adenine and Disease Exacerbation studies

Research Excerpts

Excerpt	Relevance	Reference
"A large clinic cohort of chronic hepatitis B cirrhotic patients were enrolled in a treatment program of lamivudine ± adefovir therapy."	9.15	Clinical outcomes of lamivudine-adefovir therapy in chronic hepatitis B cirrhosis. ( Aung, MO; Dan, YY; Fernandes, M; Lai, V; Lee, GH; Lee, YM; Lim, SG; Low, HC; Mak, B; Sutedja, D, 2011)
"A total of 145 lamivudine-resistant patients with chronic hepatitis B (73% cirrhotics, 86% hepatitis B e antigen negative, 92% genotype D) were treated with adefovir 10 mg in addition to lamivudine 100 mg."	9.12	Low resistance to adefovir combined with lamivudine: a 3-year study of 145 lamivudine-resistant hepatitis B patients. ( Colombo, M; Iavarone, M; Lampertico, P; Manenti, E; Sablon, E; Viganò, M, 2007)
"To evaluate the cost effectiveness of treatment of hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) with entecavir compared with lamivudine with adefovir salvage, based primarily on the results of a recent 2-year, randomised, multicentre, clinical trial (n = 709)."	9.12	Cost effectiveness of entecavir versus lamivudine with adefovir salvage in HBeAg-positive chronic hepatitis B. ( Clarke, L; Di Bisceglie, A; Gish, RG; Iloeje, UH; Kowdley, KV; Sullivan, SD; Tafesse, E; Veenstra, DL, 2007)
"This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of tenofovir disoproxil fumarate for the treatment of chronic hepatitis B, in accordance with the licensed indication, based upon the evidence submission from Gilead to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process."	8.86	Tenofovir disoproxil fumarate for the treatment of chronic hepatitis B infection. ( Colquitt, J; Cooper, K; Harris, P; Jones, J; Shepherd, J, 2010)
"To investigate the process by which quercetin suppresses atherosclerosis by upregulating MST1-mediated autophagy in RAW264."	7.91	Quercetin Suppresses the Progression of Atherosclerosis by Regulating MST1-Mediated Autophagy in ox-LDL-Induced RAW264.7 Macrophage Foam Cells. ( Cao, H; Chen, C; Jia, Q; Shen, D; Xing, S; Yan, L, 2019)
"The aims of this study were to select the patients with a potential for progression to hepatic failure due to lamivudine-resistant HBV and to standardize the treatment for patients with lamivudine-resistant HBV."	7.74	Predictive factors associated with the progression to hepatic failure caused by lamivudine-resistant HBV. ( Hino, T; Hisamochi, A; Ide, T; Koga, H; Koga, Y; Kumashiro, R; Kuwahara, R; Ogata, K; Sata, M; Takao, Y; Tanaka, K, 2008)
"Altered cyclin D1 (CD1), a cell cycle regulator, may play an important role in imparting aggressive nature to esophageal adenocarcinoma (EAC)."	7.74	Cyclin D1 guanine/adenine 870 polymorphism with altered protein expression is associated with genomic instability and aggressive clinical biology of esophageal adenocarcinoma. ( Ajani, JA; Chao, CK; Correa, A; Ensor, J; Hittelman, WN; Izzo, JG; Luthra, R; Pan, J; Swisher, SG; Wu, TT; Wu, X, 2007)
"Incomplete virological response to adefovir dipivoxil (ADV) has been observed in patients with lamivudine-resistant hepatitis B virus (HBV) infection and may be associated with developing resistance and disease progression."	7.73	Tenofovir for patients with lamivudine-resistant hepatitis B virus (HBV) infection and high HBV DNA level during adefovir therapy. ( Berg, T; Feucht, HH; Hüppe, D; Möller, B; Sarrazin, C; Spengler, U; van Bömmel, F; Wiedenmann, B; Zöllner, B, 2006)
"The susceptibility of adefovir-resistant hepatitis B virus (HBV) mutants is only reduced by 3-10-fold in in vitro studies, suggesting that virologic breakthrough and clinical deterioration are unlikely."	7.73	Adefovir-resistant hepatitis B can be associated with viral rebound and hepatic decompensation. ( Andreone, P; Cursaro, C; Fung, SK; Han, SH; Hussain, M; Keeffe, EB; Lok, AS; Marrero, JA; Rajender Reddy, K; Regev, A; Richtmyer, P, 2005)
"A large clinic cohort of chronic hepatitis B cirrhotic patients were enrolled in a treatment program of lamivudine ± adefovir therapy."	5.15	Clinical outcomes of lamivudine-adefovir therapy in chronic hepatitis B cirrhosis. ( Aung, MO; Dan, YY; Fernandes, M; Lai, V; Lee, GH; Lee, YM; Lim, SG; Low, HC; Mak, B; Sutedja, D, 2011)
"A total of 145 lamivudine-resistant patients with chronic hepatitis B (73% cirrhotics, 86% hepatitis B e antigen negative, 92% genotype D) were treated with adefovir 10 mg in addition to lamivudine 100 mg."	5.12	Low resistance to adefovir combined with lamivudine: a 3-year study of 145 lamivudine-resistant hepatitis B patients. ( Colombo, M; Iavarone, M; Lampertico, P; Manenti, E; Sablon, E; Viganò, M, 2007)
"To evaluate the cost effectiveness of treatment of hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) with entecavir compared with lamivudine with adefovir salvage, based primarily on the results of a recent 2-year, randomised, multicentre, clinical trial (n = 709)."	5.12	Cost effectiveness of entecavir versus lamivudine with adefovir salvage in HBeAg-positive chronic hepatitis B. ( Clarke, L; Di Bisceglie, A; Gish, RG; Iloeje, UH; Kowdley, KV; Sullivan, SD; Tafesse, E; Veenstra, DL, 2007)
"This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of tenofovir disoproxil fumarate for the treatment of chronic hepatitis B, in accordance with the licensed indication, based upon the evidence submission from Gilead to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process."	4.86	Tenofovir disoproxil fumarate for the treatment of chronic hepatitis B infection. ( Colquitt, J; Cooper, K; Harris, P; Jones, J; Shepherd, J, 2010)
" Treatment options for chronic hepatitis B include pegylated interferon and 4 licensed oral nucleosides/nucleotides (lamivudine, adefovir entecavir and tenofovir)."	4.84	[Chronic hepatitis B: current therapy]. ( Buffet, C, 2008)
"In spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD), the expanded cytosine adenine guanine (CAG) repeat in ATXN3 is the causal mutation, and its length is the main factor in determining the age at onset (AO) of clinical symptoms."	4.02	CAG Repeat Size Influences the Progression Rate of Spinocerebellar Ataxia Type 3. ( Brunt, ER; de Mattos, EP; de Vries, JJ; Jardim, LB; Kampinga, HH; Leotti, VB; Oliveira, CM; Te Meerman, GJ; Verbeek, DS, 2021)
"To investigate the process by which quercetin suppresses atherosclerosis by upregulating MST1-mediated autophagy in RAW264."	3.91	Quercetin Suppresses the Progression of Atherosclerosis by Regulating MST1-Mediated Autophagy in ox-LDL-Induced RAW264.7 Macrophage Foam Cells. ( Cao, H; Chen, C; Jia, Q; Shen, D; Xing, S; Yan, L, 2019)
"Adenine phosphoribosyltransferase (APRT) deficiency is a hereditary purine metabolism disorder that causes kidney stones and chronic kidney disease (CKD)."	3.91	Long-term renal outcomes of APRT deficiency presenting in childhood. ( Agustsdottir, IM; Edvardsson, VO; Indridason, OS; Palsson, R; Runolfsdottir, HL, 2019)
"To analyze the effects of preexisting lamivudine (LAM) resistance and applying antiviral treatment (adefovir [ADV] add-on LAM combination treatment) on long-term treatment outcomes, and comparing the clinical outcomes of antiviral-naïve chronic hepatitis B patients receiving entecavir (ETV) monotherapy."	3.83	Comparison of the clinical outcomes between antiviral-naïve patients treated with entecavir and lamivudine-resistant patients receiving adefovir add-on lamivudine combination treatment. ( Cho, YK; Choi, KY; Jeon, WK; Jung, YS; Kim, BI; Kim, HJ; Park, DI; Park, JH; Park, SK; Sohn, CI; Yang, HJ, 2016)
" Adefovir, entecavir, tenofovir and lamivudine (with rescue therapy in cases of viral resistance) were compared for treating adult patients with chronic hepatitis B undergoing treatment for the first time, with high levels of alanine aminotransferase, no evidence of cirrhosis and without HIV co-infection."	3.79	Incorporated antivirals for chronic hepatitis B in Brazil: a cost-effectiveness analysis. ( Acurcio, Fde A; Almeida, AM; Andrade, EI; Brandão, CM; Cherchiglia, ML; Oliveira, GL; Silva, AL, 2013)
"After adenine dosing, significant hyperphosphatemia, hypocalcemia and secondary hyperparathyroidism (2HPT) were observed during the experimental period of 15 weeks."	3.75	Vascular calcification and secondary hyperparathyroidism of severe chronic kidney disease and its relation to serum phosphate and calcium levels. ( Fujimori, A; Fukushima, S; Itoh, H; Mizukami, K; Nara, H; Okada, M; Sanagi, M; Takakura, K; Terai, K, 2009)
"The aims of this study were to select the patients with a potential for progression to hepatic failure due to lamivudine-resistant HBV and to standardize the treatment for patients with lamivudine-resistant HBV."	3.74	Predictive factors associated with the progression to hepatic failure caused by lamivudine-resistant HBV. ( Hino, T; Hisamochi, A; Ide, T; Koga, H; Koga, Y; Kumashiro, R; Kuwahara, R; Ogata, K; Sata, M; Takao, Y; Tanaka, K, 2008)
"Altered cyclin D1 (CD1), a cell cycle regulator, may play an important role in imparting aggressive nature to esophageal adenocarcinoma (EAC)."	3.74	Cyclin D1 guanine/adenine 870 polymorphism with altered protein expression is associated with genomic instability and aggressive clinical biology of esophageal adenocarcinoma. ( Ajani, JA; Chao, CK; Correa, A; Ensor, J; Hittelman, WN; Izzo, JG; Luthra, R; Pan, J; Swisher, SG; Wu, TT; Wu, X, 2007)
"Incomplete virological response to adefovir dipivoxil (ADV) has been observed in patients with lamivudine-resistant hepatitis B virus (HBV) infection and may be associated with developing resistance and disease progression."	3.73	Tenofovir for patients with lamivudine-resistant hepatitis B virus (HBV) infection and high HBV DNA level during adefovir therapy. ( Berg, T; Feucht, HH; Hüppe, D; Möller, B; Sarrazin, C; Spengler, U; van Bömmel, F; Wiedenmann, B; Zöllner, B, 2006)
"The susceptibility of adefovir-resistant hepatitis B virus (HBV) mutants is only reduced by 3-10-fold in in vitro studies, suggesting that virologic breakthrough and clinical deterioration are unlikely."	3.73	Adefovir-resistant hepatitis B can be associated with viral rebound and hepatic decompensation. ( Andreone, P; Cursaro, C; Fung, SK; Han, SH; Hussain, M; Keeffe, EB; Lok, AS; Marrero, JA; Rajender Reddy, K; Regev, A; Richtmyer, P, 2005)
"Most patients with follicular lymphoma (FL) experience multiple relapses necessitating subsequent lines of therapy."	2.87	Single-agent ibrutinib in relapsed or refractory follicular lymphoma: a phase 2 consortium trial. ( Anderson, DM; Ansell, SM; Bartlett, NL; Costello, BA; Fehniger, TA; Gomez, F; Griffith, M; Griffith, OL; Krysiak, K; Kuruvilla, JG; LaPlant, BR; Qi, J; Ramirez, C; Reeder, CB; Siegel, BA; Thye, LS, 2018)
" Venetoclax is a selective, orally bioavailable inhibitor of BCL-2 active in previously treated patients with relapsed or refractory chronic lymphocytic leukaemia."	2.87	Venetoclax for chronic lymphocytic leukaemia progressing after ibrutinib: an interim analysis of a multicentre, open-label, phase 2 trial. ( Barr, PM; Byrd, JC; Cheson, BD; Choi, M; Chyla, B; Coutre, S; Davids, MS; Furman, RR; Humerickhouse, RA; Jones, JA; Lamanna, N; Mato, AR; Potluri, J; Salem, AH; Verdugo, M; Wierda, WG; Woyach, J; Zhou, L, 2018)
"Treatment of chronic lymphocytic leukemia (CLL) has shifted from chemo-immunotherapy to targeted agents."	2.84	The evolutionary landscape of chronic lymphocytic leukemia treated with ibrutinib targeted therapy. ( Bozic, I; Burger, JA; Cibulskis, C; Farooqui, MZH; Fein, J; Getz, G; Herman, SEM; Hoellenriegel, J; Landau, DA; Leshchiner, I; Liu, D; Livitz, D; Neuberg, DS; Ravichandran, S; Rosebrock, D; Sivina, M; Sun, C; Underbayev, C; Wiestner, A; Wu, CJ; Zhang, W; Zviran, A, 2017)
"Between Sept 19, 2012, and Jan 21, 2014, 578 eligible patients were randomly assigned to ibrutinib or placebo in combination with bendamustine plus rituximab (289 in each group)."	2.82	Ibrutinib combined with bendamustine and rituximab compared with placebo, bendamustine, and rituximab for previously treated chronic lymphocytic leukaemia or small lymphocytic lymphoma (HELIOS): a randomised, double-blind, phase 3 study. ( Avigdor, A; Balasubramanian, S; Bartlett, NL; Chanan-Khan, A; Cramer, P; Demirkan, F; Dilhuydy, MS; Fraser, G; Goy, A; Grosicki, S; Hallek, M; Howes, A; Janssens, A; Karlsson, C; Loscertales, J; Mahler, M; Mato, A; Mayer, J; Panagiotidis, P; Pavlovsky, MA; Phelps, C; Pristupa, A; Pylypenko, H; Rule, S; Salman, M; Samoilova, O; Silva, RS; Sun, S; Villa, D, 2016)
"Differences in disease progression occurred from the third year on ART, whereas higher rates of switch to second-line treatment occurred in LCM from the second year."	2.75	Routine versus clinically driven laboratory monitoring of HIV antiretroviral therapy in Africa (DART): a randomised non-inferiority trial. ( Abaine, D; Aber, M; Ahimbisibwe, F; Akao, J; Akuma, S; Amuron, B; Amurwon, J; Angweng, E; Anywar, W; Atwiine, D; Atwiine, S; Awio, P; Babiker, A; Babiker, AG; Bafana, T; Bagaya, L; Bahendeka, S; Bakeinyaga, GT; Barungi, G; Bassett, M; Bohannon, J; Boocock, K; Borok, M; Bray, D; Breckenridge, A; Bulaya-Tembo, R; Buluma, E; Burke, A; Burke, C; Byakwaga, H; Byamukama, A; Byaruhanga, R; Chakonza, L; Chidziva, E; Chigwedere, E; Chimanzi, J; Chimbetete, C; Chirairo, H; Chirara, M; Chirema, O; Chitsungo, S; Chivhunga, T; Coutinho, A; Darbyshire, JH; Drasiku, A; Dunn, D; Enzama, R; Etukoit, B; Fadhiru, K; Ferrier, A; Florence, A; Foster, S; Gazzard, B; Generous, L; Gibb, DM; Gilks, C; Gilks, CF; Goodall, R; Grosskurth, H; Grundy, C; Haguma, W; Hakim, J; Hill, C; Hughes, P; Jamu, A; Jangano, M; Jones, S; Kabanda, J; Kabuye, G; Kagina, G; Kajungu, D; Kaleebu, P; Kambungu, A; Kankunda, R; Karungi, J; Kasirye, R; Katabira, E; Katabira, H; Katundu, P; Khauka, P; Kigozi, J; Kikaire, B; Kityo, C; Komugyena, J; Kulume, R; Kusiima, A; Kyomugisha, H; Labeja, O; Lara, AM; Latif, A; Levin, J; Lubwama, E; Lutwama, F; Lyagoba, F; Machingura, I; Machingura, J; Makota, S; Mambule, I; Mapinge, F; Mapuchere, C; Massa, R; Matenga, J; Matongo, M; Maweni, C; Mawora, A; McCormick, A; McLaren, A; Mdege, N; Moyo, K; Muchabaiwa, L; Mudzingwa, S; Mufuka-Kapuya, C; Muganzi, A; Mugisha, A; Mugurungi, O; Mugyenyi, P; Muhweezi, D; Muhwezi, A; Mukiibi, S; Mukose, A; Mulindwa, G; Mulindwa, M; Munderi, P; Murungi, S; Musana, H; Musoro, G; Mutowo, J; Mutsai, S; Muvirimi, C; Muyingo, S; Muzambi, M; Mwebesa, D; Mwesigwa, P; Nabankema, E; Nabongo, P; Naidoo, B; Nairuba, R; Nakahima, W; Nakazibwe, M; Nakiyingi, J; Nalumenya, R; Namale, L; Namara, W; Namata, I; Namazzi, A; Namuli, T; Namyalo, M; Nanfuka, A; Nanfuka, R; Nassuna, G; Ndembi, N; Newland, C; Ngorima, N; Nimwesiga, E; Nsibambi, D; Nyachwo, L; Nyiraguhirwa, D; Ochai, R; Ojiambo, H; Ojiambo, W; Oketta, F; Omony, W; Otim, T; Oyugi, J; Palfreeman, A; Pascoe, M; Pearce, G; Peto, L; Peto, T; Phiri, M; Pillay, D; Pozniak, A; Puddephatt, C; Rahim, S; Rauchenberger, M; Reid, A; Robertson, V; Ronald, A; Rooney, J; Ruberantwari, A; Rutikarayo, N; Sabiiti, J; Sadik, F; Sematala, F; Serwadda, D; Sheehan, S; Simango, M; Smith, M; Snowden, W; Spencer-Drake, C; Spyer, M; Ssali, F; Steens, JM; Svovanapasis, P; Takubwa, J; Taylor, K; Taziwa, F; Tinago, G; Todd, J; Tugume, S; Tukamushaba, J; Tumukunde, D; Tumusiime, C; Twijukye, C; Vere, L; Waita, R; Wakholi, BN; Walker, AS; Walusimbi, J; Wangati, K; Wanyama, J; Wapakhabulo, AC; Warambwa, C; Warara, R; Wavamunno, P; Weller, I; Whitworth, J; Wilkes, H; Winogron, D; Yirrell, D; Zalwango, A; Zalwango, E; Zawedde, C; Zengeza, E, 2010)
