1-anilino-8-naphthalenesulfonate has been researched along with Disease Exacerbation in 106 studies
1-anilino-8-naphthalenesulfonate: RN given refers to parent cpd
8-anilinonaphthalene-1-sulfonic acid : A naphthalenesulfonic acid that is naphthalene-1-sulfonic acid substituted by a phenylamino group at position 8.
| Excerpt | Relevance | Reference |
|---|---|---|
| "The addition of orlistat to a conventional weight loss regimen significantly improved oral glucose tolerance and diminished the rate of progression to the development of impaired glucose tolerance and type 2 diabetes." | 9.09 | Effects of weight loss with orlistat on glucose tolerance and progression to type 2 diabetes in obese adults. ( Boldrin, MN; Hauptman, J; Heymsfield, SB; Lucas, CP; Rissanen, A; Segal, KR; Sjöström, L; Wilding, JP, 2000) |
| "Acute pancreatitis was induced by limitation of pancreatic blood flow by clamping of inferior splenic artery for 30 min, followed by reperfusion." | 5.31 | Influence of leptin administration on the course of acute ischemic pancreatitis. ( Bilskl, J; Ceranowicz, P; Dembiński, A; Dembiński, M; Jaworek, J; Konturek, PC; Konturek, SJ; Warzecha, Z, 2002) |
| "The addition of orlistat to a conventional weight loss regimen significantly improved oral glucose tolerance and diminished the rate of progression to the development of impaired glucose tolerance and type 2 diabetes." | 5.09 | Effects of weight loss with orlistat on glucose tolerance and progression to type 2 diabetes in obese adults. ( Boldrin, MN; Hauptman, J; Heymsfield, SB; Lucas, CP; Rissanen, A; Segal, KR; Sjöström, L; Wilding, JP, 2000) |
| " Single nucleotide polymorphisms (SNPs) near the epidermal growth factor (EGF) (rs4444903), IL28B (rs12979860), and PNPLA3 (rs738409) loci are associated with treatment response, fibrosis, and hepatocellular carcinoma in non-transplant hepatitis C, but allograft population data are limited." | 3.83 | Impact of EGF, IL28B, and PNPLA3 polymorphisms on the outcome of allograft hepatitis C: a multicenter study. ( Chung, RT; Corey, KE; Curry, MP; Fuchs, BC; Gao, T; Gogela, NA; Gordon, FD; Johnson, KB; King, LY; Kothari, D; Lee, JH; Lin, MV; Misdraji, J; Mueller, JL; Nephew, LD; Simpson, MA; Tanabe, KK; Wei, L; Zheng, H, 2016) |
| "Nonalcoholic fatty liver disease (NAFLD) affects around a quarter of the global population, paralleling worldwide increases in obesity and metabolic syndrome." | 2.66 | Genetic contributions to NAFLD: leveraging shared genetics to uncover systems biology. ( Eslam, M; George, J, 2020) |
| "Nonalcoholic fatty liver disease (NAFLD), including nonalcoholic steatohepatitis (NASH), causes hepatic fibrosis, cirrhosis and hepatocellular carcinoma (HCC)." | 2.66 | Molecular Mechanisms: Connections between Nonalcoholic Fatty Liver Disease, Steatohepatitis and Hepatocellular Carcinoma. ( Goto, T; Hirotsu, Y; Kanda, T; Masuzaki, R; Moriyama, M; Omata, M, 2020) |
| "Indeed, acute pancreatitis, especially when presenting in severe forms with hyperstimulation of the pro-inflammatory response, may represent a crucial factor in the progression of COVID-19, entailing both an increase in hospitalization days and in mortality rate." | 2.66 | Involvement of the exocrine pancreas during COVID-19 infection and possible pathogenetic hypothesis: a concise review. ( De Biase, D; Fiorino, S; Gallo, C; Hong, W; Maccioni, F; Traversa, G; Zippi, M, 2020) |
| "Furthermore, NAFLD is believed to be involved in the pathogenesis of common disorders such as type 2 diabetes and cardiovascular disease." | 2.61 | Non-alcoholic fatty liver disease: causes, diagnosis, cardiometabolic consequences, and treatment strategies. ( Cusi, K; Häring, HU; Stefan, N, 2019) |
| "Nonalcoholic fatty liver disease (NAFLD), now the leading cause of liver damage worldwide, is epidemiologically associated with obesity, insulin resistance and type 2 diabetes, and is a potentially progressive condition to advanced liver fibrosis and hepatocellular carcinoma." | 2.58 | Genetics of Nonalcoholic Fatty Liver Disease: A 2018 Update. ( Baselli, GA; Valenti, LVC, 2018) |
| "Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease worldwide." | 2.58 | The genetic backgrounds in nonalcoholic fatty liver disease. ( Itoh, Y; Seko, Y; Yamaguchi, K, 2018) |
| "Both ARLD and NAFLD are multifactorial and refer to a spectrum of disease severity, ranging from steatosis through steatohepatitis to fibrosis and cirrhosis." | 2.58 | Genetics of alcoholic liver disease and non-alcoholic steatohepatitis. ( Anstee, QM; Scott, E, 2018) |
| "Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States and represents an increasingly important etiology of hepatocellular carcinoma (HCC) with annual cumulative incidence rates ranging from 2% to 12% in cohorts of NAFLD cirrhosis." | 2.53 | Hepatocellular carcinoma in patients with non-alcoholic fatty liver disease. ( Lim, JK; Nguyen, MH; Wong, CR, 2016) |
| "Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum that spans simple steatosis, through nonalcoholic steatohepatitis (NASH) to fibrosis and ultimately cirrhosis." | 2.52 | The Genetics of Nonalcoholic Fatty Liver Disease: Spotlight on PNPLA3 and TM6SF2. ( Anstee, QM; Day, CP, 2015) |
| "Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and comprises a liver disease spectrum ranging from steatosis to nonalcoholic steatohepatitis (NASH) with risk of progression to liver cirrhosis and hepatocellular carcinoma (HCC)." | 2.52 | Challenges and Management of Liver Cirrhosis: Practical Issues in the Therapy of Patients with Cirrhosis due to NAFLD and NASH. ( Halilbasic, E; Hofer, H; Kazemi-Shirazi, L; Kienbacher, C; Munda, P; Rechling, C; Trauner, M; Traussnigg, S, 2015) |
| "Non-alcoholic fatty liver disease (NAFLD) is the most frequent chronic liver disease in Western countries, ranging from simple steatosis to steatohepatitis, cirrhosis, and hepatocellular cancer." | 2.50 | Role of metabolic lipases and lipolytic metabolites in the pathogenesis of NAFLD. ( Claudel, T; Fuchs, CD; Trauner, M, 2014) |
| "NAFLD is a disease spectrum ranging from simple steatosis, through steatohepatitis to fibrosis and, ultimately, cirrhosis." | 2.49 | The genetics of NAFLD. ( Anstee, QM; Day, CP, 2013) |
| "Nonalcoholic fatty liver disease (NAFLD) in most patients involves only simple hepatic steatosis; however, a minority develop progressive steatohepatitis." | 2.47 | Genetic determinants of susceptibility and severity in nonalcoholic fatty liver disease. ( Ballestri, S; Carulli, L; Daly, AK; Day, CP; Loria, P, 2011) |
| "Thirteen hospitalized dogs with acute pancreatitis diagnosed based on clinical signs, serum cPLI concentrations, and imaging findings were enrolled." | 1.62 | Serum concentrations of canine pancreatic lipase immunoreactivity and C-reactive protein for monitoring disease progression in dogs with acute pancreatitis. ( Fosgate, GT; Keany, KM; Perry, SM; Steiner, JM; Stroup, ST, 2021) |
| "Fibrosis progression in autoimmune hepatitis can be attenuated by immunosuppressive treatment; however, some patients progress despite therapy." | 1.56 | The PNPLA3 rs738409 GG genotype is associated with poorer prognosis in 239 patients with autoimmune hepatitis. ( Großhennig, A; Kirstein, MM; Manns, MP; Marhenke, S; Mederacke, I; Mederacke, YS; Metzler, F; Vogel, A, 2020) |
| "Non-alcoholic fatty liver disease (NAFLD) is a common chronic condition caused by the accumulation of fat in the liver." | 1.56 | Validating candidate biomarkers for different stages of non-alcoholic fatty liver disease. ( Al-Otaibi, M; Al-Qarni, R; Al-Saif, F; Alfadda, AA; Alkhalidi, H; Bamehriz, F; Hassanain, M; Iqbal, M, 2020) |
| "'Severe NAFLD' was defined as the presence of steatohepatitis, NAFLD activity score ≥4 or fibrosis stage ≥2." | 1.56 | Liver transcriptomics highlights interleukin-32 as novel NAFLD-related cytokine and candidate biomarker. ( Badiali, S; Baselli, GA; Dongiovanni, P; Fracanzani, AL; Maggioni, M; Mancina, RM; Maurotti, S; Meroni, M; Montalcini, T; Pelusi, S; Pingitore, P; Prati, D; Rametta, R; Romeo, S; Rossi, G; Taliento, AE; Valenti, L, 2020) |
| "Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in children and adolescents today." | 1.51 | Genetic determinants of steatosis and fibrosis progression in paediatric non-alcoholic fatty liver disease. ( Berndt, N; Bläker, H; Bufler, P; Cadenas, C; Golka, K; Hengstler, JG; Henning, S; Holzhütter, HG; Hudert, CA; Jansen, PLM; Loddenkemper, C; Meierhofer, D; Reinders, J; Rudolph, B; Selinski, S; Thielhorn, R; Wiegand, S, 2019) |