"Type 2 diabetes is caused by defective insulin secretion and impaired insulin action."	2.71	Polymorphisms of the SUR1 (ABCC8) and Kir6.2 (KCNJ11) genes predict the conversion from impaired glucose tolerance to type 2 diabetes. The Finnish Diabetes Prevention Study. ( Eriksson, J; Hämäläinen, H; Ilanne-Parikka, P; Keinänen-Kiukaanniemi, S; Laakso, M; Laukkanen, O; Lindström, J; Pihlajamäki, J; Tuomilehto, J; Uusitupa, M; Valle, TT, 2004)
"EMT is involved in tumor metastasis because it leads to cancer cell migration and invasion, and is also associated with chemoresistance."	2.66	Regulation of Epithelial-to-Mesenchymal Transition by Alternative Translation Initiation Mechanisms and Its Implications for Cancer Metastasis. ( Bera, A; Lewis, SM, 2020)
"Those who develop disease progression on ibrutinib are a particularly high-risk population with poor outcomes."	2.58	Management of patients with chronic lymphocytic leukemia at high risk of relapse on ibrutinib therapy. ( Ayed, AO; Parikh, SA, 2018)
"Proteinuria is also now recognized as a common finding in individuals living with HIV."	2.55	Renal effects of novel antiretroviral drugs. ( Jones, R; Levy, JB; Milburn, J, 2017)
"Specialized treatment of CHB in pregnancy, coinfection, decompensated cirrhosis, and posttransplant is safe and effective."	2.48	New advances in chronic hepatitis B. ( Lee, WM; Tujios, SR, 2012)
"Those at risk for liver disease progression are usually treated with a combination of interferon (IFN) and ribavirin (RBV), which is not highly effective; it has low rates of sustained virologic response (SVR), especially for coinfected patients with HCV genotype 1 and those of African descent."	2.48	Management of patients coinfected with HCV and HIV: a close look at the role for direct-acting antivirals. ( Naggie, S; Sulkowski, MS, 2012)
"Acute renal failure is common in HIV-infected patients and is associated with acute infection and medication-related nephrotoxicity."	2.44	HIV-1 infection and the kidney: an evolving challenge in HIV medicine. ( de Silva, TI; Dockrell, DH; Griffin, MD; Post, FA, 2007)
"To address the clinical management of chronic hepatitis B virus (HBV) infection."	2.43	Management of chronic hepatitis B virus infection: current perspectives for the nurse practitioner. ( Perrillo, R, 2006)
"About 350 million people worldwide have chronic hepatitis B virus (HBV) infection."	2.42	Slowing the progression of chronic hepatitis B. Early antiviral therapy can help minimize complications. ( Jacobson, IM; Purow, DB, 2003)
"Lamivudine appears to be a safe and effective antiviral agent, which may improve or stabilize liver disease in selected patients with advanced cirrhosis and active HBV replication."	2.42	Management of patients with decompensated HBV cirrhosis. ( Fontana, RJ, 2003)
"Airway inflammation is a key factor in the mechanisms of asthma."	2.42	Mechanisms of asthma. ( Busse, WW; Rosenwasser, LJ, 2003)
"Lamivudine has been introduced as an alternative to IFN, showing at least similar efficacy, but with a wider spectrum of indications and without the adverse effects."	2.41	Drug therapy for hepatitis B. ( Regev, A; Schiff, ER, 2001)
"Oesophageal cancer is the fifth most frequent cause of cancer death world wide and most of these cancers occur in developing countries."	2.40	Molecular precursor lesions in oesophageal cancer. ( Hainaut, P; Montesano, R, 1998)
"An adenine diet was administered to male Wistar rats to induce AMC."	1.91	Towards a better understanding of arterial calcification disease progression in CKD: investigation of early pathological alterations. ( D'Haese, P; De Meyer, G; Guns, PJ; Neutel, C; Opdebeeck, B; Van den Bergh, G; Verhulst, A, 2023)
"BACKGROUND Chronic lymphocytic leukemia (CLL) is a mature B-cell neoplasm and the most common leukemia in adults in Western countries."	1.72	An 81-Year-Old Man with a 6-Year History of Chronic Lymphocytic Leukemia Presenting with Disease Flare Following Ibrutinib Discontinuation. ( Colaci, E; Giusti, D; Leonardi, G; Luppi, M; Maccaferri, M; Marasca, R; Pioli, V; Potenza, L; Pozzi, S, 2022)
"Among patients with CLL disease progression on ibrutinib, OS was significantly longer when next-line treatment was chimeric antigen receptor T-cell therapy (median not reached) or venetoclax-based treatment (median 29."	1.72	Clinical outcomes in patients with chronic lymphocytic leukemia with disease progression on ibrutinib. ( Ailawadhi, S; Braggio, E; Call, TG; Chanan-Khan, AA; Ding, W; Hampel, PJ; Hanson, CA; Kay, NE; Kenderian, SS; Koehler, AB; Leis, JF; Muchtar, E; Parikh, SA; Parrondo, R; Rabe, KG; Schwager, SM; Sher, T; Shi, M; Slager, SL; Van Dyke, DL; Wang, Y, 2022)
"Ibrutinib is an established treatment for relapsed/refractory (R/R) mantle cell lymphoma (MCL) and clinical trial data supports use at second line compared to later relapse."	1.62	Ibrutinib for mantle cell lymphoma at first relapse: a United Kingdom real-world analysis of outcomes in 211 patients. ( Arasaretnam, A; Bishton, M; Bolam, S; Creasey, T; Crosbie, N; Dawi, S; Dutton, D; Eyre, TA; Follows, G; Goradia, H; Harrison, S; Johnston, R; Kirkwood, AA; Lambert, J; Lewis, D; McCulloch, R; McKay, P; McMillan, A; Miles, O; Osborne, W; Patmore, R; Phillips, N; Robinson, A; Rule, S; Wilson, MR, 2021)
"Cardiorenal syndrome is a major cause of mortality in patients with chronic kidney disease (CKD)."	1.56	The guanylate cyclase C agonist linaclotide ameliorates the gut-cardio-renal axis in an adenine-induced mouse model of chronic kidney disease. ( Abe, T; Akiyama, Y; Asaji, K; Fukuda, S; Ho, HJ; Ito, S; Iwasaki, T; Kanemitsu, Y; Kikuchi, K; Kure, S; Matsuhashi, T; Mishima, E; Nanto-Hara, F; Oikawa, Y; Owada, Y; Saigusa, D; Soga, T; Suzuki, C; Suzuki, T; Tomioka, Y; Tsukimi, T, 2020)
"Using an orthotopic mouse breast cancer model, we show that ibrutinib inhibits the progression and metastasis of breast cancer."	1.56	Ibrutinib treatment inhibits breast cancer progression and metastasis by inducing conversion of myeloid-derived suppressor cells to dendritic cells. ( Ahirwar, DK; Ganju, RK; Halsey, G; Hamza, O; Holcomb, EA; Jha, BK; Maryala, RJ; Oghumu, S; Saljoughian, N; Satoskar, AR; Singh, B; Varikuti, S; Verma, C; Viana, AG; Volpedo, G, 2020)
" Emerging real-world-data shows similar response and survival, but higher discontinuation rates due to adverse events (AEs)."	1.51	Safety and efficacy analysis of long-term follow up real-world data with ibrutinib monotherapy in 58 patients with CLL treated in a single-center in Greece. ( Angelopoulou, M; Bitsani, C; Dimou, M; Iliakis, T; Kalyva, S; Koudouna, A; Kyrtsonis, MC; Panayiotidis, P; Papaioannou, P; Pardalis, V; Tsaftaridis, P; Vassilakopoulos, TP, 2019)
"The median times to disease progression and RT were 33."	1.51	Targeted multigene deep sequencing of Bruton tyrosine kinase inhibitor-resistant chronic lymphocytic leukemia with disease progression and Richter transformation. ( Alhalouli, T; Bueso-Ramos, C; Burger, J; Estrov, Z; Ferrajoli, A; Jain, N; Jain, P; Kanagal-Shamanna, R; Kantarjian, HM; Keating, M; Khoury, JD; Luthra, R; Medeiros, LJ; Patel, KP; Routbort, M; Wierda, W, 2019)
" These findings suggest deterioration of the humoral immune system is associated with progressive CLL and altering the dosing of IgRT to achieve higher than conventional IgG target levels may have therapeutic activity."	1.48	Association of blood IgG with tumor necrosis factor-alpha and clinical course of chronic lymphocytic leukemia. ( Huang, J; Lazarus, A; Norris, P; Shi, Y; Spaner, DE; Venema, R; Wang, G, 2018)
"In areas where chronic hepatitis B virus infection is prevalent, acute hepatitis E virus superinfection on chronic hepatitis B virus infection occurs sporadically."	1.48	Seroclearance of hepatitis B surface antigen following hepatitis E exacerbation on chronic hepatitis E and B dual infection in a renal transplant recipient: a case report. ( Chiang, YJ; Chu, YD; Yeh, CS; Yeh, CT, 2018)
"We conducted a retrospective analysis of chronic lymphocytic leukemia patients treated with ibrutinib either commercially or on clinical trials."	1.48	Toxicities and outcomes of 616 ibrutinib-treated patients in the United States: a real-world analysis. ( Bachow, SH; Barr, P; Brander, DM; Cheson, BD; Claxton, D; Dorsey, C; Goy, A; Hill, B; Howlett, C; Isaac, K; Kennard, KH; Kiselev, P; Lamanna, N; Landsburg, D; Mato, AR; Nabhan, C; Nasta, SD; Pu, J; Schuster, SJ; Skarbnik, A; Svoboda, J; Thompson, MC; Timlin, C; Ujjani, CS; Winter, A; Zent, C, 2018)
"Reasons for discontinuation include: disease progression (n = 27; 14%), toxicity (n = 15; 8%), nonresponse (n = 5; 3%), and other unrelated reasons (n = 4; 2%)."	1.48	Ibrutinib discontinuation in Waldenström macroglobulinemia: Etiologies, outcomes, and IgM rebound. ( Castillo, JJ; Dubeau, T; Guang, Y; Gustine, JN; Hunter, ZR; Meid, K; Severns, P; Treon, SP; Xu, L, 2018)
"The established treatment algorithms for chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) are currently challenged by novel classes of drugs, with ibrutinib being one of the most effective."	1.46	Hodgkin Lymphoma Transformation of Chronic Lymphocytic Leukemia Under Ibrutinib Therapy: Chance Association or Therapy-related? ( Kalpadakis, C; Koulieris, E; Moschogiannis, M; Pangalis, GA; Rontogianni, D; Sachanas, S; Tsirkinidis, P; Yiakoumis, X, 2017)
"Lenalidomide-based treatment showed clinical activity, with no unexpected toxicities, in patients with relapsed/refractory mantle cell lymphoma who previously failed ibrutinib therapy."	1.46	Observational study of lenalidomide in patients with mantle cell lymphoma who relapsed/progressed after or were refractory/intolerant to ibrutinib (MCL-004). ( Barnett, E; Bravo, MC; Ghosh, N; Goy, A; Hamadani, M; Lossos, IS; Martin, P; Phillips, T; Reeder, CB; Rule, S; Schuster, SJ; Wang, M, 2017)
"Richter syndrome (RS) is a rare event in chronic lymphocytic leukemia (CLL) that is influenced by biological factors and prior CLL treatments."	1.46	Ibrutinib treatment of a patient with relapsing chronic lymphocytic leukemia and sustained remission of Richter syndrome. ( Albi, E; Ascani, S; Aureli, P; Baldoni, S; Del Papa, B; Di Ianni, M; Dorillo, E; Falzetti, F; Sportoletti, P, 2017)
"Ninety-five consecutive patients (93 chronic lymphocytic leukemia, 2 small lymphocytic leukemia) were included in the study between May 2014 and May 2015."	1.43	Real-world results of ibrutinib in patients with relapsed or refractory chronic lymphocytic leukemia: data from 95 consecutive patients treated in a compassionate use program. A study from the Swedish Chronic Lymphocytic Leukemia Group. ( Andersson, PO; Asklid, A; Hansson, L; Karlsson, C; Karlsson, K; Lauri, B; Lundin, J; Mattsson, M; Norin, S; Österborg, A; Sandstedt, A; Winqvist, M, 2016)
"Among 31 patients who experienced disease progression following ibrutinib and underwent salvage therapy, the overall and complete response rates were 32% and 19%, respectively."	1.42	Patients with mantle cell lymphoma failing ibrutinib are unlikely to respond to salvage chemotherapy and have poor outcomes. ( Champlin, RE; Cheah, CY; Chihara, D; Fowler, NH; Hagemeister, FB; Romaguera, JE; Seymour, JF; Wang, ML, 2015)
"Chronic Obstructive Pulmonary Disease (COPD) represents a group of disorders with several underlying causes that hamper airflow into the lungs."	1.40	Combined inhibition of PDE4 and PI3Kδ modulates the inflammatory component involved in the progression of chronic obstructive pulmonary disease. ( Dharmarajan, S; Dinavahi, SS; Nyayapathy, S; Perumal, Y; Viswanadha, S, 2014)
"Acetaminophen is a safe antipyretic and analgesic drug within the clinically recommended dosage range, but overdose can cause fatal liver and or kidney damage."	1.38	Effect of acetaminophen on the progression of renal damage in adenine induced renal failure model rats. ( Arimizu, K; Chuang, VT; Hirata, S; Irie, T; Ishitsuka, Y; Kadowaki, D; Kitamura, K; Maruyama, T; Narita, Y; Otagiri, M; Sumikawa, S; Taguchi, K, 2012)
"Systemic lupus erythematosus is a polymorphic and multigenic inflammatory autoimmune disease."	1.38	Disease progression in MRL/lpr lupus-prone mice is reduced by NCS 613, a specific cyclic nucleotide phosphodiesterase type 4 (PDE4) inhibitor. ( Bourguignon, JJ; Gazi, L; Keravis, T; Lugnier, C; Monneaux, F; Muller, S; Yougbaré, I, 2012)
"Several animal models with chronic renal failure have been established and used for demonstrating complications including hyperphosphataemia."	1.35	Comparison of chronic renal failure rats and modification of the preparation protocol as a hyperphosphataemia model. ( Mizukami, K; Okada, M; Terai, K, 2008)
"Idiopathic dilated cardiomyopathy (IDC) has multiple genetic and acquired causes."	1.34	The 212A variant of the APJ receptor gene for the endogenous inotrope apelin is associated with slower heart failure progression in idiopathic dilated cardiomyopathy. ( Capestro, A; Dessì-Fulgheri, P; Forleo, C; Guida, P; Iacoviello, M; Pietrucci, F; Pitzalis, M; Rappelli, A; Romito, R; Sarzani, R; Sorrentino, S; Soura, E, 2007)
"However, in chronic renal failure (CRF), serum 1,25(OH)(2)D and Pi levels are often abnormal."	1.33	Nicotinamide prevents the development of hyperphosphataemia by suppressing intestinal sodium-dependent phosphate transporter in rats with adenine-induced renal failure. ( Eto, N; Miyata, Y; Ohno, H; Yamashita, T, 2005)
"Treatment of chronic hepatitis B (CHB) involves a number of complex and controversial issues."	1.33	Chronic hepatitis B: a critical appraisal of current approaches to therapy. ( Alberti, A; Buti, M; Cooksley, WG; Fried, MW; Gish, RG; Hadziyannis, SJ; Keeffe, EB; Liaw, YF; Naoumov, NV; Perrillo, RP; Peters, M; Schalm, S; Schiff, ER; Thio, CL; Tsai, N, 2006)
"Renal involvement in patients with systemic lupus erythematosus (SLE) varies from none to full-blown disease."	1.31	The polymorphism of monocyte chemoattractant protein-1 is associated with the renal disease of SLE. ( Chung, JH; Kim, HL; Kim, S; Kim, YS; Lee, DS; Lee, JS; Lim, CS; Yang, SH, 2002)

Research

Studies (175)

Authors

Clinical Trials (27)

Trial Overview

Trial Outcomes

Overall Survival (OS) Rate at 3 Years

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	3 (1.71)	18.2507
2000's	42 (24.00)	29.6817
2010's	100 (57.14)	24.3611
2020's	30 (17.14)	2.80

Authors	Studies
Langerbeins, P	2
Zhang, C	4
Robrecht, S	1
Cramer, P	3
Fürstenau, M	1
Al-Sawaf, O	1
von Tresckow, J	1
Fink, AM	1
Kreuzer, KA	2
Vehling-Kaiser, U	1
Tausch, E	1
Müller, L	1
Eckart, MJ	1
Schlag, R	1
Freier, W	1
Gaska, T	1
Balser, C	1
Reiser, M	1
Stauch, M	1
Wendtner, CM	2
Fischer, K	2
Stilgenbauer, S	3
Eichhorst, B	2
Hallek, M	3
Jain, P	6
Zhao, S	2
Lee, HJ	2
Hill, HA	1
Ok, CY	1
Kanagal-Shamanna, R	3
Hagemeister, FB	2
Fowler, N	2
Fayad, L	2
Yao, Y	4
Liu, Y	8
Moghrabi, OB	1
Navsaria, L	1
Feng, L	1
Nogueras Gonzalez, GM	1
Xu, G	2
Thirumurthi, S	1
Santos, D	1
Iliescu, C	1
Tang, G	1
Medeiros, LJ	3
Vega, F	1
Avellaneda, M	1
Badillo, M	1
Flowers, CR	1
Wang, L	4
Wang, ML	3
Ito, S	5
Manabe, E	1
Dai, Y	1
Ishihara, M	1
Tsujino, T	1
Shanafelt, TD	1
Wang, XV	1
Hanson, CA	2
Paietta, EM	1
O'Brien, S	5
Barrientos, J	1
Jelinek, DF	1
Braggio, E	2
Leis, JF	2
Zhang, CC	1
Coutre, SE	1
Barr, PM	5
Cashen, AF	1
Mato, AR	6
Singh, AK	1
Mullane, MP	1
Little, RF	1
Erba, H	1
Stone, RM	1
Litzow, M	1
Tallman, M	1
Kay, NE	2
Jurczak, W	2
Jerkeman, M	1
Trotman, J	1
Zinzani, PL	1
Belada, D	1
Boccomini, C	1
Flinn, IW	1
Giri, P	1
Goy, A	6
Hamlin, PA	1
Hermine, O	1
Hernández-Rivas, JÁ	1
Hong, X	1
Kim, SJ	2
Lewis, D	2
Mishima, Y	1
Özcan, M	1
Perini, GF	1
Pocock, C	1
Song, Y	2
Spurgeon, SE	1
Storring, JM	1
Walewski, J	1
Zhu, J	3
Qin, R	1
Henninger, T	1
Deshpande, S	1
Howes, A	2
Le Gouill, S	1
Dreyling, M	2
Pozzi, S	1
Potenza, L	1
Giusti, D	1
Colaci, E	1
Pioli, V	1
Leonardi, G	1
Maccaferri, M	1
Luppi, M	1
Marasca, R	1
Hampel, PJ	1
Rabe, KG	1
Call, TG	1
Ding, W	1
Chanan-Khan, AA	1
Kenderian, SS	1
Muchtar, E	2
Wang, Y	9
Ailawadhi, S	1
Koehler, AB	1
Parrondo, R	1
Schwager, SM	1
Sher, T	1
Shi, M	1
Van Dyke, DL	1
Slager, SL	1
Parikh, SA	3
Van den Bergh, G	1
Opdebeeck, B	1
Neutel, C	1
Guns, PJ	1
De Meyer, G	1
D'Haese, P	1
Verhulst, A	1
Shuvy, M	1
Abedat, S	1
Eliaz, R	1
Abu-Rmeileh, I	1
Abu-Snieneh, A	1
Ben-Dov, IZ	1
Meir, K	1
Pereg, D	1
Beeri, R	1
Lotan, C	1
Nanto-Hara, F	1
Kanemitsu, Y	2
Fukuda, S	3
Kikuchi, K	3
Asaji, K	2
Saigusa, D	1
Iwasaki, T	1
Ho, HJ	1
Mishima, E	3
Suzuki, T	3
Suzuki, C	3
Tsukimi, T	1
Matsuhashi, T	1
Oikawa, Y	1
Akiyama, Y	3
Kure, S	1
Owada, Y	1
Tomioka, Y	3
Soga, T	3
Abe, T	3
Abeykoon, JP	1
Zanwar, S	1
Ansell, SM	2
Gertz, MA	1
Kumar, S	1
Manske, M	1
Novak, AJ	1
King, R	1
Greipp, P	1
Go, R	1
Inwards, D	1
Habermann, T	1
Witzig, TE	1
Thompson, CA	1
Dingli, D	1
Lacy, MQ	1
Leung, N	1
Dispenzieri, A	1
Gonsalves, W	1
Warsame, R	1
Kyle, RA	1
Rajkumar, V	1
Kapoor, P	1
Das, AA	1
Chakravarty, D	1
Bhunia, D	1
Ghosh, S	1
Mandal, PC	1
Siddiqui, KN	1
Bandyopadhyay, A	1
Wu, L	1
Pei, Y	1
Zhu, Y	2
Jiang, M	1
Wang, C	4
Cui, W	1
Zhang, D	1
Cao, H	1
Jia, Q	1
Yan, L	1
Chen, C	1
Xing, S	1
Shen, D	1
Tissino, E	1
Pozzo, F	1
Benedetti, D	1
Caldana, C	1
Bittolo, T	1
Rossi, FM	1
Bomben, R	1
Nanni, P	1
Chivilò, H	1
Cattarossi, I	1
Zaina, E	1
Norris, K	1
Polesel, J	1
Gentile, M	3
Tripepi, G	1
Moia, R	1
Santinelli, E	1
Innocenti, I	2
Olivieri, J	1
D'Arena, G	2
Laurenti, L	3
Zaja, F	1
Pozzato, G	1
Chiarenza, A	1
Di Raimondo, F	2
Rossi, D	1
Pepper, C	1
Hartmann, TN	1
Gaidano, G	2
Del Poeta, G	2
Gattei, V	1
Zucchetto, A	1
Varikuti, S	1
Singh, B	2
Volpedo, G	1
Ahirwar, DK	1
Jha, BK	1
Saljoughian, N	1
Viana, AG	1
Verma, C	1
Hamza, O	1
Halsey, G	1
Holcomb, EA	1
Maryala, RJ	1
Oghumu, S	1
Ganju, RK	1
Satoskar, AR	1
Lin, VS	1
Lew, TE	1
Handunnetti, SM	1
Blombery, P	2
Nguyen, T	1
Westerman, DA	1
Kuss, BJ	1
Tam, CS	3
Roberts, AW	1
Seymour, JF	3
Anderson, MA	1
Halim, AA	1
Alsayed, B	1
Embarak, S	1
Yaseen, T	1
Dabbous, S	1
Fontaine, O	1
Dueluzeau, R	1
Raibaud, P	1
Chabanet, C	1
Popoff, MR	1
Badoual, J	1
Gabilan, JC	1
Andremont, A	1
Gómez, L	1
Andrés, S	1
Sánchez, J	1
Alonso, JM	1
Rey, J	1
López, F	1
Jiménez, A	1
Yan, Z	1
Zhou, L	2
Zhao, Y	3
Wang, J	6
Huang, L	3
Hu, K	1
Liu, H	4
Wang, H	3
Guo, Z	1
Huang, H	5
Yang, R	1
Owen, TW	1
Al-Kaysi, RO	1
Bardeen, CJ	1
Cheng, Q	1
Wu, S	1
Cheng, T	1
Zhou, X	1
Wang, B	4
Zhang, Q	5
Wu, X	4
Ochiai, T	1
Ishiguro, H	2
Nakano, R	2
Kubota, Y	2
Hara, M	1
Sunada, K	1
Hashimoto, K	1
Kajioka, J	1
Fujishima, A	1
Jiao, J	3
Gai, QY	3
Wang, W	2
Zang, YP	2
Niu, LL	2
Fu, YJ	3
Wang, X	4
Yao, LP	1
Qin, QP	1
Wang, ZY	1
Liu, J	4
Aleksic Sabo, V	1
Knezevic, P	1
Borges-Argáez, R	1
Chan-Balan, R	1
Cetina-Montejo, L	1
Ayora-Talavera, G	1
Sansores-Peraza, P	1
Gómez-Carballo, J	1
Cáceres-Farfán, M	1
Jang, J	1
Akin, D	1
Bashir, R	1
Yu, Z	1
Jiang, H	1
He, C	2
Xiao, Z	1
Xu, J	2
Sun, Q	1
Han, D	1
Lei, H	1
Zhao, K	2
Zhu, L	1
Li, X	4
Fu, H	2
Wilson, BK	1
Step, DL	1
Maxwell, CL	1
Gifford, CA	1
Richards, CJ	1
Krehbiel, CR	1
Warner, JM	1
Doerr, AJ	1
Erickson, GE	1
Guretzky, JA	1
Rasby, RJ	1
Watson, AK	1
Klopfenstein, TJ	1
Sun, Y	4
Liu, Z	4
Pham, TD	1
Lee, BK	1
Yang, FC	1
Wu, KH	1
Lin, WP	1
Hu, MK	1
Lin, L	3
Shao, J	1
Sun, M	1
Zhang, X	7
Xu, N	1
Wang, R	1
Liu, S	2
He, H	1
Dong, X	2
Yang, M	2
Yang, Q	1
Duan, S	1
Yu, Y	2
Han, J	2
Chen, L	2
Yang, X	1
Li, W	4
Wang, T	3
Campbell, DA	1
Gao, K	1
Zager, RA	1
Johnson, ACM	1
Guillem, A	1
Keyser, J	1
Steubl, D	1
Schneider, MP	1
Meiselbach, H	1
Nadal, J	1
Schmid, MC	1
Saritas, T	1
Krane, V	1
Sommerer, C	1
Baid-Agrawal, S	1
Voelkl, J	1
Kotsis, F	1
Köttgen, A	1
Eckardt, KU	1
Scherberich, JE	1
Li, H	4
Yao, L	2
Sun, L	3
Zhu, Z	1
Naren, N	1
Zhang, XX	2
Gentile, GL	1
Rupert, AS	1
Carrasco, LI	1
Garcia, EM	1
Kumar, NG	1
Walsh, SW	1
Jefferson, KK	1
Guest, RL	1
Samé Guerra, D	1
Wissler, M	1
Grimm, J	1
Silhavy, TJ	1
Lee, JH	2
Yoo, JS	1
Kim, Y	1
Kim, JS	2
Lee, EJ	1
Roe, JH	1
Delorme, M	1
Bouchard, PA	1
Simon, M	1
Simard, S	1
Lellouche, F	1
D'Urzo, KA	1
Mok, F	1
D'Urzo, AD	1
Koneru, B	1
Lopez, G	1
Farooqi, A	1
Conkrite, KL	1
Nguyen, TH	1
Macha, SJ	1
Modi, A	1
Rokita, JL	1
Urias, E	1
Hindle, A	1
Davidson, H	1
Mccoy, K	1
Nance, J	1
Yazdani, V	1
Irwin, MS	1
Yang, S	1
Wheeler, DA	1
Maris, JM	1
Diskin, SJ	1
Reynolds, CP	1
Abhilash, L	1
Kalliyil, A	1
Sheeba, V	1
Hartley, AM	2
Meunier, B	2
Pinotsis, N	1
Maréchal, A	2
Xu, JY	1
Genko, N	1
Haraux, F	1
Rich, PR	1
Kamalanathan, M	1
Doyle, SM	1
Xu, C	1
Achberger, AM	1
Wade, TL	1
Schwehr, K	1
Santschi, PH	1
Sylvan, JB	1
Quigg, A	1
Leong, W	1
Xu, W	2
Gao, S	1
Zhai, X	1
Gilson, E	1
Ye, J	1
Lu, Y	1
Yan, R	1
Zhang, Y	6
Hu, Z	1
You, Q	1
Cai, Q	1