| "Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver illness with a genetically heterogeneous background that can be accompanied by considerable morbidity and attendant health care costs." | 1.51 | GWAS and enrichment analyses of non-alcoholic fatty liver disease identify new trait-associated genes and pathways across eMERGE Network. ( Benoit, B; Carey, DJ; Carrell, DS; Carroll, RJ; Cobb, BL; Connolly, JJ; Crosslin, DR; Divanovic, S; Gharavi, AG; Hakonarson, H; Harley, ITW; Harley, JB; Huang, Y; Jarvik, GP; Kullo, IJ; Larson, EB; Li, R; Lingren, T; Mentch, FD; Murphy, S; Namjou, B; Niu, X; Pacheco, JA; Parameswaran, S; Ritchie, MD; Stanaway, IB; Verma, S; Wei, WQ; Williams, MS; Xanthakos, SA, 2019) |
| "In human breast cancer, high LIPG expression was observed in a limited subset of tumours and was significantly associated with shorter metastasis-free survival in node-negative, untreated patients." | 1.51 | LIPG-promoted lipid storage mediates adaptation to oxidative stress in breast cancer. ( Adawy, A; Cadenas, C; Claus, M; Edlund, K; Franckenstein, D; Frank, S; Gianmoena, K; Glotzbach, A; Grgas, K; Hayen, H; Hellwig, B; Hengstler, JG; Käfferlein, HU; Lesjak, MS; Madjar, K; Marchan, R; Mardinoglu, A; Micke, P; Pontén, F; Rahnenführer, J; Schmidt, M; Schriewer, A; Stewart, JD; Thaler, S; Vosbeck, S; Watzl, C; Zhang, C, 2019) |
| "Identifying NAFLD patients at risk of progression is crucial to orient medical care and resources." | 1.48 | Combining Genetic Variants to Improve Risk Prediction for NAFLD and Its Progression to Cirrhosis: A Proof of Concept Study. ( Antonelli-Incalzi, R; Baiocchini, A; Carotti, S; Cecere, R; De Vincentis, A; Del Nonno, F; Dell'Unto, C; Delle Monache, M; Galati, G; Gallo, P; Giannelli, V; Morini, S; Pellicelli, AM; Picardi, A; Rosati, D; Valentini, F; Vespasiani-Gentilucci, U, 2018) |
| "The ability of lipolysis in breast cancer cells were measured, as well as the expression of the rate-limiting lipase ATGL and fatty acid transporter FABP5." | 1.48 | Utilization of adipocyte-derived lipids and enhanced intracellular trafficking of fatty acids contribute to breast cancer progression. ( Li, Y; Ren, G; Sun, J; Tan, J; Tan, Y; Wang, Y; Xiang, T; Xing, L; Yang, D; Zeng, B, 2018) |
| "Non-alcoholic fatty liver disease (NAFLD) has a prevalence of approximately 30% in western countries, and is emerging as the first cause of liver cirrhosis and hepatocellular carcinoma (HCC)." | 1.48 | Promoting genetics in non-alcoholic fatty liver disease: Combined risk score through polymorphisms and clinical variables. ( Antonelli-Incalzi, R; Dell'Unto, C; Gallo, P; Picardi, A; Vespasiani-Gentilucci, U; Volpentesta, M, 2018) |
| "Advanced liver fibrosis was neither associated with PNPLA3 (p = 0." | 1.42 | The Impact of PNPLA3 rs738409 SNP on Liver Fibrosis Progression, Portal Hypertension and Hepatic Steatosis in HIV/HCV Coinfection. ( Aichelburg, MC; Bota, S; Bucsics, T; Ferenci, P; Grabmeier-Pfistershammer, K; Mandorfer, M; Payer, BA; Peck-Radosavljevic, M; Reiberger, T; Scheiner, B; Schwabl, P; Stättermayer, A; Trauner, M, 2015) |
| "Although most hepatocellular carcinoma (HCC) is related to chronic viral hepatitis or alcoholic liver disease, the incidence of NAFLD-related HCC is increasing." | 1.40 | Carriage of the PNPLA3 rs738409 C >G polymorphism confers an increased risk of non-alcoholic fatty liver disease associated hepatocellular carcinoma. ( Anstee, QM; Burt, AD; Daly, AK; Day, CP; Dufour, JF; Leathart, JB; Liu, YL; Patman, GL; Piguet, AC; Reeves, HL, 2014) |
| "Since hyperglycemia aggravates acute pancreatitis and also activates the receptor for advanced glycation endproducts (RAGE) in other organs, we explored if RAGE is expressed in the pancreas and if its expression is regulated during acute pancreatitis and hyperglycemia." | 1.39 | Impact of hyperglycemia and acute pancreatitis on the receptor for advanced glycation endproducts. ( Bürtin, F; Butschkau, A; Genz, B; Kroemer, T; Kuhla, A; Sempert, K; Timm, F; Vollmar, B; Zechner, D, 2013) |
| "The etiology of NAFLD is multifactorial." | 1.39 | PNPLA3, a genetic marker of progressive liver disease, still hiding its metabolic function? ( Burnol, AF; Dubuquoy, C; Moldes, M, 2013) |
| "Obesity is an emerging risk factor for chronic kidney disease (CKD) in the developed world." | 1.39 | Orlistat, an under-recognised cause of progressive renal impairment. ( Coutinho, AK; Glancey, GR, 2013) |
| "We identify BSSL as a marker for HIV-1 disease progression and emergence of X4 variants." | 1.38 | HIV-1 disease progression is associated with bile-salt stimulated lipase (BSSL) gene polymorphism. ( Bakker, M; Kootstra, NA; Paxton, WA; Pollakis, G; Stax, MJ; Tanck, MW; van 't Wout, AB, 2012) |
| "We defined various liver fibrosis phenotypes on the basis of METAVIR scores, with and without taking the duration of HCV infection into account." | 1.38 | Genome-wide association study identifies variants associated with progression of liver fibrosis from HCV infection. ( Abel, L; Argiro, L; Bibert, S; Bochud, PY; Boland, A; Booth, DR; Bourlière, M; Bousquet, L; Bréchot, C; Casanova, JL; Cerny, A; Dufour, JF; George, J; Guergnon, J; Halfon, P; Heim, MH; Hirsch, H; Jacobson, IM; Jouanguy, E; Kutalik, Z; Malinverni, R; Martinetti, G; Moradpour, D; Müllhaupt, B; Munteanu, M; Nalpas, B; Negro, F; Patin, E; Pol, S; Poynard, T; Rice, CM; Semela, D; Stewart, G; Suppiah, V; Talal, AH; Theodorou, I, 2012) |
| "The severity of acute pancreatitis was assessed 0 h or 1, 2, 3, 5 and 10 days after the last dose of cerulein." | 1.36 | Role of hormonal axis, growth hormone - IGF-1, in the therapeutic effect of ghrelin in the course of cerulein-induced acute pancreatitis. ( Ceranowicz, D; Ceranowicz, P; Cieszkowski, J; Dembinski, A; Kato, I; Kusnierz-Cabala, B; Kuwahara, A; Tomaszewska, R; Warzecha, Z, 2010) |
| " Clinically cardiac adverse events were defined as need for reoperation (n = 88; 46%), reintervention (n = 58; 30%), or angina (n = 89; 46%)." | 1.35 | Gene polymorphisms in APOE, NOS3, and LIPC genes may be risk factors for cardiac adverse events after primary CABG. ( Beiras-Fernandez, A; Eifert, S; Lohse, P; Nollert, G; Rasch, A; Reichart, B, 2009) |
| "To evaluate coronary atherosclerosis, we used CSI (coronary stenosis index) calculated from coronary angiograms." | 1.33 | CETP (cholesteryl ester transfer protein) promoter -1337 C>T polymorphism protects against coronary atherosclerosis in Japanese patients with heterozygous familial hypercholesterolaemia. ( Higashikata, T; Inazu, A; Katsuda, S; Kawashiri, MA; Kobayashi, J; Mabuchi, H; Miwa, K; Nohara, A; Takata, M; Yamagishi, M, 2006) |
| "Chronic pancreatitis is a common cause of exocrine pancreatic insufficiency (EPI) in humans and cats but is rarely recognised in dogs in which pancreatic acinar atrophy (PAA) is reportedly more common." | 1.32 | Exocrine pancreatic insufficiency as an end stage of pancreatitis in four dogs. ( Watson, PJ, 2003) |
| "Acute pancreatitis was induced by limitation of pancreatic blood flow by clamping of inferior splenic artery for 30 min, followed by reperfusion." | 1.31 | Influence of leptin administration on the course of acute ischemic pancreatitis. ( Bilskl, J; Ceranowicz, P; Dembiński, A; Dembiński, M; Jaworek, J; Konturek, PC; Konturek, SJ; Warzecha, Z, 2002) |
| "The following were recorded: disease progression (CDC class), nutritional status (weight Z-score), CD4 lymphocyte count, drug treatment during the previous 12 months, presence of opportunistic infections, clinical evidence of acute pancreatitis (increased serum pancreatic enzymes associated with vomiting, abdominal distention, and intolerance when eating)." | 1.30 | Serum pancreatic enzymes in human immunodeficiency virus-infected children. A collaborative study of the Italian Society of Pediatric Gastroenterology and Hepatology. ( Bastoni, K; Bavusotto, A; Boccia, MC; Canani, RB; Carroccio, A; Fontana, M; Guarino, A; Montalto, G; Spagnuolo, MI; Verghi, F; Zuin, G, 1998) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 5 (4.72) | 18.2507 |
| 2000's | 15 (14.15) | 29.6817 |
| 2010's | 71 (66.98) | 24.3611 |
| 2020's | 15 (14.15) | 2.80 |
| Authors | Studies |
|---|---|
| Oliveira, CP | 1 |
| Liu, Q | 1 |
| Li, L | 2 |
| Xu, D | 1 |
| Zhu, J | 1 |
| Huang, Z | 1 |
| Yang, J | 2 |
| Cheng, S | 1 |
| Gu, Y | 1 |
| Zheng, L | 1 |
| Zhang, X | 2 |
| Shen, H | 1 |
| Eslam, M | 1 |
| George, J | 2 |
| Crisan, D | 1 |
| Grigorescu, M | 1 |
| Crisan, N | 1 |
| Craciun, R | 1 |
| Lupsor, M | 1 |
| Radu, C | 1 |
| Grigorescu, MD | 1 |
| Suciu, A | 1 |
| Epure, F | 1 |
| Avram, L | 1 |
| Leach, N | 1 |
| Daijo, K | 1 |
| Nakahara, T | 1 |
| Inagaki, Y | 1 |
| Nanba, M | 1 |
| Nishida, Y | 1 |
| Uchikawa, S | 1 |
| Kodama, K | 1 |
| Oya, K | 1 |
| Morio, K | 1 |
| Fujino, H | 1 |
| Ono, A | 1 |
| Murakami, E | 1 |
| Yamauchi, M | 1 |
| Kawaoka, T | 1 |
| Miki, D | 1 |
| Tsuge, M | 1 |
| Hiramatsu, A | 1 |
| Hayes, CN | 1 |
| Imamura, M | 1 |
| Aikata, H | 1 |
| Ochi, H | 2 |
| Chayama, K | 2 |
| Baselli, GA | 2 |
| Dongiovanni, P | 5 |
| Rametta, R | 2 |
| Meroni, M | 1 |
| Pelusi, S | 1 |
| Maggioni, M | 2 |
| Badiali, S | 1 |
| Pingitore, P | 2 |
| Maurotti, S | 1 |
| Montalcini, T | 2 |
| Taliento, AE | 1 |
| Prati, D | 1 |
| Rossi, G | 1 |
| Fracanzani, AL | 2 |
| Mancina, RM | 3 |
| Romeo, S | 3 |
| Valenti, L | 6 |
| Kanda, T | 1 |
| Goto, T | 1 |
| Hirotsu, Y | 1 |
| Masuzaki, R | 1 |
| Moriyama, M | 1 |
| Omata, M | 1 |
| Mederacke, YS | 1 |
| Kirstein, MM | 2 |
| Großhennig, A | 1 |
| Marhenke, S | 2 |
| Metzler, F | 1 |
| Manns, MP | 1 |
| Vogel, A | 2 |
| Mederacke, I | 1 |
| Attané, C | 1 |
| Muller, C | 1 |
| Al-Qarni, R | 1 |
| Iqbal, M | 1 |
| Al-Otaibi, M | 1 |
| Al-Saif, F | 1 |
| Alfadda, AA | 1 |
| Alkhalidi, H | 1 |
| Bamehriz, F | 1 |
| Hassanain, M | 1 |
| Lim, MA | 1 |
| Pranata, R | 1 |
| Jabłońska, J | 1 |
| Kluska, M | 1 |
| Lin, XJ | 1 |
| Liu, R | 1 |
| Li, C | 2 |
| Yi, X | 1 |
| Fu, B | 1 |
| Walker, MJ | 1 |
| Xu, XM | 1 |
| Sun, G | 1 |
| Lin, CH | 1 |
| Lan, NSR | 1 |
| Yeap, BB | 1 |
| Fegan, PG | 1 |
| Green, G | 1 |
| Rankin, JM | 1 |
| Dwivedi, G | 1 |
| Habibi, A | 1 |
| Karami, S | 1 |
| Varmira, K | 1 |
| Hadadi, M | 1 |
| Zhang, M | 1 |
| Li, Q | 1 |
| Lan, X | 1 |
| Li, X | 1 |
| Zhang, Y | 2 |
| Wang, Z | 1 |
| Zheng, J | 1 |
| Eskandari-Sedighi, G | 1 |
| Cortez, LM | 1 |
| Daude, N | 1 |
| Shmeit, K | 1 |
| Sim, V | 1 |
| Westaway, D | 1 |
| Weigand, S | 1 |
| O'Connor, M | 1 |
| Blažek, P | 1 |
| Kantenwein, V | 1 |
| Friedrich, L | 1 |
| Grebmer, C | 1 |
| Schaarschmidt, C | 1 |
| von Olshausen, G | 1 |
| Reents, T | 1 |
| Deisenhofer, I | 1 |
| Lennerz, C | 1 |
| Kolb, C | 1 |
| Iwata, H | 1 |
| Sassa, N | 1 |
| Kato, M | 2 |
| Murase, Y | 1 |
| Seko, S | 1 |
| Kawanishi, H | 1 |
| Hattori, R | 1 |
| Gotoh, M | 1 |
| Tsuzuki, T | 1 |
| Chen, D | 1 |
| Zhang, J | 1 |
| Chen, YP | 2 |
| Li, Y | 3 |
| Zhou, M | 1 |
| Waterhouse, GIN | 1 |
| Sun, J | 2 |
| Shi, W | 1 |
| Ai, S | 1 |
| Manne, ASN | 1 |
| Hegde, AR | 1 |
| Raut, SY | 1 |
| Rao, RR | 1 |
| Kulkarni, VI | 1 |
| Mutalik, S | 1 |
| Jafari, R | 1 |
| Hectors, SJ | 1 |
| Koehne de González, AK | 1 |
| Spincemaille, P | 1 |
| Prince, MR | 1 |
| Brittenham, GM | 1 |
| Wang, Y | 2 |
| Banini, BA | 1 |
| Kumar, DP | 1 |
| Cazanave, S | 1 |
| Seneshaw, M | 1 |
| Mirshahi, F | 1 |
| Santhekadur, PK | 1 |
| Wang, L | 1 |
| Guan, HP | 1 |
| Oseini, AM | 1 |
| Alonso, C | 1 |
| Bedossa, P | 1 |
| Koduru, SV | 1 |
| Min, HK | 1 |
| Sanyal, AJ | 1 |
| Zippi, M | 1 |
| Hong, W | 1 |
| Traversa, G | 1 |
| Maccioni, F | 1 |
| De Biase, D | 1 |
| Gallo, C | 1 |
| Fiorino, S | 1 |
| Gao, Y | 1 |
| Xie, H | 1 |
| Selen, ES | 1 |
| Choi, J | 1 |
| Wolfgang, MJ | 1 |
| Keany, KM | 1 |
| Fosgate, GT | 1 |
| Perry, SM | 1 |
| Stroup, ST | 1 |
| Steiner, JM | 1 |
| Gulley, JL | 1 |
| Rajan, A | 1 |
| Spigel, DR | 1 |
| Iannotti, N | 1 |
| Chandler, J | 1 |
| Wong, DJL | 1 |
| Leach, J | 1 |
| Edenfield, WJ | 1 |
| Wang, D | 1 |
| Grote, HJ | 1 |
| Heydebreck, AV | 1 |
| Chin, K | 1 |
| Cuillerot, JM | 1 |
| Kelly, K | 1 |
| Kawamura, Y | 1 |
| Ikeda, K | 1 |
| Arase, Y | 1 |
| Fujiyama, S | 1 |
| Hosaka, T | 1 |
| Kobayashi, M | 2 |
| Saitoh, S | 1 |
| Sezaki, H | 1 |
| Akuta, N | 1 |
| Suzuki, F | 1 |
| Suzuki, Y | 1 |
| Kumada, H | 2 |
| DeWeerdt, S | 1 |
| Seko, Y | 1 |
| Yamaguchi, K | 1 |
| Itoh, Y | 1 |
| Stickel, F | 1 |
| Buch, S | 1 |
| Nischalke, HD | 1 |
| Weiss, KH | 1 |
| Gotthardt, D | 1 |
| Fischer, J | 1 |
| Rosendahl, J | 1 |
| Marot, A | 1 |
| Elamly, M | 1 |
| Casper, M | 1 |
| Lammert, F | 1 |
| McQuillin, A | 1 |
| Zopf, S | 1 |
| Spengler, U | 1 |
| Eyer, F | 1 |
| von Felden, J | 1 |
| Wege, H | 1 |
| Buch, T | 1 |
| Schafmayer, C | 1 |
| Braun, F | 1 |
| Deltenre, P | 1 |
| Berg, T | 1 |
| Morgan, MY | 1 |
| Hampe, J | 1 |
| Lu, FB | 1 |
| Hu, ED | 1 |
| Xu, LM | 1 |
| Chen, L | 1 |
| Wu, JL | 1 |
| Li, H | 1 |
| Chen, DZ | 1 |
| Jiménez-Sousa, MÁ | 1 |
| Gómez-Moreno, AZ | 1 |
| Pineda-Tenor, D | 1 |
| Sánchez-Ruano, JJ | 1 |
| Fernández-Rodríguez, A | 1 |
| Artaza-Varasa, T | 1 |
| Gómez-Sanz, A | 1 |
| Martín-Vicente, M | 1 |
| Vázquez-Morón, S | 1 |
| Resino, S | 1 |
| Scott, E | 1 |
| Anstee, QM | 5 |
| Vespasiani-Gentilucci, U | 2 |
| Dell'Unto, C | 2 |
| De Vincentis, A | 1 |
| Baiocchini, A | 1 |
| Delle Monache, M | 1 |
| Cecere, R | 1 |
| Pellicelli, AM | 1 |
| Giannelli, V | 1 |
| Carotti, S | 1 |
| Galati, G | 1 |
| Gallo, P | 2 |
| Valentini, F | 1 |
| Del Nonno, F | 1 |
| Rosati, D | 1 |
| Morini, S | 1 |
| Antonelli-Incalzi, R | 2 |
| Picardi, A | 2 |
| Yang, D | 1 |
| Xing, L | 1 |
| Tan, Y | 1 |
| Zeng, B | 1 |
| Xiang, T | 1 |
| Tan, J | 1 |
| Ren, G | 1 |
| Parajuli, N | 1 |
| Takahara, S | 1 |
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| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Association of Anesthesia Technique With Morbidity and Mortality in Patients With COVID-19 and Surgery for Hip Fracture: a Retrospective Population Cohort Study[NCT05133648] | 1,000 participants (Anticipated) | Observational | 2023-01-05 | Active, not recruiting | |||
| PAveMenT: Phase Ib Study of Palbociclib and Avelumab in Metastatic AR+ Triple Negative Breast Cancer[NCT04360941] | Phase 1 | 45 participants (Anticipated) | Interventional | 2020-08-11 | Recruiting | ||
| A Phase I, Open-label, Multiple-ascending Dose Trial to Investigate the Safety, Tolerability, Pharmacokinetics, Biological and Clinical Activity of Avelumab (MSB0010718C) in Subjects With Metastatic or Locally Advanced Solid Tumors and Expansion to Select[NCT01772004] | Phase 1 | 1,756 participants (Actual) | Interventional | 2013-01-31 | Completed | ||
| The Role of Microbiome Reprogramming on Liver Fat Accumulation[NCT03914495] | 57 participants (Actual) | Interventional | 2019-05-21 | Terminated (stopped due to PI carefully considered multiple factors and decided to close study to any further enrollment.) | |||
| Comparative Clinical Study to Evaluate the Possible Beneficial Effect of Empagliflozin Versus Pioglitazone on Non-diabetic Patients With Non-Alcoholic Steatohepatitis[NCT05605158] | Phase 3 | 56 participants (Anticipated) | Interventional | 2022-11-30 | Not yet recruiting | ||
| 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 | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Apparent terminal half-life was defined as the time required for the serum concentration of drug to decrease 50 percent in the final stage of its elimination. (NCT01772004)
Timeframe: Pre-infusion, at end of 1-hour infusion (Day 1), 0.5, 1, 2, 4, 6,12, 24, 36, 48 hours after end of infusion
| Intervention | Hours (Median) |
|---|---|
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 61.425 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 89.064 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 97.440 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 108.671 |
Area under the serum concentration versus time curve from time zero to the last sampling time t at which the concentration is at or above the lower limit of quantification (LLLQ). AUC(0-t) was calculated according to the mixed log-linear trapezoidal rule. (NCT01772004)
Timeframe: Pre-infusion, at end of 1-hour infusion (Day 1), 0.5, 1, 2, 4, 6,12, 24, 36, 48 hours after end of infusion
| Intervention | Hours*micrograms per milliliter (Mean) |
|---|---|
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 1040 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 6080 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 22749.4 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 45100 |
The AUC(0-inf) was estimated by determining the total area under the curve of the concentration versus time curve extrapolated to infinity. (NCT01772004)