Trial	Phase	Enrollment	Study Type	Start Date	Status
A Placebo-Controlled, Double-Blind, Randomized, Multicenter, Three Arm Phase III Trial to Compare the Efficacy and Safety of Ibrutinib vs. Placebo in Previously Untreated Binet Stage A Chronic Lymphocytic Leukemia Patients With Risk of Early Disease Progr[NCT02863718]	Phase 3	515 participants (Actual)	Interventional	2014-04-30	Completed
A Phase II Study of Ibrutinib Plus Rituximab With Hyper-CVAD Consolidation in Newly Diagnosed Young Patients With Mantle Cell Lymphoma: A Window Period for Bioimmunotherapy Before Chemotherapy[NCT02427620]	Phase 2	131 participants (Anticipated)	Interventional	2015-06-03	Active, not recruiting
A Phase II Study of Ibrutinib Plus Rituximab in Patients With Relapsed/Refractory Mantle Cell Lymphoma or Elderly Patients With Newly Diagnosed MCL[NCT01880567]	Phase 2	113 participants (Actual)	Interventional	2013-07-15	Active, not recruiting
A Randomized Phase III Study of Ibrutinib (PCI-32765)-Based Therapy vs Standard Fludarabine, Cyclophosphamide, and Rituximab (FCR) Chemoimmunotherapy in Untreated Younger Patients With Chronic Lymphocytic Leukemia (CLL)[NCT02048813]	Phase 3	529 participants (Actual)	Interventional	2014-02-20	Active, not recruiting
A Randomized, Double-blind, Placebo-controlled Phase 3 Study of the Bruton's Tyrosine Kinase (BTK) Inhibitor, PCI-32765 (Ibrutinib), in Combination With Bendamustine and Rituximab (BR) in Subjects With Newly Diagnosed Mantle Cell Lymphoma[NCT01776840]	Phase 3	523 participants (Actual)	Interventional	2013-05-16	Active, not recruiting
Phase 2 Trial of Single-Agent Ibrutinib (PCI-32765) in Relapsed or Refractory Follicular Lymphoma[NCT01849263]	Phase 2	41 participants (Actual)	Interventional	2013-04-02	Active, not recruiting
A Multicenter, Observational Study to Evaluate the Effectiveness of Lenalidomide (Revlimid®) in Subjects With Mantle Cell Lymphoma Who Have Relapsed or Progressed After Treatment With Ibrutinib or Are Refractory or Intolerant to Ibrutinib.[NCT02341781]		30 participants (Actual)	Observational	2015-04-30	Completed
A Phase 2 Open-Label Study of the Efficacy and Safety of ABT-199 (GDC-0199) in Chronic Lymphocytic Leukemia Subjects With Relapse or Refractory to B-Cell Receptor Signaling Pathway Inhibitor Therapy[NCT02141282]	Phase 2	127 participants (Actual)	Interventional	2014-09-10	Completed
Treatment Patterns, Outcomes, and Patient-Reported Health-Related Quality of Life: A Prospective Disease Registry of Patients With Mantle Cell Lymphoma Treated With Novel Agents[NCT03816683]		229 participants (Actual)	Observational	2019-04-01	Active, not recruiting
Ibrutinib vs Ibrutinib + Rituximab (i vs iR) in Patients With Relapsed (CLL)[NCT02007044]	Phase 2	208 participants (Anticipated)	Interventional	2013-12-06	Active, not recruiting
A Phase 1 Dose-ranging Study to Investigate the Safety, Tolerability, and Pharmacokinetics of MRG-106 Following Local Intratumoral, Subcutaneous, and Intravenous Administration in Subjects With Various Lymphomas and Leukemias[NCT02580552]	Phase 1	66 participants (Actual)	Interventional	2016-02-09	Completed
Phase III Randomized Study to Investigate the Use of Acalabrutinib in the Treatment of Patients With Early Stage CLL With High Risk of Early Disease Progression[NCT04178798]	Phase 3	22 participants (Actual)	Interventional	2019-12-09	Active, not recruiting
An Open-label, Phase 1b/2, Safety and Efficacy Study of the Bruton's Tyrosine Kinase (Btk) Inhibitor, PCI-32765, and Ofatumumab in Subjects With Relapsed/Refractory Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma and Prolymphocytic Leukemia[NCT01217749]	Phase 1/Phase 2	71 participants (Actual)	Interventional	2010-12-31	Completed
A Phase 1b/2 Fixed-dose Study of Bruton's Tyrosine Kinase (Btk) Inhibitor, PCI-32765, in Chronic Lymphocytic Leukemia[NCT01105247]	Phase 1/Phase 2	133 participants (Actual)	Interventional	2010-05-31	Completed
A Randomized, Multicenter, Open-label, Phase 3 Study of the Bruton's Tyrosine Kinase (BTK) Inhibitor Ibrutinib (PCI-32765) Versus Ofatumumab in Patients With Relapsed or Refractory Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma[NCT01578707]	Phase 3	391 participants (Actual)	Interventional	2012-06-30	Completed
A Phase 2 Study of the Bruton's Tyrosine Kinase (Btk) Inhibitor, PCI-32765(Ibrutinib), in Relapsed and Refractory Patients With Chronic Lymphocytic Leukemia (CLL)/Small Lymphocytic Lymphoma (SLL) and B-cell Prolymphocytic Leukemia (B-PLL)[NCT01589302]	Phase 2	154 participants (Actual)	Interventional	2012-05-21	Active, not recruiting
Effect of Spironolactone on the Progression of Coronary Calcification in Peritoneal Dialysis Patients[NCT03314493]	Phase 3	33 participants (Actual)	Interventional	2014-11-07	Completed
Randomized, Double-blind, Placebo-controlled Phase 3 Study of Ibrutinib, a Bruton's Tyrosine Kinase (BTK) Inhibitor, in Combination With Bendamustine and Rituximab (BR) in Subjects With Relapsed or Refractory Chronic Lymphocytic Leukemia/Small Lymphocytic[NCT01611090]	Phase 3	578 participants (Actual)	Interventional	2012-09-19	Completed
A Phase 2 Study to Assess the Safety and Efficacy of TGR-1202 in Patients With Chronic Lymphocytic Leukemia (CLL) Who Are Intolerant to Prior BTK (Bruton Tyrosine Kinase) or PI3K-Delta (Phosphoinositide-3-kinase) Inhibitor Therapy[NCT02742090]	Phase 2	51 participants (Actual)	Interventional	2016-04-21	Completed
A Phase 2 Study of the Efficacy and Safety of ACP-196 in Subjects With Relapsed/Refractory CLL and Intolerant of Ibrutinib Therapy[NCT02717611]	Phase 2	60 participants (Actual)	Interventional	2016-03-08	Active, not recruiting
Severe Impairment of Solute-Free Water Clearance in Patients With HIV Infection[NCT01869010]		30 participants (Actual)	Observational	2010-01-31	Completed
EuroSIDA Prospective Observational Cohort Study on Clinical and Virological Outcome of European Patients Infected With HIV[NCT02699736]		23,000 participants (Actual)	Observational [Patient Registry]	1994-01-31	Enrolling by invitation
The SETPOINT Study - A Randomized Study of the Effect of Immediate Treatment With Potent Antiretroviral Therapy Versus Observation With Treatment as Indicated in Newly Infected HIV-1 Infected Subjects: Does Early Therapy After the Virologic Setpoint?[NCT00090779]	Phase 2	130 participants (Actual)	Interventional	2005-01-31	Terminated (stopped due to The DSMB concluded that the findings regarding the primary analysis would persist and that no additional study goals would be achieved by continuing the study.)
The Finnish Diabetes Prevention Study: A Follow-up Study on the Effect of a Dietary and Exercise Intervention in the Prevention of Diabetes and Its Vascular Complications[NCT00518167]		522 participants (Actual)	Interventional	1993-11-30	Active, not recruiting
A Phase 2, Randomized, Double-Blind Study Exploring the Efficacy, Safety and Tolerability of Tenofovir Disoproxil Fumarate (DF) Monotherapy Versus Emtricitabine Plus Tenofovir DF Fixed-Dose Combination Therapy in Subjects Currently Being Treated With Adef[NCT00307489]	Phase 2	106 participants (Actual)	Interventional	2006-03-31	Completed
Efficacy of Adefovir and Lamivudine Combination Therapy in Patients With Entecavir Resistance[NCT01546116]	Phase 4	20 participants (Actual)	Interventional	2010-02-28	Completed
A Phase II, Randomized Trial of Amprenavir as Part of Dual Protease Inhibitor Regimens (Placebo-Controlled) in Combination With Abacavir, Efavirenz, and Adefovir Dipivoxil Versus Amprenavir Alone in HIV-Infected Subjects With Prior Exposure to Approved Pr[NCT00000912]	Phase 2	475 participants	Interventional		Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Overall survival was defined as time from randomization to death from any cause or date last known alive. Overall survival rate at 3 years was estimated using the method of Kaplan-Meier. (NCT02048813)
Timeframe: Assessed every 3 months until progression; after progression, assessed every 3 months for first 2 years, every 6 months for years 3-5, up to 4 years and 8 months

Progression-free Survival (PFS) Rate at 3 Years

Intervention	Proportion of participants (Number)
Arm A (Ibrutinib, Rituximab)	0.988
Arm B (Rituximab, Fludarabine Phosphate, Cyclophosphamide)	0.915

"PFS was defined as the time from randomization to CLL progression or death, whichever occurred first. Progression is characterized by any of the following:~≥ 50% increase from nadir since start of treatment (tx) in the sum of the products of at least 2 lymph nodes on 2 consecutive examinations 2 weeks apart~≥ 50% increase from nadir since start of tx in the size of liver and/or spleen~≥ 50% increase in the absolute number of circulating lymphocytes not due to tumor flare reaction. The absolute lymphocyte count must be ≥ 5x10^9/L to qualify as disease progression.~Transformation to a more aggressive histology (e.g. Richter's syndrome or prolymphocytic leukemia with > 55% prolymphocytes). For patients who achieve a complete response or nodular partial response, progression is defined as recurrence of circulating leukemia cell clone in the peripheral blood and an absolute lymphocyte count > 5x10^9/L and/or recurrence of palpable lymphadenopathy > 1.5 cm by physical exam." (NCT02048813)
Timeframe: Assessed every 3 months until progression up to 4 years and 8 months

Area Under the Concentration Curve of Ibrutinib During 24 Hours After Dosing at Steady State

Intervention	Proportion of participants (Number)
Arm A (Ibrutinib, Rituximab)	0.894
Arm B (Rituximab, Fludarabine Phosphate, Cyclophosphamide)	0.729

Area under the concentration curve of ibrutinib during 24 hours after dosing at steady state was determined using PopPK modeling. (NCT01776840)
Timeframe: Day 2 of Cycles 1, 2 and 3 (each cycle was of 28 days)

Complete Response Rate

Intervention	nanogramhour per milliliter (ngh/mL) (Mean)
Ibrutinib + BR (Treatment B)	425

Complete response (CR) rate is defined as the percentage of participants who achieve CR (based on investigator assessment) on or prior to the initiation of subsequent anticancer therapy. Criteria for CR: disappearance of all evidence of disease; mass of any size permitted if positron emission tomography (PET) negative; regression to normal size on computed tomography (CT); spleen and liver: not palpable, nodules disappeared; bone marrow: infiltrate cleared on repeat biopsy. (NCT01776840)
Timeframe: Up to 97 months

Duration of Complete Response (DoCR)

Intervention	percentage of participants (Number)
Ibrutinib + BR (Treatment B)	65.5
Placebo + BR (Treatment A)	57.6

Duration of complete response (DoCR) was defined as the interval between the date of initial documentation of a CR and the date of first documented evidence of PD or death whichever occurs first, for participants who achieved CR. (NCT01776840)
Timeframe: Up to 97 months

Duration of Response (DoR)

Intervention	months (Median)
Ibrutinib + BR (Treatment B)	NA
Placebo + BR (Treatment A)	78.1

Duration of Response (DoR) was defined as the interval between the date of initial documentation of a response including PR and the date of first documented evidence of PD or death. (NCT01776840)
Timeframe: Up to 97 months

Maximum Observed Plasma Concentration of Ibrutinib

Intervention	months (Median)
Ibrutinib + BR (Treatment B)	81
Placebo + BR (Treatment A)	63.5

Maximum observed plasma concentration of ibrutinib was determined using PopPK modeling. (NCT01776840)
Timeframe: Day 2 of Cycles 1, 2 and 3 (each cycle was of 28 days)

Minimal Residual Disease (MRD)-Negative Response Rate

Intervention	ng/mL (Mean)
Ibrutinib + BR (Treatment B)	74.5

Minimal residual disease negative rate was defined as the percentage of participants with a best overall response of CR with MRD-negative disease status (that is, <5 mantle cell lymphoma [MCL] cell per 10,000 leukocytes for detection using the MRD assay), as assessed by flow cytometry of a bone marrow and/or peripheral blood sample. (NCT01776840)
Timeframe: Up to 97 months

Minimum Observed Plasma Concentration of Ibrutinib

Intervention	percentage of participants (Number)
Ibrutinib + BR (Treatment B)	62.1
Placebo + BR (Treatment A)	56.5

Minimum observed plasma concentration of ibrutinib was determined using PopPK modeling. (NCT01776840)
Timeframe: Day 2 of Cycles 1, 2 and 3 (each cycle was of 28 days)

Number of Participants With Treatment-emergent Adverse Events (TEAEs)

Intervention	nanograms per milliliter (ng/mL) (Mean)
Ibrutinib + BR (Treatment B)	3.90

Number of participants with TEAEs were reported. Treatment-emergent adverse events are defined as adverse events with onset or worsening on or after date of first dose of study treatment up to and including 30 days after date of last dose of study medication, or the initiation of subsequent anticancer therapy, whichever is earlier. (NCT01776840)
Timeframe: Up to 97 months

Oral Plasma Clearance (CL/F) of Ibrutinib

Intervention	Participants (Count of Participants)
Ibrutinib + BR (Treatment B)	259
Placebo + BR (Treatment A)	257

CL/F of Ibrutinib was determined using population pharmacokinetics (PopPK modeling). (NCT01776840)
Timeframe: Day 2 of Cycles 1, 2 and 3 (each cycle was of 28 days)