Timeframe: Pre-infusion, at end of 1-hour infusion (Day 1), 0.5, 1, 2, 4, 6,12, 24, 36, 48 hours after end of infusion
| Intervention | Hours*micrograms per milliliter (Mean) |
|---|---|
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 1290 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 6850 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 25920.9 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 46600 |
Cmax is the maximum observed serum concentration obtained directly from the concentration versus time curve. (NCT01772004)
Timeframe: Pre-infusion, at end of 1-hour infusion (Day 1), 0.5, 1, 2, 4, 6,12, 24, 36, 48 hours after end of infusion
| Intervention | Micrograms per milliliter (mcg/mL) (Mean) |
|---|---|
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 18.7 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 81.9 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 249.048 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 489 |
DLT: defined using National Cancer Institute Common Toxicity Criteria for Adverse Events Version 4.0, as any one of following: any Grade (Gr) >=3toxicity that is possibly/probably/ definitely related to avelumab, except for any of following: Gr 3 infusion-related reaction resolving within 6 hours and controlled with medical management, Transient Gr 3 flu-like symptoms/fever, which is controlled with medical management, Transient Gr 3 fatigue, local reactions, headache, nausea, emesis that resolves to <= Gr 1, Gr3 diarrhea, Gr 3 skin toxicity, Gr 3 liver function test increase that resolves to <= Gr1 in < 7 days after medical management has been initiated, Single laboratory values out of normal range that were unlikely related to study treatment according to investigator, did not have any clinical correlate, and resolved to <= Gr1 within 7 days with adequate medical management and tumor flare phenomenon defined as local pain, irritation/rash localized at sites of known/suspected tumor. (NCT01772004)
Timeframe: Dose Escalation: Baseline up to Week 3
| Intervention | Participants (Count of Participants) |
|---|---|
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 0 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 0 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 0 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 1 |
Serum samples were analyzed by a validated electrochemiluminescence immunoassay to detect the presence of antidrug antibodies (ADA). Number of participants with ADA positive results for Avelumab were reported. (NCT01772004)
Timeframe: Dose Escalation: Baseline up to Day 1023
| Intervention | Participants (Count of Participants) |
|---|---|
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 0 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 2 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 0 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 0 |
Tmax is time to reach maximum observed serum concentration obtained directly from the concentration versus time curve. (NCT01772004)
Timeframe: Pre-infusion, at end of 1-hour infusion (Day 1), 0.5, 1, 2, 4, 6,12, 24, 36, 48 hours after end of infusion
| Intervention | Hours (Median) |
|---|---|
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 1.500 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 1.500 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 1.500 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 1.717 |
Duration of response according to modified irRC, per investigator assessment was calculated for each participant with a confirmed response (immune-related complete response [irCR] or immune-related partial response [irPR]) as the time from the first observation of response to the first observation of documented disease progression (or death within 12 weeks of the last tumor assessment). irCR: Complete disappearance of all tumor lesions (both index and non-index lesions with no new measurable/unmeasurable lesions). irPR: At least 30% reduction from baseline in the sum of the longest diameter (SLD) of all lesions). Results were calculated based on Kaplan-Meier estimates. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Months (Median) |
|---|---|
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 21.13 |
| Primary Expansion Cohort: NSCLC, First Line | NA |
| Primary Expansion Cohort: Metastatic Breast Cancer | 8.31 |
| Primary Expansion Cohort: GC/GEJC Progressed | 4.14 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 22.23 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | NA |
| Secondary Expansion Cohort: Melanoma | NA |
| Secondary Expansion Cohort: Mesothelioma | 15.21 |
| Secondary Expansion Cohort: Urothelial Carcinoma | NA |
| Secondary Expansion Cohort: Ovarian Cancer | NA |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 10.61 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | NA |
| Efficacy Expansion Cohort: Ovarian Cancer | NA |
| Efficacy Expansion Cohort: Urothelial Carcinoma | NA |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | NA |
| Efficacy Expansion Cohort: HNSCC | NA |
Duration of response according to RECIST 1.1, per investigator assessment was calculated for each participant with a confirmed response (complete response [CR] or partial response [PR]) as the time from the first observation of response to the first observation of documented disease progression (or death within 12 weeks of the last tumor assessment). CR: Disappearance of all evidence of target and non-target lesions. PR: At least 30 percent (%) reduction from baseline in the sum of the longest diameter (SLD) of all lesions. Results were calculated based on Kaplan-Meier estimates. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Months (Median) |
|---|---|
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 17.48 |
| Primary Expansion Cohort: NSCLC, First Line | 12.02 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 8.33 |
| Primary Expansion Cohort: GC/GEJC Progressed | 3.48 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 21.42 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 8.41 |
| Secondary Expansion Cohort: Melanoma | NA |
| Secondary Expansion Cohort: Mesothelioma | 15.21 |
| Secondary Expansion Cohort: Urothelial Carcinoma | NA |
| Secondary Expansion Cohort: Ovarian Cancer | 10.38 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 9.94 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | NA |
| Efficacy Expansion Cohort: Ovarian Cancer | NA |
| Efficacy Expansion Cohort: Urothelial Carcinoma | NA |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | NA |
| Efficacy Expansion Cohort: HNSCC | NA |
The irPFS time was defined as the time from first administration of study treatment until first documentation of immune-related progressive disease (irPD) or death when death occurred within 12 weeks of the last tumor assessment or first administration of study treatment (whichever was later). irPD: sum of the longest diameters of target and new measurable lesions increases greater than or equal to [>=] 20%, confirmed by a repeat, consecutive observations at least 4 weeks from the date first documented. The analysis of irPFS will be performed with a Kaplan-Meier method. Data for immune related progression-free survival time has been reported. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Months (Median) |
|---|---|
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 4.04 |
| Primary Expansion Cohort: NSCLC, First Line | 6.93 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 1.64 |
| Primary Expansion Cohort: GC/GEJC Progressed | 1.81 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 4.14 |
| Secondary Expansion Cohort: Colorectal Cancer | 2.79 |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | NA |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 3.81 |
| Secondary Expansion Cohort: Melanoma | 6.83 |
| Secondary Expansion Cohort: Mesothelioma | 6.18 |
| Secondary Expansion Cohort: Urothelial Carcinoma | 4.07 |
| Secondary Expansion Cohort: Ovarian Cancer | 4.04 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 8.34 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 6.90 |
| Efficacy Expansion Cohort: Ovarian Cancer | 2.60 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 2.46 |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 1.35 |
| Efficacy Expansion Cohort: HNSCC | 2.83 |