Oral Volume of Distribution at Steady State of Ibrutinib

Intervention	liter per hour (L/h) (Mean)
Ibrutinib + BR (Treatment B)	1123

Oral volume of distribution at steady state of ibrutinib was determined using PopPK modeling. (NCT01776840)
Timeframe: Day 2 of Cycles 1, 2 and 3 (each cycle was of 28 days)

Overall Survival

Intervention	liter (Mean)
Ibrutinib + BR (Treatment B)	7286

Overall survival is defined as the time from the date of randomization to the date of the participant's death. (NCT01776840)
Timeframe: Up to 97 months

Percentage of Participants With Overall Response

Intervention	months (Median)
Ibrutinib + BR (Treatment B)	NA
Placebo + BR (Treatment A)	NA

Percentage of participants with overall response that is participants who achieved CR or PR was reported. Criteria for CR: disappearance of all evidence of disease; mass of any size permitted if PET negative; regression to normal size on CT; spleen and liver: not palpable, nodules disappeared; bone marrow: infiltrate cleared on repeat biopsy. Criteria for PR: greater than or equal to (>=) 50% decrease in sum of the diameter of all target lesions compared with baseline, in absence of new lesions or unequivocal progression of non-target lesions. (NCT01776840)
Timeframe: Up to 97 months

Progression-free Survival (PFS)

Intervention	percentage of participants (Number)
Ibrutinib + BR (Treatment B)	89.7
Placebo + BR (Treatment A)	88.5

Progression-free survival (PFS) is defined as the interval between the date of randomization to the date of disease progression (PD) or relapse from complete response (CR) or death, whichever is first reported. Disease assessments were based on the 2007 Revised Response Criteria for Malignant Lymphoma. PD is defined as any new lesion or increase by 50 percent (%) of previously involved sites from nadir (PD criteria: Appearance of new nodal lesion 1.5 centimeters [cm] in any axis, 50% increase in sum of product of diameters [SPD] of greater than [>] 1 node or 50% increase in longest diameter of previously identified node 1 cm in short axis). (NCT01776840)
Timeframe: Up to 97 months

Time to Response

Intervention	months (Median)
Ibrutinib + BR (Treatment B)	80.6
Placebo + BR (Treatment A)	52.9

Time to response was defined as the interval between the date of randomization and the date of initial documentation of a response. (NCT01776840)
Timeframe: Up to 97 months

Time to Worsening (TTW) in the Lymphoma (Lym) Subscale of the Functional Assessment of Cancer Therapy-Lymphoma (FACT-Lym) Questionnaire

Intervention	months (Median)
Ibrutinib + BR (Treatment B)	2.79
Placebo + BR (Treatment A)	2.79

"Time to worsening in the Lymphoma subscale of the FACT-Lym, defined as the interval from the date of randomization to the start date of worsening of participant symptoms. Worsening was defined by a 5-point decrease from baseline, death, or a missing assessment due to being too ill, whichever occurred first. FACT-Lym Lymphoma subscale contains 15 questions, scores from 0 to 4 for each question (higher the worse). Lymphoma subscale score is the total of reverse scores, range 0 to 60. Higher scores indicate a better quality of life." (NCT01776840)
Timeframe: Up to 97 months

Time-to-Next Treatment

Intervention	months (Median)
Ibrutinib + BR (Treatment B)	17.4
Placebo + BR (Treatment A)	22.2

Time-to-next treatment was measured from the date of randomization to the start date of any anti-mantle cell lymphoma (anti-MCL) treatment subsequent to the study treatment. (NCT01776840)
Timeframe: Up to 97 months

Duration of Response

Intervention	months (Median)
Ibrutinib + BR (Treatment B)	NA
Placebo + BR (Treatment A)	92.0

"Duration of response is defined as the time from first evidence of a response to the first documented time of progressive disease (PD). Response and Progression were assessed using the Cheson et al. Revised Response Criteria for Malignant Lymphoma. > > A CR is defined as the disappearance of all evidence of disease. A PR is defined as ≥ 50% decrease in the sum of the products of dimensions (SPD) of up to 6 largest dominant masses; no increase in size of other nodes and regression on CT, and no increase in size of liver/spleen.Estimated using the method of Kaplan-Meier.>~> Progressive Disease (PD) is defined as any new lesion or increase by ≥ 50% of previously involved sites from nadir." (NCT01849263)
Timeframe: Time from the date at which the patient's objective status is first noted to be a CR or PR to the earliest date progression is documented, assessed up to 5 years

Overall Response Rate

Intervention	months (Median)
Treatment (Ibrutinib)	13.9

"Overall response rate defined as a partial response (PR) or complete response (CR) as the objective status at any time during treatment, evaluated using the Cheson et al. Revised Response Criteria for Malignant Lymphoma. Ninety-five percent binomial confidence intervals for the true success proportion will be calculated.~A CR is defined as the disappearance of all evidence of disease. A PR is defined as ≥ 50% decrease in the sum of the products of dimensions (SPD) of up to 6 largest dominant masses; no increase in size of other nodes and regression on CT, and no increase in size of liver/spleen." (NCT01849263)
Timeframe: Up to 5 years

Overall Survival

Intervention	proportion of participants (Number)
Treatment (Ibrutinib)	0.375

Overall Survival is defined as the time from registration to death due to any cause. Estimated using the method of Kaplan-Meier. (NCT01849263)
Timeframe: Assessed up to 5 years

Progression-free Survival

Intervention	months (Median)
Treatment (Ibrutinib)	NA

Progression-Free Survival is defined as the time from registration to documented progression or death due to any cause, whichever occurs first. Estimated using the method of Kaplan-Meier. (NCT01849263)
Timeframe: Time from registration to progression or death due to any cause, assessed up to 5 years

Time to Response

Intervention	months (Median)
Treatment (Ibrutinib)	14.0

Time to response is defined for all evaluable patients who have achieved a confirmed response as the time from the date of registration to the date at which the patient's objective status is first noted to be a CR or PR.The median and 95% confidence interval will be calculated using the methods of Kaplan-Meier. (NCT01849263)
Timeframe: Time from the date of registration to the date at which the patient's objective status is first noted to be a CR or PR, assessed up to 5 years

Time to Subsequent Treatment

Intervention	months (Median)
Treatment (Ibrutinib)	4.6

Time to subsequent treatment is defined as the time from registration to the date of initiation of subsequent treatment for lymphoma. The distribution of time to subsequent treatment will be estimated using the method of Kaplan-Meier. (NCT01849263)
Timeframe: Time from registration to the date of initiation of subsequent treatment for lymphoma, assessed up to 5 years

Time to Treatment Failure

Intervention	months (Median)
Treatment (Ibrutinib)	17.7

Time to treatment failure is defined as the time from registration to the date of treatment discontinuation due to any reason. The distribution of time to treatment failure will be estimated using the method of Kaplan-Meier. (NCT01849263)
Timeframe: Time from registration to the date of treatment discontinuation due to any reason, assessed up to 5 years

Duration of Response (DOR)

Intervention	months (Median)
Treatment (Ibrutinib)	10.0

DOR is defined as the number of days from the date of first response (complete response [CR], complete response with incomplete marrow recovery [CRi], nodular partial remission [nPR], or partial remission [PR]) to the earliest recurrence or progressive disease. DOR was analyzed by Kaplan-Meier (K-M) methodology. (NCT02141282)
Timeframe: At Wk 5, Day 1; Wk 8, Day 1; Wk 12, Day 1; Wk 16, Day 1; Wk 20, Day 1; Wk 24, Day 1; Wk 36, Day 1; every 12 wks after Wk 36; Final Visit; estimated median time on follow-up was 1694 d for ibrutinib failure cohort and 1942 d for idelalisib failure cohort

Overall Response Rate (ORR)

Intervention	months (Median)
ABT-199 After Ibrutinib Therapy: Main and Expansion Cohorts	35.1
ABT-199 After Idelalisib Therapy: Main and Expansion Cohorts	55.4

Overall response rate is defined as the percentage of participants with an overall response (per the investigator assessment) 2008 Modified International Workshop for Chronic Lymphocytic Leukemia (IWCLL) National Cancer Institute-Working Group (NCI-WG) criteria. (NCT02141282)
Timeframe: At Wk 5, Day 1; Wk 8, Day 1; Wk 12, Day 1; Wk 16, Day 1; Wk 20, Day 1; Wk 24, Day 1; Wk 36, Day 1; every 12 wks after Wk 36; Final Visit; estimated median time on follow-up was 1694 d for ibrutinib failure cohort and 1942 d for idelalisib failure cohort

Overall Survival (OS)

Intervention	percentage of participants (Number)
ABT-199 After Ibrutinib Therapy: Main and Expansion Cohorts	64.8
ABT-199 After Idelalisib Therapy: Main and Expansion Cohorts	69.4

OS is defined as the number of days from the date of first dose to the date of death for all dosed participants. For participants who did not die, their data was censored at the date of last study visit or the last known date to be alive, whichever was later. OS was estimated using Kaplan-Meier methodology. (NCT02141282)
Timeframe: At Wk 5, Day 1; Wk 8, Day 1; Wk 12, Day 1; Wk 16, Day 1; Wk 20, Day 1; Wk 24, Day 1; Wk 36, Day 1; every 12 wks after Wk 36; Final Visit; estimated median time on follow-up was 1694 d for ibrutinib failure cohort and 1942 d for idelalisib failure cohort

Progression-free Survival (PFS)

Intervention	months (Median)
ABT-199 After Ibrutinib Therapy: Main and Expansion Cohorts	69.6
ABT-199 After Idelalisib Therapy: Main and Expansion Cohorts	NA

PFS is defined as the number of days from the date of first dose to the date of earliest disease progression (PD) or death. PFS was analyzed by Kaplan-Meier methodology. (NCT02141282)
Timeframe: At Wk 5, Day 1; Wk 8, Day 1; Wk 12, Day 1; Wk 16, Day 1; Wk 20, Day 1; Wk 24, Day 1; Wk 36, Day 1; every 12 wks after Wk 36; Final Visit; estimated median time on follow-up was 1694 d for ibrutinib failure cohort and 1942 d for idelalisib failure cohort

Time to Next Anti-Chronic Lymphocytic Leukemia Treatment (TNNT)

Intervention	months (Median)
ABT-199 After Ibrutinib Therapy: Main and Expansion Cohorts	24.7
ABT-199 After Idelalisib Therapy: Main and Expansion Cohorts	43.4

TNNT is defined as the number of days from the date of the first dose of venetoclax to the date of first dose of any non-protocol anti-leukemia therapy (NPT) or death from any cause. For participants who did not take NPT, their data was censored at the last known date to be free of NPT. TTNT was analyzed by Kaplan-Meier methodology. (NCT02141282)
Timeframe: Collected every 3 months for a period of 5 years after the last participant had enrolled into the study

Time to Progression (TTP)

Intervention	months (Median)
ABT-199 After Ibrutinib Therapy: Main and Expansion Cohorts	24.0
ABT-199 After Idelalisib Therapy: Main and Expansion Cohorts	37.8

"TTP is defined as the number of days from the date of first dose to the date of earliest disease progression (PD).~TTP was analyzed by Kaplan-Meier (K-M) methodology." (NCT02141282)
Timeframe: At Wk 5, Day 1; Wk 8, Day 1; Wk 12, Day 1; Wk 16, Day 1; Wk 20, Day 1; Wk 24, Day 1; Wk 36, Day 1; every 12 wks after Wk 36; Final Visit; estimated median time on follow-up was 1694 d for ibrutinib failure cohort and 1942 d for idelalisib failure cohort

Percentage of Participants With Minimal Residual Disease (MRD) Negativity Status

Intervention	months (Median)
ABT-199 After Ibrutinib Therapy: Main and Expansion Cohorts	36.1
ABT-199 After Idelalisib Therapy: Main and Expansion Cohorts	43.4

The rate of MRD response is defined as the percentage of participants who had MRD negative status. (NCT02141282)
Timeframe: Assessed at Week 24, Day 1; after the first Complete Response, Complete Remission with Incomplete Marrow Recovery, or Partial Response; at 12-week interval visits until two consecutive negative MRD levels were reported

Number of Participants With Treatment Emergent Adverse Events (AEs)

Intervention	percentage of participants (Number)
	Peripheral blood	Bone marrow
ABT-199 After Ibrutinib Therapy: Main and Expansion Cohorts	30.8	6.6
ABT-199 After Idelalisib Therapy: Main and Expansion Cohorts	25.0	11.1

Number of participants who had experienced at least one treatment emergent AE (NCT01217749)
Timeframe: From first dose of study treatment to within 30 days of last dose or until study closure

Percentage of Participants Achieving Response

Intervention	participants (Number)
Group 1	27
Group 2	20
Group 3	24

The primary endpoint for the study was overall response rate (ORR), defined as the proportion of participants who achieved a best overall response of complete response (CR), CR with incomplete blood count recovery (Cri), or partial response (PR), according to the guidelines from the International Workshop on Chronic Lymphocytic Leukemia (IWCLL1) published in 2008 for CLL participants and International Working Group for non-Hodgkin's lymphoma (IWG NHL) 2007 criteria for SLL participants, with the modification that treatment-related lymphocytosis will not be considered progressive disease, as evaluated by the investigators. Assessment of disease is based on radiological exams, physical exam, hematological evaluations and, when appropriate, bone marrow results. (NCT01217749)
Timeframe: The median follow-up time on study for all treated participants is 12.5 (range 0.5-19.6) months

Progression Free Survival (PFS) at 12 Months

Intervention	percentage of participants (Number)
Group 1	92.6
Group 2	80.0
Group 3	70.8

"Progressive disease for CLL (Hallek) is characterized by ≥1 of the following:~Appearance of any new lesion, eg lymph nodes (> 1.5 cm), de novo hepatomegaly or splenomegaly, or other organ infiltrates~Increase of ≥50%~in longest diameter of any previous site~in hepatomegaly or splenomegaly~in blood lymphocytes with ≥5x109/L B cells with enlarging lymph node, liver, or spleen~Progressive disease for B cell lymphoma (Cheson) is characterized by any new lesion or increase by ≥ 50% of previously involved sites from nadir:~Appearance of a new lesion(s) >1.5 cm in any axis, ≥ 50% increase in the SPD of >1 node, or ≥50% increase in longest diameter of a previously identified node >1 cm in short axis~Lesions PET+ if FDG-avid lymphoma or PET+ before therapy~50% increase from nadir in the SPD of any liver or spleen lesions~New or recurrent BM involvement~Increase of ≥50% in blood lymphocytes with ≥5x109/L B cells within enlarging lymph node, liver, or spleen" (NCT01217749)
Timeframe: From first dose of study treatment until disease progression, death, or until 12 months

Safety During Dose-Limiting Toxicity (DLT) Observation Period

Intervention	percentage of event free participants (Mean)
Group 1	88.7
Group 2	85.0
Group 3	75.0

Number of dose-limiting toxicities observed in the first 6 participants enrolled in treatment Groups 1 and 2 (NCT01217749)
Timeframe: 56 days for Group 1 and 28 days for Group 2

Food Effect Cohort Assessments

Intervention	participants who experienced DLT (Number)
Group 1	0
Group 2	0

Geometric mean ratio (Fed/Fasted) for PCI-32765 AUClast. The data were collected at 0, 0.5, 1, 2, 4, 6, 24 h post-dose. The AUClast was calculated from 0 up to 24 hours post-dose. (NCT01105247)
Timeframe: Fed was assessed on either Day 8 or Day 15 and Fasted was assessed on the remaining day as cross-over design.