Serum samples were analyzed by a validated electrochemiluminescence immunoassay to detect the presence of antidrug antibodies (ADA). Number of participants with ADA positive results for Avelumab were reported. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Participants (Count of Participants) |
|---|---|
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 17 |
| Primary Expansion Cohort: NSCLC, First Line | 9 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 17 |
| Primary Expansion Cohort: GC/GEJC Progressed | 3 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 6 |
| Secondary Expansion Cohort: Colorectal Cancer | 0 |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | 0 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 4 |
| Secondary Expansion Cohort: Melanoma | 5 |
| Secondary Expansion Cohort: Mesothelioma | 3 |
| Secondary Expansion Cohort: Urothelial Carcinoma | 2 |
| Secondary Expansion Cohort: Ovarian Cancer | 5 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 5 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 3 |
| Efficacy Expansion Cohort: Ovarian Cancer | 5 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 17 |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 6 |
| Efficacy Expansion Cohort: HNSCC | 5 |
Overall survival time was measured as time in months first administration of trial treatment to death. The analysis of OS time was performed with a Kaplan-Meier method. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Months (Median) |
|---|---|
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 8.57 |
| Primary Expansion Cohort: NSCLC, First Line | 14.23 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 8.38 |
| Primary Expansion Cohort: GC/GEJC Progressed | 6.64 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 11.07 |
| Secondary Expansion Cohort: Colorectal Cancer | 11.20 |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | 19.32 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 10.55 |
| Secondary Expansion Cohort: Melanoma | 17.22 |
| Secondary Expansion Cohort: Mesothelioma | 10.71 |
| Secondary Expansion Cohort: Urothelial Carcinoma | 13.70 |
| Secondary Expansion Cohort: Ovarian Cancer | 11.17 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | NA |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 16.85 |
| Efficacy Expansion Cohort: Ovarian Cancer | 9.13 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 6.97 |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 3.35 |
| Efficacy Expansion Cohort: HNSCC | 7.98 |
The PFS time (based on investigator assessments), according to the RECIST 1.1, was defined as the time from first administration of study treatment until first documentation of progressive disease (PD) or death when death occurred within 12 weeks of the last tumor assessment or first administration of study treatment (whichever was later). PD was defined as at least a 20% increase in the sum of longest diameter (SLD), taking as reference the smallest SLD recorded from baseline or the appearance of 1 or more new lesions and unequivocal progression of non-target lesions. The analysis of PFS was performed with a Kaplan-Meier method. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Months (Median) |
|---|---|
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 2.66 |
| Primary Expansion Cohort: NSCLC, First Line | 4.04 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 1.35 |
| Primary Expansion Cohort: GC/GEJC Progressed | 1.38 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 2.76 |
| Secondary Expansion Cohort: Colorectal Cancer | 1.41 |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | 5.39 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 2.56 |
| Secondary Expansion Cohort: Melanoma | 3.06 |
| Secondary Expansion Cohort: Mesothelioma | 4.11 |
| Secondary Expansion Cohort: Urothelial Carcinoma | 2.69 |
| Secondary Expansion Cohort: Ovarian Cancer | 2.60 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 8.28 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 5.55 |
| Efficacy Expansion Cohort: Ovarian Cancer | 1.45 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 1.41 |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 1.31 |
| Efficacy Expansion Cohort: HNSCC | 1.77 |
Duration of response according to modified irRC, per investigator assessment was calculated for each participant with a confirmed response (immune-related complete response [irCR] or immune-related partial response [irPR]) as the time from the first observation of response to the first observation of documented disease progression (or death within 12 weeks of the last tumor assessment). irCR: Complete disappearance of all tumor lesions (both index and non-index lesions with no new measurable/unmeasurable lesions). irPR: At least 30% reduction from baseline in the sum of the longest diameter (SLD) of all lesions). Results were calculated based on Kaplan-Meier estimates. (NCT01772004)
Timeframe: Efficacy Expansion: Baseline up to Day 1072
| Intervention | Months (Median) |
|---|---|
| Efficacy Expansion Cohort: Ovarian Cancer | NA |
| Efficacy Expansion Cohort: Urothelial Carcinoma | NA |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | NA |
| Efficacy Expansion Cohort: HNSCC | NA |
The PFS time (based on IERC), according to the RECIST 1.1, was defined as the time from first administration of study treatment until first documentation of progressive disease (PD) or death when death occurred within 12 weeks of the last tumor assessment or first administration of study treatment (whichever was later). PD was defined as at least a 20% increase in the sum of longest diameter (SLD), taking as reference the smallest SLD recorded from baseline or the appearance of 1 or more new lesions and unequivocal progression of non-target lesions. The analysis of PFS was performed with a Kaplan-Meier method. (NCT01772004)
Timeframe: Efficacy Expansion: Baseline up to Day 1072
| Intervention | Months (Median) |
|---|---|
| Efficacy Expansion Cohort: Ovarian Cancer | 1.87 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 1.45 |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 1.31 |
| Efficacy Expansion Cohort: HNSCC | 1.41 |
Adverse event(AE): any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with use of study drug, whether or not related to study drug. A serious adverse event(SAE) was an AE that resulted in any of following outcomes: death; life threatening; persistent/significant disability/incapacity; initial or prolonged inpatient hospitalization; congenital anomaly/birth defect or was otherwise considered medically important. Treatment-emergent events were events between first dose of study drug that were absent before treatment or that worsened relative to pre-treatment state up to 30 days after last administration.TEAEs included both Serious TEAEs and non-serious TEAEs. Severity of TEAEs were graded using National Cancer Institute-Common Terminology Criteria for Adverse Events (NCI-CTCAE) version 4.0 toxicity grades, as follows: Grade 1= Mild, Grade 2= Moderate, Grade 3= Severe, Grade 4= Life-threatening and Grade 5= Death. (NCT01772004)
Timeframe: Up to Day 2511
| Intervention | Participants (Count of Participants) | ||||||
|---|---|---|---|---|---|---|---|
| Participants with TEAEs | Participants with TEAEs with Grade 1 severity | Participants with TEAEs with Grade 2 severity | Participants with TEAEs with Grade 3 severity | Participants with TEAEs with Grade 4 severity | Participants with TEAEs with Grade 5 severity | Participants with TEAEs with missing Grade | |
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 4 | 0 | 0 | 2 | 0 | 2 | 0 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 15 | 1 | 4 | 6 | 2 | 2 | 0 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg Weekly | 8 | 2 | 3 | 3 | 0 | 0 | 0 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 21 | 2 | 6 | 11 | 1 | 1 | 0 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 13 | 1 | 4 | 4 | 0 | 4 | 0 |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 130 | 2 | 30 | 51 | 12 | 35 | 0 |
| Efficacy Expansion Cohort: HNSCC | 149 | 14 | 43 | 54 | 12 | 25 | 1 |
| Efficacy Expansion Cohort: Ovarian Cancer | 103 | 7 | 30 | 45 | 6 | 15 | 0 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 204 | 15 | 46 | 82 | 16 | 45 | 0 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 88 | 14 | 19 | 41 | 4 | 10 | 0 |
| Primary Expansion Cohort: GC/GEJC Progressed | 60 | 5 | 9 | 29 | 7 | 10 | 0 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 161 | 22 | 58 | 45 | 12 | 24 | 0 |
| Primary Expansion Cohort: NSCLC, First Line | 156 | 3 | 45 | 68 | 15 | 25 | 0 |
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 182 | 11 | 54 | 66 | 19 | 32 | 0 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 50 | 1 | 10 | 25 | 8 | 6 | 0 |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | 17 | 5 | 5 | 7 | 0 | 0 | 0 |
| Secondary Expansion Cohort: Colorectal Cancer | 21 | 2 | 9 | 6 | 1 | 3 | 0 |
| Secondary Expansion Cohort: Melanoma | 50 | 2 | 17 | 21 | 5 | 5 | 0 |
| Secondary Expansion Cohort: Mesothelioma | 53 | 2 | 21 | 23 | 3 | 4 | 0 |
| Secondary Expansion Cohort: Ovarian Cancer | 122 | 11 | 52 | 42 | 3 | 14 | 0 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 62 | 7 | 25 | 20 | 6 | 4 | 0 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 19 | 1 | 5 | 10 | 1 | 2 | 0 |
| Secondary Expansion Cohort: Urothelial Carcinoma | 44 | 3 | 10 | 18 | 6 | 7 | 0 |
"AE was defined as any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of study drug, whether or not related to study drug. Treatment-emergent events were the events between first dose of study drug that were absent before treatment or that worsened relative to pre-treatment state up to 30 days after last administration. TEAEs included both Serious TEAEs and non-serious TEAEs. Treatment related AE was defined as having a Possible or Related relationship to study treatment, as assessed by the Investigator. Severity of Treatment-Related TEAEs were graded using NCI-CTCAE version 4.0 toxicity grades, as follows: Grade 1= Mild, Grade 2= Moderate, Grade 3= Severe, Grade 4= Life-threatening and Grade 5= Death." (NCT01772004)
Timeframe: Baseline up to Day 2511
| Intervention | Participants (Count of Participants) | ||||||
|---|---|---|---|---|---|---|---|
| Participants with Treatment-Related TEAEs | Participants with Treatment-Related TEAEs with Grade 1 severity | Participants with Treatment-Related TEAEs with Grade 2 severity | Participants with Treatment-Related TEAEs with Grade 3 severity | Participants with Treatment-Related TEAEs with Grade 4 severity | Participants with Treatment-Related TEAEs with Grade 5 severity | Participants with Treatment-Related TEAEs with missing Grade | |
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 3 | 1 | 1 | 1 | 0 | 0 | 0 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 14 | 7 | 3 | 3 | 1 | 0 | 0 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg Weekly | 7 | 2 | 4 | 1 | 0 | 0 | 0 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 17 | 6 | 8 | 2 | 1 | 0 | 0 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 9 | 5 | 4 | 0 | 0 | 0 | 0 |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 71 | 25 | 33 | 11 | 1 | 1 | 0 |
| Efficacy Expansion Cohort: HNSCC | 83 | 39 | 34 | 9 | 1 | 0 | 0 |
| Efficacy Expansion Cohort: Ovarian Cancer | 65 | 30 | 26 | 8 | 1 | 0 | 0 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 144 | 50 | 70 | 20 | 3 | 1 | 0 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 57 | 27 | 22 | 7 | 0 | 1 | 0 |
| Primary Expansion Cohort: GC/GEJC Progressed | 28 | 14 | 9 | 4 | 1 | 0 | 0 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 118 | 52 | 46 | 13 | 5 | 2 | 0 |
| Primary Expansion Cohort: NSCLC, First Line | 109 | 29 | 60 | 17 | 3 | 0 | 0 |
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 146 | 46 | 71 | 21 | 8 | 0 | 0 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 41 | 12 | 21 | 8 | 0 | 0 | 0 |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | 15 | 8 | 6 | 1 | 0 | 0 | 0 |
| Secondary Expansion Cohort: Colorectal Cancer | 16 | 4 | 9 | 3 | 0 | 0 | 0 |
| Secondary Expansion Cohort: Melanoma | 39 | 15 | 20 | 4 | 0 | 0 | 0 |
| Secondary Expansion Cohort: Mesothelioma | 43 | 8 | 30 | 3 | 2 | 0 | 0 |
| Secondary Expansion Cohort: Ovarian Cancer | 86 | 46 | 31 | 7 | 2 | 0 | 0 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 51 | 20 | 23 | 3 | 5 | 0 | 0 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 14 | 4 | 9 | 1 | 0 | 0 | 0 |
| Secondary Expansion Cohort: Urothelial Carcinoma | 32 | 11 | 18 | 2 | 1 | 0 | 0 |
irBOR defined as best response of any of immune related complete response (irCR), immune related partial response (irPR), immune related stable disease (irSD) and immune related progressive disease (irPD) recorded from baseline until immune related disease progression and determined according to modified irRC per investigator assessment. irCR: Complete disappearance of all tumor lesions (both index and non-index lesions with no new measurable/unmeasurable lesions). irPR: At least 30% reduction from baseline in the sum of the longest diameter (SLD) of all lesions). irSD: SLD of target and new measurable lesions neither irCR, irPR, or irPD. irPD: SLD of target and new measurable lesions increases greater than or equal to [>=] 20%, confirmed by a repeat, consecutive observations at least 4 weeks from the date first documented. Number of participants with immune-related best overall response in each category (irCR, irPR, irSD, irPD) was reported. (NCT01772004)
Timeframe: Dose Escalation: Baseline up to Day 1023
| Intervention | Participants (Count of Participants) | ||||
|---|---|---|---|---|---|
| Immune-related Complete Response | Immune-related Partial Response | Immune-related Stable Disease | Immune-related Progressive Disease | Not Evaluable | |
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 0 | 0 | 2 | 0 | 2 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 0 | 1 | 8 | 4 | 2 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 0 | 1 | 14 | 1 | 5 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 0 | 0 | 8 | 5 | 0 |
Percentage of PD-L1 receptors occupied by avelumab on human lymphocytes (CD3+ T-cells) was assessed by flow cytometry on peripheral blood mononuclear cell (PBMC) samples. Greater than or equal to [>=] 85 percent [%] of cell viability was required for reliable receptor occupancy assessment. (NCT01772004)
Timeframe: Pre-infusion on Day 1; 48 hours after infusion on Day 3; Pre-infusion on Days 15, 43, and 85
| Intervention | Percentage of receptors (Mean) |
|---|---|
| Day 15 | |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 93.2 |
Percentage of PD-L1 receptors occupied by avelumab on human lymphocytes (CD3+ T-cells) was assessed by flow cytometry on peripheral blood mononuclear cell (PBMC) samples. Greater than or equal to [>=] 85 percent [%] of cell viability was required for reliable receptor occupancy assessment. (NCT01772004)
Timeframe: Pre-infusion on Day 1; 48 hours after infusion on Day 3; Pre-infusion on Days 15, 43, and 85
| Intervention | Percentage of receptors (Mean) | ||
|---|---|---|---|
| Day 1 | Day 3 | Day 15 | |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 0.0 | 84.7 | 85.0 |
Percentage of PD-L1 receptors occupied by avelumab on human lymphocytes (CD3+ T-cells) was assessed by flow cytometry on peripheral blood mononuclear cell (PBMC) samples. Greater than or equal to [>=] 85 percent [%] of cell viability was required for reliable receptor occupancy assessment. (NCT01772004)
Timeframe: Pre-infusion on Day 1; 48 hours after infusion on Day 3; Pre-infusion on Days 15, 43, and 85
| Intervention | Percentage of receptors (Mean) | |||
|---|---|---|---|---|
| Day 1 | Day 3 | Day 15 | Day 43 | |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 0.0 | 80.1 | 90.0 | 96.8 |
Percentage of PD-L1 receptors occupied by avelumab on human lymphocytes (CD3+ T-cells) was assessed by flow cytometry on peripheral blood mononuclear cell (PBMC) samples. Greater than or equal to [>=] 85 percent [%] of cell viability was required for reliable receptor occupancy assessment. (NCT01772004)
Timeframe: Pre-infusion on Day 1; 48 hours after infusion on Day 3; Pre-infusion on Days 15, 43, and 85
| Intervention | Percentage of receptors (Mean) | |||
|---|---|---|---|---|
| Day 3 | Day 15 | Day 43 | Day 85 | |
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 92.5 | 75.7 | 30.3 | 19.8 |