Number of Participants With Treatment Emergent Adverse Events (AEs)

Intervention	(Number)
Food Effect Cohort	1.65

Number of participants who had experienced at least one treatment emergent AEs. (NCT01105247)
Timeframe: From first dose to within 30 days of last dose of PCI-32765

Percentage of Participants Achieving Response

Intervention	Participants (Number)
PCI-32765	116
Food Effect	11

Response criteria are as outlined in the IWCLL 2008 criteria (Hallek 2008) and as assessed by investigator, e.g. response requires 50% reduction in lymph node size. (NCT01105247)
Timeframe: The median follow-up time for all treated patients are 21 month, range (0.7 month, 29 months).

Progression Free Survival Rate at 24 Months

Intervention	Percentage of Participants (Number)
Treatment Naive	71
Relapsed/ Refractory	75.3
Food Effect	56.3

Criteria for progression are as outlined in the IWCLL 2008 criteria (Hallek 2008) and as assessed by investigator, e.g. progression defined as a 50% increase in lymph node size. (NCT01105247)
Timeframe: The median follow-up time for all treated patients are 21 month, range (0.7 month, 29 months).

OS (Overall Survival)

Intervention	Percentage of Participants (Number)
Treatment Naive	96.3
Relapsed/ Refractory	73.6
Food- Effect	NA

OS analysis was conducted at the time of study closure, with no adjustment for crossover from the ofatumumab arm to the ibrutinib arm (NCT01578707)
Timeframe: OS analysis was conducted at the time of study closure, including up to 6 years of study follow-up

Overall Response Rate (ORR) by Independent Review Committee (IRC)

Intervention	months (Median)
Ofatumumab (Arm A)	65.1
Ibrutinib (Arm B)	67.7

Overall Response Rate per the IWCLL 2008 criteria as assessed by IRC, limited to the time of primary analysis 06 November 2013 (NCT01578707)
Timeframe: About 18 months after the first subject was enrolled

Overall Response Rate (ORR) by Investigator

Intervention	percentage of participants (Number)
Ofatumumab (Arm A)	4.1
Ibrutinib (Arm B)	42.6

Overall response per the IWCLL 2008 criteria as assessed by Investigator with up to 6 years of study follow-up (NCT01578707)
Timeframe: From study initiation to study closure, including up to 6 years of study follow-up

PFS (Progression Free Survival) by Independent Review Committee (IRC), Limited to the Time of Primary Analysis 06 November 2013

Intervention	percentage of participants (Number)
Ofatumumab (Arm A)	22.4
Ibrutinib (Arm B)	87.7

The primary objective of this study was to evaluate the efficacy of ibrutinib compared to ofatumumab based on independent review committee (IRC) assessment of progression-free survival (PFS) according to 2008 IWCLL guidelines. (NCT01578707)
Timeframe: Analysis was conducted after observing approximately 117 PFS events, which occurred about 18 months after the first subject was enrolled.

Progression Free Survival (PFS) by Investigator With up to 6 Years of Study Follow-up

Intervention	months (Median)
Ofatumumab (Arm A)	8.1
Ibrutinib (Arm B)	NA

Long-Term Progression Free Survival as assessed by the investigator with up to 6 years of study follow-up (NCT01578707)
Timeframe: From study initiation to study closure, including up to 6 years of study follow-up

Rate of Sustained Hemoglobin and Platelet Improvement

Intervention	months (Median)
Ofatumumab (Arm A)	8.1
Ibrutinib (Arm B)	44.1

Proportion of subjects with hemoglobin (HgB) increase >=20 g/L and platelet (PLT) increase >=50% over baseline continuously for >=56 days without blood transfusions or growth factors. (NCT01578707)
Timeframe: From study initiation to study closure, including up to 6 years of study follow-up

Cancer-Specific Stress as Measured by the Impact of Event Scale-Revised (IES-R)

Intervention	percentage of participants (Number)
	Hgb Improvement in patient with baseline anemia	Platelet improvement in baseline thrombocytopenia
Ibrutinib (Arm B)	69.7	78.4
Ofatumumab (Arm A)	32.6	9.4

Cancer-Specific Stress was measured by the Impact of Event Scale-Revised Participants rated the intensity of these feelings using a five-point Likert scale ranging from 0=not at all to 4=extremely. Patients rated the frequency of their feelings or events for the previous week before treatment. The items were summed for a total score that ranged from 0 to 64 (NCT01589302)
Timeframe: Up to 2 years

Cognitive-Affective Depressive Symptoms as Measured by the Beck Depression Inventory-2nd Edition (BDI-II)

The Beck Depression Inventory-2nd edition is a 21-item measure of depressive symptoms. Scores were calculated representing the cognitive-affective and the somatic symptoms associated with depression (e.g. sadness, pessimism, loss of pleasure) during past month on scale from 0 to 3. Items were summed, with higher scores indicating more depressive symptoms. The scores on the scale from range from 0 to 42. (NCT01589302)
Timeframe: at 5 months

Effectiveness of Ibrutinib Bridging Patients to Allogeneic Stem Cell Transplant and Outcome of Patients Following This Intervention

The number of participants with successful Allogenic Stem Cell Transplant (NCT01589302)
Timeframe: Up to 2 years

Fatigue Symptom Inventory (FSI) Interference Quality of Life as Measured by a 11-item Total Disruption Index Sub Scale of Fatigue Symptoms Inventory

The Fatigue Interference quality of life measures is a 11-item self reported questionnaire used to measure frequency, severity and daily pattern of fatigue Symptoms as well as impact of QOL in the past week. The Total Disruption Index (TDI) an 7 item subset of FSI was used. Items were rated on a 11-point Likert scale from 0=no interference to 10=extreme interference. Total scores could range from 0 to 70, with higher scores indicating greater fatigue interference. (NCT01589302)
Timeframe: at 5 months

Mental Health Quality of Life Was Measured by the Mental Component Summary Score of the Medical Outcomes Study

SF-12 assesses aspects of quality of life including physical functioning, role functioning-physical, bodily pain, general health perceptions, vitality, social functioning, role functioning-emotional, and mental health. Subscale raw scores are transformed to put each subscale on a 0-100 range with higher scores indicative of greater functioning. Subscale scores are standardized based on US General Population norms and aggregated based on factor score coefficients into two component scores: the Physical Component Summary (PCS) and the Mental Component Summary (MCS). Component scores are norm-based t-scores meaning scores above 50 indicate better functioning than average functioning while scores below 50 indicate worse functioning. (NCT01589302)
Timeframe: at 5 months

Negative Mood Quality of Life Measured by a 37-item Questionnaire

The Profile of Mood States-Short Form (POMS-SF) yields six subscales, Tension, Depression, Anger, Vigor, Fatigue, and Confusion. A total mood disturbance score is found by summing the six subscales. Total Mood Disturbance (TMD) scores range from -24 to 124 with higher scores indicating greater mood disturbance. (NCT01589302)
Timeframe: at 5 months

Physical Health Quality of Life as Measured by a 12 Item Short-Form Health Survey

Physical Health Quality of life measures were administered during screening and on Days 1 (±3), of Cycle 1, Day 1 (±3), of Cycle 2 and on day 1 (±7) of Cycles 3, 6, and then every 3 months thru Cycle 24 and at time of progression and /or end of treatment. SF-12 assesses aspects of quality of life including physical functioning, role functioning-physical, bodily pain, general health perceptions, vitality, social functioning, role functioning-emotional, and mental health. Subscale raw scores are transformed to put each subscale on a 0-100 range with higher scores indicative of greater functioning. Subscale scores are standardized based on US General Population norms and aggregated based on factor score coefficients into two component scores: the Physical Component Summary (PCS) and the Mental Component Summary (MCS). Component scores are norm-based t-scores meaning scores above 50 indicate better functioning than average functioning while scores below 50 indicate worse functioning. (NCT01589302)
Timeframe: up to 5 months

Resistance Studies of Ibrutinib

Percentage of patients with BTK C481S mutation or PLCG2 mutation (NCT01589302)
Timeframe: Up to 4 years

Sleep Through Quality of Life as Measured by a Medical Outcomes Study-Sleep Scale

Sleep problems quality of life measures is a six-item sleep problems index I of the Medical Outcomes Study-Sleep Scale used to assess sleep problems. Participants reported how often they experience six specific difficulties with sleep on a 6-point Likert scale (1=All of the time to 6=None of the time). Scores transformed into a 0-100 scale with higher scores indicating greater sleep problems. (NCT01589302)
Timeframe: at 5 months

2-year Kaplan-Meier Estimate of OS for Relapsed and Refractory CLL Patients Treated With Single Agent PCI-32765

Time from date of first treatment with ibrutinib until the date of progression or death from any cause. Those alive and progression free are censored at the date of last clinical assessment. (NCT01589302)
Timeframe: 2 years

Best Overall Response Rate Using the Revised International Workshop on Chronic Lymphocytic Leukemia (IWCLL) Working Group Guidelines

Responders were subjects who achieved a complete response (CR), partial response (PR) or PR with persistent lymphocytosis. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT01589302)
Timeframe: up to 2 years

Determine the 2 Year Progression-free Survival (PFS) of Single Agent PCI-32765 in Patients With Relapsed and Refractory CLL.

We will summarize our findings for this endpoint independently as well within each cohort (del17p vs other cytogenetic groups). We will evaluate the proportion of patients who are progression-free and alive at two years or have gone on to transplant (treatment successes) over the total number of evaluable patients; eligible patients who received at least one dose of therapy are considered evaluable. Assuming that the number of treatment successes as defined above is binomially distributed, we will also include 95% binomial confidence intervals for the estimates corresponding to each cohort. (NCT01589302)
Timeframe: up to 2 years

Number of Patients With 6 Month ORR of Single Agent Ibrutinib in Relapsed and Refractory CLL Patients

The 6 month overall response rates overall response rate (ORR). Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT01589302)
Timeframe: Up to 6 months

Number of Patients With Adverse Events, Graded According to the NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 4.0

Adverse events grade 3 or higher using the National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE) version 4.0 with the attribution of either definite, possible or probable related. (NCT01589302)
Timeframe: Up to 2 years post treatment

Percentage of Patients With Overall Survival (OS)

Time from date of first treatment with ibrutinib until the date of death from any cause or the date of last contact for those alive. (NCT01589302)
Timeframe: 2 years

Change From Baseline in Beta2 Microglobulin at End of Treatment (EOT)

Change from baseline in beta2 microglobulin at end of treatment at time of primary analysis was reported. (NCT01611090)
Timeframe: Baseline to EOT (Up to 2 years)

Change From Baseline in EORTC QLQ-C30 Physical Functioning Score at End of Treatment

"EORTC QLQ-C30 Physical Functioning Score is a questionnaire to assess quality of life of cancer patients. It is composed of 30 items, multi-item measure (28 items) and 2 single-item measures. For the multiple item measure, 4-point scale is used and the score for each item range from 1 = not at all to 4 = very much. Higher scores indicate worsening. The 2 single-item measure involves question about the overall health and overall quality of life which was rated on a 7-point scale ranging from 1 = very poor to 7 = excellent. Lower scores indicate worsening. All scale and item scores were linearly transformed to be in range from 0-100. A higher score represents a higher (better) level of functioning, or a higher (worse) level of symptoms." (NCT01611090)
Timeframe: Baseline to EOT (up to 2 years)

Change From Baseline in EuroQol-5 Dimension-5 Level (EQ-5D-5L) Utility Score Scale at End of Treatment

The EuroQol-5 is a five dimensional health state classification. Each dimension is assessed on a 3-point ordinal scale (1=no problems, 2=some problems, 3=extreme problems). The responses to the five EQ-5D dimensions were scored using a utility-weighted algorithm to derive an EQ-5D health status index score between 0 to 1. High score indicating a high level of utility. (NCT01611090)
Timeframe: Baseline to EOT (up to 2 years)

Change From Baseline in EuroQol-5 Dimension-5 Level (EQ-5D-5L) Visual Analog Scale at End of Treatment

The EQ-5D questionnaire is a brief, generic health-related quality of life assessment (HRQOL) that can also be used to incorporate participant preferences into health economic evaluations. The EQ-5D questionnaire assesses HRQOL in terms of degree of limitation on 5 health dimensions (mobility, self-care, usual activities, pain/discomfort, anxiety/depression) and as overall health using a visual analog scale with response options ranging from 0 (worst imaginable health) to 100 (best imaginable health). (NCT01611090)
Timeframe: Baseline to EOT (up to 2 years)

Change From Baseline in FACIT-Fatigue Scale at End of Treatment

FACIT-Fatigue is an instrument for use as a measure of the effect of fatigue in patients with cancer and other chronic diseases. Responses to the 13-item FACIT Fatigue Scale are reported on a 5-point categorical response scale ranging from 0 (not at all) to 4 (very much). The sum of all responses resulted in the FACIT-Fatigue score for a total possible score of 0 (worst score) to 52 (best score). (NCT01611090)
Timeframe: Baseline to EOT (up to 2 years)

Median Time to Clinically Meaningful Improvement in FACIT-Fatigue Scale

Time to improvement is defined as the time interval (months) from randomization to the first observation of improvement. FACIT-Fatigue is an instrument for use as a measure of the effect of fatigue in patients with cancer and other chronic diseases. Responses to the 13-item FACIT Fatigue Scale are reported on a 5-point categorical response scale ranging from 0 (not at all) to 4 (very much). The sum of all responses resulted in the FACIT-Fatigue score for a total possible score of 0 (worst score) to 52 (best score). (NCT01611090)
Timeframe: Up to 2 years

Number of Participants Who Received Subsequent Antineoplastic Therapy

Number of participants who received subsequent antineoplastic therapy was reported. (NCT01611090)
Timeframe: Up to 5 years

Number of Participants With Clinically Relevant Shifts in Disease-Related Symptoms

The disease-related symptoms included fatigue, weight loss, fevers, night sweats, abdominal discomfort/splenomegaly and anorexia. (NCT01611090)
Timeframe: From the date of randomization to disease progression (Up to 2 years)

Overall Response Rate (ORR)

ORR defined as number of participants achieving a complete response (CR), complete response with incomplete marrow recovery (CRi), nodular partial response (nPR) or partial response (PR). IWCLL 2008 criteria: CR- No lymphadenopathy and hepatosplenomegaly, no constitutional symptoms, neutrophils >1.5*10^9/liter (L), platelets >100*10^9/L, Hgb >11 gram per deciliter (g/dL) and absolute lymphocyte count <4000/microliter (mcL); CRi- CR with incomplete recovery of bone marrow; nPR- participants meet criteria for CR, but the bone marrow biopsy shows B-lymphoid nodules, may represent a clonal infiltrate; PR-2 of the following when abnormal at baseline: >=50% decrease in ALC, >=50% decrease in sum products of up to 6 lymph nodes, >=50% decrease in enlargement of spleen or liver; and 1 of the following: neutrophils >1.5*10^9/L, Platelets >100*10^9/L and Hgb>11 g/dL or >=50% improvement over baseline in any of these; no new enlarged nodes or new hepatosplenomegaly. (NCT01611090)
Timeframe: Up to 5 years