BOR was determined according to RECIST v1.1 and as per investigator assessment. BOR is defined as the best response of any of complete response (CR), partial response (PR), stable disease (SD) and progressive disease (PD) recorded from date of randomization until disease progression or recurrence (taking the smallest measurement recorded since start of treatment as reference). CR: Disappearance of all evidence of target and non-target lesions. PR: At least 30 percent (%) reduction from baseline in the sum of the longest diameter (SLD) of all lesions. SD =Neither sufficient increase to qualify for PD nor sufficient shrinkage to qualify for PR. PD is defined as at least a 20 % increase in the SLD, taking as reference the smallest SLD recorded from baseline or appearance of 1 or more new lesions and unequivocal progression of non-target lesions. Number of participants with best overall response in each category (CR, PR, SD, PD) was reported. (NCT01772004)
Timeframe: Dose Escalation: Baseline up to Day 2511
| Intervention | Participants (Count of Participants) | ||||
|---|---|---|---|---|---|
| Complete Response | Partial Response | Stable Disease | Progressive Disease | Not Evaluable | |
| Dose Escalation Cohort: Avelumab 1.0 mg/kg | 0 | 0 | 2 | 0 | 2 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg | 0 | 1 | 8 | 4 | 2 |
| Dose Escalation Cohort: Avelumab 10.0 mg/kg Weekly | 0 | 1 | 4 | 1 | 2 |
| Dose Escalation Cohort: Avelumab 20.0 mg/kg | 0 | 1 | 14 | 3 | 3 |
| Dose Escalation Cohort: Avelumab 3.0 mg/kg | 0 | 0 | 8 | 5 | 0 |
Confirmed Best Overall Response (BOR) was determined according to Response Evaluation Criteria in Solid Tumors (RECIST) v1.1and as adjudicated by an Independent Endpoint Review Committee (IERC) is defined as best response of any of complete response (CR), partial response (PR), stable disease (SD) and progressive disease (PD) recorded from date of randomization until disease progression/recurrence (taking smallest measurement recorded since start of treatment as reference). CR: Disappearance of all evidence of target/non-target lesions. PR: At least 30% reduction from baseline in sum of longest diameter (SLD) of all lesions. SD: Neither sufficient increase to qualify for PD nor sufficient shrinkage to qualify for PR. PD: at least a 20% increase in SLD, taking as reference smallest SLD recorded from baseline/appearance of 1or more new lesions and unequivocal progression of non-target lesions. Number of participants with BOR in each category (CR, PR, SD, PD) were reported. (NCT01772004)
Timeframe: Secondary Urothelial Carcinoma Dose Expansion: Baseline up to Day 931
| Intervention | Participants (Count of Participants) | |||||
|---|---|---|---|---|---|---|
| Complete Response | Partial Response | Stable Disease | Non-CR/Non-PD | Progressive Disease | Not Evaluable | |
| Secondary Expansion Cohort: Urothelial Carcinoma | 6 | 1 | 16 | 0 | 16 | 5 |
BOR was determined according to RECIST v1.1 and as per investigator assessment. BOR is defined as the best response of any of complete response (CR), partial response (PR), stable disease (SD) and progressive disease (PD) recorded from date of randomization until disease progression or recurrence (taking the smallest measurement recorded since start of treatment as reference). CR: Disappearance of all evidence of target and non-target lesions. PR: At least 30 percent (%) reduction from baseline in the sum of the longest diameter (SLD) of all lesions. SD = Neither sufficient increase to qualify for PD nor sufficient shrinkage to qualify for PR. PD is defined as at least a 20 % increase in the SLD, taking as reference the smallest SLD recorded from baseline or appearance of 1 or more new lesions and unequivocal progression of non-target lesions. Number of participants with best overall response in each category (CR, PR, SD, PD) was reported. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Participants (Count of Participants) | ||||
|---|---|---|---|---|---|
| Complete Response | Partial Response | Stable Disease | Progressive Disease | Not Evaluable | |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 1 | 7 | 23 | 80 | 21 |
| Efficacy Expansion Cohort: HNSCC | 5 | 15 | 50 | 66 | 17 |
| Efficacy Expansion Cohort: Ovarian Cancer | 3 | 4 | 37 | 46 | 13 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 7 | 24 | 45 | 87 | 35 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 2 | 4 | 45 | 29 | 10 |
| Primary Expansion Cohort: GC/GEJC Progressed | 0 | 4 | 13 | 36 | 7 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 1 | 4 | 41 | 107 | 15 |
| Primary Expansion Cohort: NSCLC, First Line | 3 | 28 | 68 | 40 | 17 |
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 2 | 24 | 66 | 68 | 24 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 0 | 3 | 21 | 22 | 4 |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | 0 | 0 | 10 | 5 | 3 |
| Secondary Expansion Cohort: Colorectal Cancer | 0 | 0 | 9 | 9 | 3 |
| Secondary Expansion Cohort: Melanoma | 4 | 7 | 16 | 17 | 7 |
| Secondary Expansion Cohort: Mesothelioma | 1 | 4 | 26 | 18 | 4 |
| Secondary Expansion Cohort: Ovarian Cancer | 1 | 11 | 53 | 51 | 9 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 1 | 9 | 38 | 11 | 3 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 0 | 2 | 13 | 4 | 1 |
| Secondary Expansion Cohort: Urothelial Carcinoma | 2 | 4 | 20 | 14 | 4 |
irBOR defined as best response of any of immune related complete response (irCR), immune related partial response (irPR), immune related stable disease (irSD) and immune related progressive disease (irPD) recorded from baseline until immune related disease progression and determined according to modified irRC per investigator assessment. irCR: Complete disappearance of all tumor lesions (both index and non-index lesions with no new measurable/unmeasurable lesions). irPR: At least 30% reduction from baseline in the sum of the longest diameter (SLD) of all lesions). irSD: SLD of target and new measurable lesions neither irCR, irPR, or irPD. irPD: SLD of target and new measurable lesions increases greater than or equal to [>=] 20%, confirmed by a repeat, consecutive observations at least 4 weeks from the date first documented. Number of participants with immune-related best overall response in each category (irCR, irPR, irSD, irPD) was reported. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Participants (Count of Participants) | ||||
|---|---|---|---|---|---|
| Immune-related Complete Response | Immune-related Partial Response | Immune-related Stable Disease | Immune-related Progressive Disease | Not Evaluable | |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 1 | 7 | 29 | 62 | 33 |
| Efficacy Expansion Cohort: HNSCC | 6 | 15 | 61 | 44 | 27 |
| Efficacy Expansion Cohort: Ovarian Cancer | 3 | 4 | 44 | 33 | 19 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 10 | 24 | 61 | 62 | 41 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 2 | 4 | 53 | 0 | 31 |
| Primary Expansion Cohort: GC/GEJC Progressed | 0 | 5 | 20 | 0 | 35 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 1 | 6 | 60 | 69 | 32 |
| Primary Expansion Cohort: NSCLC, First Line | 4 | 31 | 78 | 21 | 22 |
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 2 | 26 | 80 | 36 | 40 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 0 | 3 | 26 | 14 | 7 |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | 0 | 0 | 3 | 1 | 14 |
| Secondary Expansion Cohort: Colorectal Cancer | 0 | 0 | 9 | 5 | 7 |
| Secondary Expansion Cohort: Melanoma | 4 | 7 | 20 | 11 | 9 |
| Secondary Expansion Cohort: Mesothelioma | 1 | 4 | 31 | 10 | 7 |
| Secondary Expansion Cohort: Ovarian Cancer | 1 | 15 | 61 | 27 | 21 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 1 | 10 | 40 | 6 | 5 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 0 | 2 | 15 | 1 | 2 |
| Secondary Expansion Cohort: Urothelial Carcinoma | 2 | 5 | 21 | 10 | 6 |
PD-L1 assessment was performed using immunohistochemistry. PD-L1 expression status was classified as positive or negative based on the following cut-offs: For tumor cells: Participants were considered PD-L1 expression positive (negative): - if at least (less than) 5% of the tumor cells show PD-L1 membrane staining >= 1+, respectively. This was used as the primary cut-off; - if at least (less than) 25% of the tumor cells show PD-L1 membrane staining >=2+, respectively. This was considered as secondary cut-off; - if at least (less than) 1% of the tumor cells show PD-L1 membrane staining >=1+, respectively. This was used as the tertiary cut-off; - if at least (less than) 50% of the tumor cells show PD-L1 membrane staining >=1+, respectively. This was used as the '50% cut-off'; - if at least (less than) 80% of the tumor cells show PD-L1 membrane staining ≥1+, respectively. This was used as the '80% cut-off'. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Participants (Count of Participants) |