Overall Survival (OS)

OS was defined as the interval between the date of randomization and the date of death from any cause. (NCT01611090)
Timeframe: Up to 5 years

Percentage of Participants With Minimal Residual Disease (MRD)-Negative Response

MRD-negative response was defined as the percentage of participants who reach MRD negative disease status (less than 1 chronic lymphocytic leukemia [CLL] cell per 10,000 leukocytes) in either bone marrow or peripheral blood. All randomized participants were included in this analysis. Participants with missing MRD data were considered non-responders. (NCT01611090)
Timeframe: Up to 5 years

Progression-free Survival (PFS)

PFS was defined as the interval between the date of randomization and the date of disease progression or death, whichever was first reported. IWCLL 2008 criteria for PD: New enlarged nodes >1.5 cm, new hepatomegaly or splenomegaly, or other new organ infiltrates, bone lesion, ascites, or pleural effusion confirmed due to chronic lymphocytic leukemia (CLL); >=50% increase in existing lymph nodes; >=50% increase in enlargement of liver or spleen; >=50% increase from baseline in lymphocyte count (and to >=5*10^9/L) or >=50% increase from nadir count confirmed on >=2 serial assessments if absolute lymphocyte count (ALC) >=30,000 per microliter and lymphocyte doubling time is rapid, unless considered treatment-related lymphocytosis; new cytopenia (Hemoglobin b [Hgb] or platelets) attributable to CLL; and transformation to a more aggressive histology. (NCT01611090)
Timeframe: Up to 5 years

Change From Baseline in EORTC QLQ-CLL 16 Domain Scores at End of Treatment

The EORTC QLQ-CLL 16 is a 16-item disease specific module that comprises 5 domains of patient-reported health status important in CLL. There are three multi-item scales that include fatigue (2 items), treatment side effects and disease symptoms (8 items), and infection (4 items), and 2 single-item scales on social activities and future health worries. Responses are measured on a 4 point scale ranging from 1 (not at all) to 4 (very much). (NCT01611090)
Timeframe: Baseline to EOT (up to 2 years)

Percentage of Participants With Sustained Hematologic Improvement

Sustained hematologic improvement was defined as hematological improvement that was sustained continuously for greater than or equal to (>=) 56 days without blood transfusion or growth factors: 1) Platelet counts greater than (>)100* 109/liter (L) if baseline less than or equal to (<=) 100*109/L or increase >= 50 percent (%) over baseline; 2) Hemoglobin >11 gram per deciliters (g/dL) if baseline <= 11 g/dL or increase >= 2 g/dL over baseline. (NCT01611090)
Timeframe: Up to 5 years

Duration of Response

"The duration of response of ACP-196 (acalabrutinib) in subjects with relapsed / refractory CLL who are intolerant of ibrutinib therapy.~DOR is calculated as date of disease progression or death (censoring date for censored subjects) - date of achieving the first CR, CRi, nPR, or PR + 1." (NCT02717611)
Timeframe: From the date of the first dose until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 5 years)

Overall Survival

The overall survival of ACP-319 (acalabrutinib) in subjects with relapsed/refractory CLL who are intolerant of ibrutinib therapy (NCT02717611)
Timeframe: From date of the first dose until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 5 years).

Progression-Free Survival

"The progression-free survival of ACP-196 (acalabrutinib) in subjects with relapsed / refractory CLL who are intolerant of ibrutinib therapy.~PFS is calculated as date of disease progression or death (censoring date for censored subjects) - first dose date + 1." (NCT02717611)
Timeframe: From the date of the first dose until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 5 years).

The Overall Response Rate (ORR) of ACP-196 (Acalabrutinib)

"The overall response rate (ORR) of ACP-196 (acalabrutinib) in subjects with relapsed / refractory CLL who are intolerant of ibrutinib therapy.~ORR is defined as the proportion of subjects achieving a best overall response (BOR) of either complete remission (CR), complete remission with incomplete bone marrow recovery (CRi), nodular partial remission (nPR), or partial remission (PR) at or before initiation of subsequent anticancer therapy. ORR will be analyzed per investigator's assessment." (NCT02717611)
Timeframe: From date of the first dose until the date of first documented progression or date of death from any cause, whichever came first, assessed up to approximately 4 years and 7 months). 1 cycle = 28 days

Time-to-Next Treatment

"The time to next treatment of ACP-196 (acalabrutinib) in subjects with relapsed / refractory CLL who are intolerant of ibrutinib therapy.~TTNT is defined as the time from date of first acalabrutinib treatment to date of institution of subsequent anticancer therapy for CLL or death due to any cause, whichever comes first. Subjects who do not have the above specified events prior to the data cutoff date will be censored at the date of last visit. TTNT will be calculated as follows:~(Earlier date of institution of subsequent anticancer therapy for CLL or date of death due to any cause) - date of first dose + 1. For censored subjects, date of last visit will replace earlier date of use of subsequent anticancer therapy for CLL or date of death due to any cause in the calculation." (NCT02717611)
Timeframe: From date of the first dose until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 5 years)

Number of Participants Experiencing Either a CDC Category B or C Diagnosis, CD4<200 Cells/mm^3 or CD4 Percent <14%.

Number of Participants in IT Arm Off Treatment Before 36 Weeks

The study provided fixed-dose combination emtricitabine/tenofovir DF 200/300 mg orally once daily and lopinavir/ritonavir 200/50 mg administered either as two tablets twice daily or four tablets once daily, for the first 36 weeks for individuals in the IT arm. (NCT00090779)
Timeframe: At Week 36

Number of Participants Meeting Clinical, Virologic, or Immunologic Criteria for Treatment Initiation or Re-initiation

The clinical, virologic, or immunologic criteria for treatment initiation or re-initiation include CD4 count below 350 cells/mm^3 on two consecutive determinations at least 4 weeks apart, at least 12 weeks into the study or 12 weeks post-treatment discontinuation, (2) confirmed CD4 count below 200 cells/mm^3 or CD4 percent below 14% at any time on study, (3) confirmed HIV-1 RNA level above 750,000 copies/mL 4 weeks into the study or above 200,000 copies/mL 12 weeks or more into the study, or (4) CDC Category B or C diagnosis. (NCT00090779)
Timeframe: 96 weeks since randomization

Ranked Log10 HIV-1 RNA Viral Load (log10 Copies/mL) Averaged at 72 and 76 Weeks for the IT Arm and DT Arm

"The primary endpoint is (i) the average of log10 viral loads (VL) at wks 72 and 76 for participants who continued to wk 72 off ARV for the DT arm, (ii) average wk 72 and 76 VL for those who continued to wk 36 off ARV for the IT arm and (iii) an assigned VL rank for the failures who needed ARVs or met criteria for entry into Step 2 prior to these study visits. The assigned rank for the failures was either the last observed rank carried forward or the worst rank relative to the other possible outcomes. This approach was designed to, if anything, bias against finding a treatment effect. To illustrate, consider five participants who enter the study (A, B, C, D, and E), 4 of whom (A, B, C, D) make it to 72 wks off therapy with RNA levels that increase from A to D. Participant E enters Step 2 at wk 12, at which time his RNA is in the 50th percentile. This rank would be carried forward, so the rank order of the log10 HIV-1 RNA endpoints would be A B E C D." (NCT00090779)
Timeframe: At Weeks 72 and 76

Ranked log10 HIV-1 RNA Viral Load (log10 Copies/mL) Averaged at Weeks 72 and 76 for the IT Arm and Ranked log10 HIV-1 RNA Viral Load (log10 Copies/mL) Averaged at Weeks 36 and 40 for the DT Arm

"The primary endpoint is (i) average wk 36 and 40 VL for those who continued to wk 36 off ARV for the DT arm, (ii) average wk 72 and 76 VL for those who continued to wk 36 off ARV for the IT arm and (iii) an assigned VL rank for the failures who needed ARVs or met criteria for entry into Step 2 prior to these study visits. The assigned rank for the failures was either the last observed rank carried forward or the worst rank relative to the other possible outcomes. This approach was designed to, if anything, bias against finding a treatment effect. To illustrate, consider five participants who enter the study (A, B, C, D, and E), 4 of whom (A, B, C, D) make it to 72 wks off therapy with RNA levels that increase from A to D. Participant E enters Step 2 at wk 12, at which time his RNA is in the 50th percentile. This rank would be carried forward, so the rank order of the log10 HIV-1 RNA endpoints would be A B E C D." (NCT00090779)
Timeframe: IT arm (weeks 72 and 76) and DT arm ( weeks 36 and 40)

Change in CD4 Counts Cells/mm^3 From Week 36 for IT Arm and From Week 0 for DT Arm

(NCT00090779)
Timeframe: IT arm (weeks 36, 60, 72, 84 and 96) and DT arm (weeks 0, 24, 36, 48 and 60)

Time From Study Entry in DT Arm Participants or From Week 36 in IT Arm Participants to Meeting the Clinical, Virologic, or Immunologic Criteria for Treatment Initiation or Re-initiation

5th, 10th, 25th, 50th, 75th and 90th percentiles in weeks from randomization for DT arm or from week 36 for IT arm to meeting the criteria for treatment initiation or re-initiation which include two consecutive CD4 count below 350 cells/mm^3 at least 4 weeks apart, at least 12 weeks into the study or 12 weeks post-treatment discontinuation, confirmed CD4 count below 200 cells/mm^3 or CD4 percent below 14% at any time on study, confirmed HIV-1 RNA level above 750,000 copies/mL 4 weeks into the study or above 200,000 copies/mL 12 weeks or more into the study, or CDC Category B or C diagnosis. (NCT00090779)
Timeframe: 96 weeks since randomization

Time to Meeting the Clinical, Virologic, or Immunologic Criteria for Treatment Initiation or Re-initiation

5th, 10th, 25th, 50th, 75th and 90th percentiles in weeks from randomization to meeting the criteria for treatment initiation or re-initiation which include CD4 count below 350 cells/mm^3 on two consecutive measurements at least 4 weeks apart, at least 12 weeks into the study or 12 weeks post-treatment discontinuation, confirmed CD4 count below 200 cells/mm^3 or CD4 percent below 14% at any time on study, confirmed HIV-1 RNA level above 750,000 copies/mL 4 weeks into the study or above 200,000 copies/mL 12 weeks or more into the study, or CDC Category B or C diagnosis. (NCT00090779)
Timeframe: 96 weeks since randomization

Time to Treatment Initiation or Death

5th, 10th, 25th, 50th and 75th percentiles in weeks from randomization to treatment initiation or death (NCT00090779)
Timeframe: 5 years since randomization

Change From Baseline in Alanine Aminotransferase (ALT) Levels at Week 168

Change From Baseline in Alanine Aminotransferase (ALT) Levels at Week 48

Change From Baseline in log10 Plasma HBV DNA Levels at Week 168

Change From Baseline in log10 Plasma HBV DNA Levels at Week 48

HBeAg Seroconversion at Week 48

Defined as having negative serum HBeAg and positive serum antibody to HBeAg [anti-HBe] for subjects with positive serum HBeAg at baseline. (NCT00307489)
Timeframe: 48 Weeks

HBsAg Loss at Week 168

Defined as having negative serum HBsAg for subjects with positive HBsAg at baseline. (NCT00307489)
Timeframe: 168 weeks

HBsAg Loss at Week 48

Defined as having negative serum HBsAg for subjects with positive HBsAg at baseline. (NCT00307489)
Timeframe: 48 Weeks

Hepatitis B Early Antigen (HBeAg) Loss at Week 168

Defined as having negative serum HBeAg for subjecst with positive HBeAg at baseline. (NCT00307489)
Timeframe: 168 weeks

Hepatitis B Early Antigen (HBeAg) Loss at Week 48

Defined as having negative serum HBeAg for subjects with positive HBeAg at baseline. (NCT00307489)
Timeframe: 48 Weeks

Hepatitis B Surface Antigen (HBsAg) Seroconversion at Week 168

Defined as having negative serum BHsAg and positive serum antibody to HBsAg (anti-HBs) for subject with positive serum BHsAg at baseline. (NCT00307489)
Timeframe: 168 weeks

Hepatitis B Surface Antigen (HBsAg) Seroconversion at Week 48

Defined as having negative serum HBsAg and positive serum antibody to HBsAg [anti-HBs] for subject with positive serum HBsAg at baseline. (NCT00307489)
Timeframe: 48 Weeks

Percentage of Participants With Normal ALT at Week 168

ULN for males = 43 U/L; ULN for females = 34 U/L (NCT00307489)
Timeframe: 168 weeks

Percentage of Participants With Normal ALT at Week 48

Percentage of Participants With Normalized ALT at Week 168

Subjects with elevated ALT at baseline that return to normal by Week 48. (NCT00307489)
Timeframe: 168 weeks

Percentage of Participants With Normalized ALT at Week 48

Subjects with elevated ALT at baseline that return to normal by Week 48. (NCT00307489)
Timeframe: 48 Weeks

Percentage of Participants With Plasma HBV DNA < 169 Copies/mL at Week 168

P-values were from a Cochran-Mantel-Haenszel test, controlling for baseline HBeAg status and prior lamivudine use. (NCT00307489)
Timeframe: 168 weeks

Intervention	patients (Number)
	Anemia	Febrible Neutropenia	Leukocytosis	Atrial Fibrillation	Diarrhea	Gastric Hemorrhage	Gastrointestinal Disorders-other	Mucositis Oral	Nausea	Death	Edema Limb	Fatigue	General Disorders and Admin Site Conditions	Cholecystitis	Bronchial Infection	Infections and Infestations-other	Lung Infection	Otitis Media	Sepsis	Skin Infection	Urinary Tract Infection	Alanine Aminotransferase Increased	Blood Bilirubin Increased	Lymphocyte Count Decreased	Lymphocyte Count Increased	Neutrophil Count Decreased	Platelet Count Decreased	White Blood Cell Decreased	Hyperuricemia	Hypophosphatemia	Arthralgia	Arthritis	Hematuria	Hypoxia	Respiratory Failure	Rash Maculo-papular	Hematoma	Hypertension
Treatment (Ibrutinib)	13	2	18	1	2	1	1	1	2	1	1	1	2	1	1	4	10	1	2	2	1	1	1	14	54	40	8	10	4	1	2	1	2	1	1	1	1	7

Intervention	milligram per liter (mg/L) (Mean)
Ibrutinib+BR	-0.46
Placebo+BR	-0.23

Intervention	Units on a scale (Mean)
Ibrutinib+BR	-2.1
Placebo+BR	-4.1

Intervention	Units on a scale (Mean)
Ibrutinib+BR	-4.3
Placebo+BR	4.0

Intervention	Units on a scale (Mean)
Ibrutinib+BR	-0.9
Placebo+BR	0.0

Intervention	Units on the scale (Mean)
	Lost weight	Dry mouth	Bruises	Abdominal discomfort	Temperature going up and down	Night sweats	Skin problems	Feel ill	Feel lethargic	Felt slowed down	Limited in planning activities	Worried about health in the future	Trouble with chest infections	Trouble with other infections	Repeated courses of antibiotics	Worried about picking up infection
Ibrutinib+BR	0.1	0.3	0.1	0.1	0.1	-0.6	0.4	0.1	0.1	0.3	0.2	0.0	0.2	0.7	0.9	0.3
Placebo+BR	0.0	0.1	0.0	0.0	0.0	-0.3	0.3	0.2	0.0	0.0	0.1	0.0	0.0	0.1	0.0	0.2

Intervention	Change in Log10 transformed CD4 Counts (Mean)
	IT arm (wk 60- wk 36) vs. DT arm (wk 24- wk 0)	IT arm (wk 72- wk 36) vs. DT arm (wk 36- wk 0)	IT arm (wk 84- wk 36) vs. DT arm (wk 48- wk 0)	IT arm (wk 96- wk 36) vs. DT arm (wk 60- wk 0)
DT Arm	-0.02	-0.03	-0.06	-0.02
IT Arm	-0.11	-0.10	-0.10	-0.12

Intervention	weeks (Number)
	5th percentile	10th percentile	25th percentile	50th percentile	75th percentile	90th percentile
DT Arm	6.9	12.3	26.3	60.0	96.0	96.0
IT Arm	5.1	10.4	22.7	58.1	NA	NA

Article	Year
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
Regulation of Epithelial-to-Mesenchymal Transition by Alternative Translation Initiation Mechanisms and Its Implications for Cancer Metastasis. International journal of molecular sciences, 2020, Jun-07, Volume: 21, Issue:11 Topics: Adenine; Animals; Disease Progression; Epithelial-Mesenchymal Transition; Humans; Models, Biological	2020
Incorporating acalabrutinib, a selective next-generation Bruton tyrosine kinase inhibitor, into clinical practice for the treatment of haematological malignancies. British journal of haematology, 2021, Volume: 193, Issue:1 Topics: Adenine; Agammaglobulinaemia Tyrosine Kinase; Aged; Aged, 80 and over; Benzamides; Clinical Trials a	2021
Adenine-induced chronic kidney disease in rats. Nephrology (Carlton, Vic.), 2018, Volume: 23, Issue:1 Topics: Adenine; Animals; Bone Diseases; Cardiovascular Diseases; Disease Models, Animal; Disease Progressio	2018
Management of patients with chronic lymphocytic leukemia at high risk of relapse on ibrutinib therapy. Leukemia & lymphoma, 2018, Volume: 59, Issue:10 Topics: Adenine; Agammaglobulinaemia Tyrosine Kinase; Biomarkers, Tumor; Clinical Trials as Topic; Disease P	2018
Ibrutinib Use Complicated by Progressive Multifocal Leukoencephalopathy. Oncology, 2018, Volume: 95, Issue:5 Topics: Adenine; Aged; Antineoplastic Agents; Disease Progression; Fatal Outcome; Female; Humans; Leukemia,	2018
Renal effects of novel antiretroviral drugs. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2017, 03-01, Volume: 32, Issue:3 Topics: Adenine; Alanine; Anti-HIV Agents; Atazanavir Sulfate; Cobicistat; Creatinine; Disease Progression;	2017
[Role of tenofovir in HIV and hepatitis C virus coinfection]. Enfermedades infecciosas y microbiologia clinica, 2008, Volume: 26 Suppl 8 Topics: Adenine; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Antiviral Agents; Chemical and Drug	2008
[Chronic hepatitis B: current therapy]. Bulletin de l'Academie nationale de medecine, 2008, Volume: 192, Issue:8 Topics: Adenine; Antiviral Agents; Carcinoma, Hepatocellular; Disease Progression; Guanine; Hepatitis B Vacc	2008
Tenofovir disoproxil fumarate for the treatment of chronic hepatitis B infection. Health technology assessment (Winchester, England), 2010, Volume: 14 Suppl 1 Topics: Adenine; Alanine Transaminase; Antiviral Agents; Cost-Benefit Analysis; Disease Progression; Hepatit	2010
The impact of human immunodeficiency virus on viral hepatitis. Liver international : official journal of the International Association for the Study of the Liver, 2011, Volume: 31 Suppl 1 Topics: Adenine; Antiviral Agents; Deoxycytidine; Disease Progression; Drug Therapy, Combination; Emtricitab	2011
New advances in chronic hepatitis B. Current opinion in gastroenterology, 2012, Volume: 28, Issue:3 Topics: Adenine; Antiviral Agents; Coinfection; Disease Progression; Drug Resistance, Viral; Female; Guanine	2012
Management of patients coinfected with HCV and HIV: a close look at the role for direct-acting antivirals. Gastroenterology, 2012, Volume: 142, Issue:6 Topics: Adenine; Anti-HIV Agents; Antiviral Agents; Coinfection; Deoxycytidine; Dideoxynucleosides; Disease	2012
Adenine phosphoribosyltransferase deficiency. Clinical journal of the American Society of Nephrology : CJASN, 2012, Volume: 7, Issue:9 Topics: Adenine; Adenine Phosphoribosyltransferase; Allopurinol; Animals; Biomarkers; Disease Progression; E	2012
Long-term therapy with nucleoside/nucleotide analogues for chronic hepatitis B in Asian patients. Antiviral therapy, 2013, Volume: 18, Issue:7 Topics: Adenine; Antiviral Agents; Asian People; Carcinoma, Hepatocellular; Disease Progression; Drug Resist	2013
Management of patients with decompensated HBV cirrhosis. Seminars in liver disease, 2003, Volume: 23, Issue:1 Topics: Adenine; Antiviral Agents; Carcinoma, Hepatocellular; Disease Progression; Drug Resistance; Hepatiti	2003
Mechanisms of asthma. The Journal of allergy and clinical immunology, 2003, Volume: 111, Issue:3 Suppl Topics: Adenine; Adult; Albuterol; Asthma; Bronchodilator Agents; Chemokines; Child; Cytokines; Disease Prog	2003
Slowing the progression of chronic hepatitis B. Early antiviral therapy can help minimize complications. Postgraduate medicine, 2003, Volume: 114, Issue:1 Topics: Adenine; Administration, Oral; Adult; Alanine Transaminase; Antiviral Agents; Biomarkers; Child; Dis	2003
Care of patients with chronic hepatitis B and HIV co-infection: recommendations from an HIV-HBV International Panel. AIDS (London, England), 2005, Feb-18, Volume: 19, Issue:3 Topics: Adenine; Antiviral Agents; Comorbidity; Deoxycytidine; Disease Progression; Drug Monitoring; Emtrici	2005
Management of chronic hepatitis B virus infection: current perspectives for the nurse practitioner. Journal of the American Academy of Nurse Practitioners, 2006, Volume: 18, Issue:5 Topics: Acute Disease; Adenine; Algorithms; Antiviral Agents; Carcinoma, Hepatocellular; Carrier State; Dise	2006
Chronic hepatitis B with advanced fibrosis or cirrhosis: impact of antiviral therapy. Reviews in gastroenterological disorders, 2007,Spring, Volume: 7, Issue:2 Topics: Adenine; Antiviral Agents; Disease Progression; DNA, Viral; Drug Resistance, Viral; Guanine; Hepatit	2007
HIV-1 infection and the kidney: an evolving challenge in HIV medicine. Mayo Clinic proceedings, 2007, Volume: 82, Issue:9 Topics: Acute Disease; Acute Kidney Injury; Adenine; AIDS-Associated Nephropathy; Angiotensin-Converting Enz	2007
Molecular precursor lesions in oesophageal cancer. Cancer surveys, 1998, Volume: 32 Topics: Adenine; Adenocarcinoma; Base Pairing; Carcinoma, Squamous Cell; Clone Cells; Disease Progression; E	1998
Drug therapy for hepatitis B. Advances in internal medicine, 2001, Volume: 46 Topics: Adenine; Antiviral Agents; Disease Progression; Female; Hepatitis B, Chronic; Humans; Interferons; L	2001
Treatment of hepatitis B and C following liver transplantation. Current gastroenterology reports, 2002, Volume: 4, Issue:1 Topics: Adenine; Antiviral Agents; Clinical Trials as Topic; Disease Progression; Drug Resistance; Drug Ther	2002

Article	Year
The CLL12 trial: ibrutinib vs placebo in treatment-naïve, early-stage chronic lymphocytic leukemia. Blood, 2022, 01-13, Volume: 139, Issue:2 Topics: Adenine; Adult; Aged; Aged, 80 and over; Disease Progression; Double-Blind Method; Female; Humans; K	2022
Ibrutinib With Rituximab in First-Line Treatment of Older Patients With Mantle Cell Lymphoma. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2022, 01-10, Volume: 40, Issue:2 Topics: Adenine; Age Factors; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Bioma	2022
Ibrutinib With Rituximab in First-Line Treatment of Older Patients With Mantle Cell Lymphoma. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2022, 01-10, Volume: 40, Issue:2 Topics: Adenine; Age Factors; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Bioma	2022
Ibrutinib With Rituximab in First-Line Treatment of Older Patients With Mantle Cell Lymphoma. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2022, 01-10, Volume: 40, Issue:2 Topics: Adenine; Age Factors; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Bioma	2022
Ibrutinib With Rituximab in First-Line Treatment of Older Patients With Mantle Cell Lymphoma. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2022, 01-10, Volume: 40, Issue:2 Topics: Adenine; Age Factors; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Bioma	2022
Long-term outcomes for ibrutinib-rituximab and chemoimmunotherapy in CLL: updated results of the E1912 trial. Blood, 2022, 07-14, Volume: 140, Issue:2 Topics: Adenine; Antineoplastic Combined Chemotherapy Protocols; Cyclophosphamide; Disease Progression; Huma	2022
Ibrutinib plus Bendamustine and Rituximab in Untreated Mantle-Cell Lymphoma. The New England journal of medicine, 2022, 06-30, Volume: 386, Issue:26 Topics: Adenine; Aged; Antineoplastic Combined Chemotherapy Protocols; Bendamustine Hydrochloride; Disease P	2022
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
The Egyptian journal of chest diseases and tuberculosis, 2016, Volume: 65, Issue:1 Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor P	2016
Ibrutinib for Chronic Lymphocytic Leukemia with The New England journal of medicine, 2020, 07-30, Volume: 383, Issue:5 Topics: Adenine; Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Disease Progression; Female; Follow-	2020
Assessment of ibrutinib plus rituximab in front-line CLL (FLAIR trial): study protocol for a phase III randomised controlled trial. Trials, 2017, 08-22, Volume: 18, Issue:1 Topics: Adenine; Adolescent; Adult; Aged; Antineoplastic Agents, Immunological; Antineoplastic Combined Chem	2017
Single-agent ibrutinib in relapsed or refractory follicular lymphoma: a phase 2 consortium trial. Blood, 2018, 01-11, Volume: 131, Issue:2 Topics: Adenine; Agammaglobulinaemia Tyrosine Kinase; Aged; Aged, 80 and over; CARD Signaling Adaptor Protei	2018
Venetoclax for chronic lymphocytic leukaemia progressing after ibrutinib: an interim analysis of a multicentre, open-label, phase 2 trial. The Lancet. Oncology, 2018, Volume: 19, Issue:1 Topics: Adenine; Administration, Oral; Adult; Agammaglobulinaemia Tyrosine Kinase; Aged; Aged, 80 and over;	2018
The evolutionary landscape of chronic lymphocytic leukemia treated with ibrutinib targeted therapy. Nature communications, 2017, 12-19, Volume: 8, Issue:1 Topics: Adenine; Adult; Agammaglobulinaemia Tyrosine Kinase; Aged; Aged, 80 and over; Antineoplastic Combine	2017
Randomized trial of ibrutinib vs ibrutinib plus rituximab in patients with chronic lymphocytic leukemia. Blood, 2019, 03-07, Volume: 133, Issue:10 Topics: Adenine; Adult; Aged; Aged, 80 and over; Antineoplastic Agents, Immunological; Antineoplastic Combin	2019
HIV disease progression in seroconvertors from the CAPRISA 004 tenofovir gel pre-exposure prophylaxis trial. Journal of acquired immune deficiency syndromes (1999), 2015, Jan-01, Volume: 68, Issue:1 Topics: Adenine; Disease Progression; Female; Gels; HIV Infections; Humans; Organophosphonates; Placebos; Pr	2015
The CLL12 trial protocol: a placebo-controlled double-blind Phase III study of ibrutinib in the treatment of early-stage chronic lymphocytic leukemia patients with risk of early disease progression. Future oncology (London, England), 2015, Volume: 11, Issue:13 Topics: Adenine; Adult; Aged; Aged, 80 and over; Disease Progression; Disease-Free Survival; Double-Blind Me	2015
Ibrutinib combined with bendamustine and rituximab compared with placebo, bendamustine, and rituximab for previously treated chronic lymphocytic leukaemia or small lymphocytic lymphoma (HELIOS): a randomised, double-blind, phase 3 study. The Lancet. Oncology, 2016, Volume: 17, Issue:2 Topics: Adenine; Adult; Aged; Aged, 80 and over; Anemia; Antineoplastic Combined Chemotherapy Protocols; Atr	2016
Routine versus clinically driven laboratory monitoring of HIV antiretroviral therapy in Africa (DART): a randomised non-inferiority trial. Lancet (London, England), 2010, Jan-09, Volume: 375, Issue:9709 Topics: Adenine; Adolescent; Adult; Africa; Aged; Anemia; Anti-Retroviral Agents; CD4 Lymphocyte Count; Crea	2010
Clinical outcomes of lamivudine-adefovir therapy in chronic hepatitis B cirrhosis. Journal of clinical gastroenterology, 2011, Volume: 45, Issue:9 Topics: Adenine; Aged; Antiviral Agents; Cohort Studies; Disease Progression; Drug Therapy, Combination; Fem	2011
The setpoint study (ACTG A5217): effect of immediate versus deferred antiretroviral therapy on virologic set point in recently HIV-1-infected individuals. The Journal of infectious diseases, 2012, Jan-01, Volume: 205, Issue:1 Topics: Adenine; Adult; Anti-HIV Agents; Deoxycytidine; Disease Progression; Drug Administration Schedule; D	2012
Polymorphisms of the SUR1 (ABCC8) and Kir6.2 (KCNJ11) genes predict the conversion from impaired glucose tolerance to type 2 diabetes. The Finnish Diabetes Prevention Study. The Journal of clinical endocrinology and metabolism, 2004, Volume: 89, Issue:12 Topics: Adenine; Adult; Alleles; ATP-Binding Cassette Transporters; Confidence Intervals; Diabetes Mellitus,	2004
Cost effectiveness of entecavir versus lamivudine with adefovir salvage in HBeAg-positive chronic hepatitis B. PharmacoEconomics, 2007, Volume: 25, Issue:11 Topics: Adenine; Anti-HIV Agents; Antiviral Agents; Cohort Studies; Cost-Benefit Analysis; Disease Progressi	2007
Low resistance to adefovir combined with lamivudine: a 3-year study of 145 lamivudine-resistant hepatitis B patients. Gastroenterology, 2007, Volume: 133, Issue:5 Topics: Adenine; Adult; Aged; Antiviral Agents; Disease Progression; DNA, Viral; Drug Resistance, Viral; Dru	2007
Dual vs single protease inhibitor therapy following antiretroviral treatment failure: a randomized trial. JAMA, 2002, Jul-10, Volume: 288, Issue:2 Topics: Adenine; Adult; Alkynes; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Benzoxazines; Carba	2002