|---|---|
| PD-L1 expression status - 1% cutoff | |
| Primary Expansion Cohort: GC/GEJC Progressed | 20 |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 26 |
PD-L1 assessment was performed using immunohistochemistry. PD-L1 expression status was classified as positive or negative based on the following cut-offs: For tumor cells: Participants were considered PD-L1 expression positive (negative): - if at least (less than) 5% of the tumor cells show PD-L1 membrane staining >= 1+, respectively. This was used as the primary cut-off; - if at least (less than) 25% of the tumor cells show PD-L1 membrane staining >=2+, respectively. This was considered as secondary cut-off; - if at least (less than) 1% of the tumor cells show PD-L1 membrane staining >=1+, respectively. This was used as the tertiary cut-off; - if at least (less than) 50% of the tumor cells show PD-L1 membrane staining >=1+, respectively. This was used as the '50% cut-off'; - if at least (less than) 80% of the tumor cells show PD-L1 membrane staining ≥1+, respectively. This was used as the '80% cut-off'. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Participants (Count of Participants) | ||
|---|---|---|---|
| PD-L1 expression status - 1% cutoff | PD-L1 expression status - 5% cutoff | PD-L1 expression status - 25% cutoff | |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 39 | 16 | 6 |
PD-L1 assessment was performed using immunohistochemistry. PD-L1 expression status was classified as positive or negative based on the following cut-offs: For tumor cells: Participants were considered PD-L1 expression positive (negative): - if at least (less than) 5% of the tumor cells show PD-L1 membrane staining >= 1+, respectively. This was used as the primary cut-off; - if at least (less than) 25% of the tumor cells show PD-L1 membrane staining >=2+, respectively. This was considered as secondary cut-off; - if at least (less than) 1% of the tumor cells show PD-L1 membrane staining >=1+, respectively. This was used as the tertiary cut-off; - if at least (less than) 50% of the tumor cells show PD-L1 membrane staining >=1+, respectively. This was used as the '50% cut-off'; - if at least (less than) 80% of the tumor cells show PD-L1 membrane staining ≥1+, respectively. This was used as the '80% cut-off'. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Participants (Count of Participants) | |||
|---|---|---|---|---|
| PD-L1 expression status - 1% cutoff | PD-L1 expression status - 5% cutoff | PD-L1 expression status - 25% cutoff | PD-L1 expression status - 50% cutoff | |
| Secondary Expansion Cohort: Colorectal Cancer | 5 | 1 | 0 | 1 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 87 | 25 | 3 | 13 |
PD-L1 assessment was performed using immunohistochemistry. PD-L1 expression status was classified as positive or negative based on the following cut-offs: For tumor cells: Participants were considered PD-L1 expression positive (negative): - if at least (less than) 5% of the tumor cells show PD-L1 membrane staining >= 1+, respectively. This was used as the primary cut-off; - if at least (less than) 25% of the tumor cells show PD-L1 membrane staining >=2+, respectively. This was considered as secondary cut-off; - if at least (less than) 1% of the tumor cells show PD-L1 membrane staining >=1+, respectively. This was used as the tertiary cut-off; - if at least (less than) 50% of the tumor cells show PD-L1 membrane staining >=1+, respectively. This was used as the '50% cut-off'; - if at least (less than) 80% of the tumor cells show PD-L1 membrane staining ≥1+, respectively. This was used as the '80% cut-off'. (NCT01772004)
Timeframe: Dose Expansion: Baseline up to Day 2023
| Intervention | Participants (Count of Participants) | ||||
|---|---|---|---|---|---|
| PD-L1 expression status - 1% cutoff | PD-L1 expression status - 5% cutoff | PD-L1 expression status - 25% cutoff | PD-L1 expression status - 50% cutoff | PD-L1 expression status - 80% cutoff | |
| Efficacy Expansion Cohort: HNSCC | 107 | 93 | 48 | 51 | 28 |
| Efficacy Expansion Cohort: Ovarian Cancer | 45 | 23 | 6 | 4 | 0 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 87 | 72 | 25 | 34 | 25 |
| Primary Expansion Cohort: NSCLC, First Line | 88 | 76 | 50 | 53 | 38 |
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 122 | 84 | 53 | 54 | 41 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 15 | 12 | 3 | 5 | 2 |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | 0 | 0 | 0 | 0 | 0 |
| Secondary Expansion Cohort: Melanoma | 19 | 15 | 7 | 8 | 2 |
| Secondary Expansion Cohort: Mesothelioma | 22 | 16 | 8 | 5 | 2 |
| Secondary Expansion Cohort: Ovarian Cancer | 76 | 32 | 3 | 2 | 2 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 20 | 11 | 2 | 1 | 0 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 4 | 1 | 0 | 0 | 0 |
| Secondary Expansion Cohort: Urothelial Carcinoma | 14 | 13 | 5 | 5 | 3 |
Serum Ctrough concentration of Avelumab is reported. (NCT01772004)
Timeframe: At Day 15, 29, 43, 57, 71, 85, 99, 127 and 169
| Intervention | Microgram per milliliter (Mean) | ||||
|---|---|---|---|---|---|
| Day 15 | Day 29 | Day 43 | Day 85 | Day 127 | |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | 28.8 | 31.6 | 32.3 | 37.9 | 44.2 |
Serum Ctrough concentration of Avelumab is reported. (NCT01772004)
Timeframe: At Day 15, 29, 43, 57, 71, 85, 99, 127 and 169
| Intervention | Microgram per milliliter (Mean) | |||||
|---|---|---|---|---|---|---|
| Day 15 | Day 29 | Day 43 | Day 57 | Day 71 | Day 85 | |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 18.1 | 18.6 | 19.8 | 16.2 | 19.6 | 19.3 |
Serum Ctrough concentration of Avelumab is reported. (NCT01772004)
Timeframe: At Day 15, 29, 43, 57, 71, 85, 99, 127 and 169
| Intervention | Microgram per milliliter (Mean) | |||||
|---|---|---|---|---|---|---|
| Day 15 | Day 29 | Day 43 | Day 85 | Day 127 | Day 169 | |
| Secondary Expansion Cohort: Colorectal Cancer | 22.4 | 25.5 | 23.2 | 8.03 | 34.2 | 10.5 |
Serum Ctrough concentration of Avelumab is reported. (NCT01772004)
Timeframe: At Day 15, 29, 43, 57, 71, 85, 99, 127 and 169
| Intervention | Microgram per milliliter (Mean) | ||||||
|---|---|---|---|---|---|---|---|
| Day 15 | Day 29 | Day 43 | Day 57 | Day 71 | Day 85 | Day 169 | |
| Efficacy Expansion Cohort: HNSCC | 20.1 | 27.0 | 29.0 | 30.6 | 31.1 | 35.6 | 32.5 |
| Efficacy Expansion Cohort: Ovarian Cancer | 22.3 | 23.9 | 27.7 | 28.5 | 30.4 | 31.2 | 28.3 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 17.6 | 21.3 | 25.2 | 24.1 | 24.2 | 28.0 | 37.3 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 25.1 | 27.4 | 29.4 | 25.5 | 27.8 | 34.4 | 43.6 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (First Line) | 26.9 | 35.7 | 35.7 | 39.8 | 38.4 | 39.7 | 47.1 |
Serum Ctrough concentration of Avelumab is reported. (NCT01772004)
Timeframe: At Day 15, 29, 43, 57, 71, 85, 99, 127 and 169
| Intervention | Microgram per milliliter (Mean) | |||||||
|---|---|---|---|---|---|---|---|---|
| Day 15 | Day 29 | Day 43 | Day 57 | Day 71 | Day 85 | Day 127 | Day 169 | |
| Primary Expansion Cohort: Metastatic Breast Cancer | 23.7 | 26.5 | 29.7 | 28.9 | 29.9 | 28.9 | 33.1 | 31.9 |
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 20.4 | 23.5 | 24.6 | 26.2 | 27.9 | 27.8 | 36.9 | 36.6 |
| Secondary Expansion Cohort: Melanoma | 22.3 | 23.8 | 29.3 | 29.9 | 28.8 | 35.6 | 58.6 | 35.3 |
| Secondary Expansion Cohort: Mesothelioma | 21.7 | 20.7 | 23.6 | 18.2 | 21.0 | 23.7 | 25.9 | 28.7 |
| Secondary Expansion Cohort: Ovarian Cancer | 23.1 | 27.7 | 28.4 | 27.3 | 33.4 | 39.1 | 40.7 | 49.3 |
| Primary Expansion Cohort: GC/GEJC (Progressed/Non Progressed) | 22.5 | 25.6 | 28.3 | 26.5 | 28.1 | 29.7 | 39.1 | 31.4 |
| Secondary Expansion Cohort: Adrenocortical Carcinoma | 17.8 | 17.3 | 20.6 | 22.2 | 22.0 | 24.9 | 28.8 | 24.7 |
| Secondary Expansion Cohort: Urothelial Carcinoma | 21.3 | 26.2 | 28.1 | 29.7 | 29.4 | 34.7 | 35.7 | 38.8 |
Serum Ctrough concentration of Avelumab is reported. (NCT01772004)
Timeframe: At Day 15, 29, 43, 57, 71, 85, 99, 127 and 169
| Intervention | Microgram per milliliter (Mean) | |||||||
|---|---|---|---|---|---|---|---|---|
| Day 15 | Day 29 | Day 43 | Day 57 | Day 71 | Day 85 | Day 99 | Day 169 | |
| Primary Expansion Cohort: NSCLC, First Line | 18.3 | 23.5 | 23.8 | 23.4 | 31.0 | 27.7 | 28.8 | 39.1 |
Serum concentration at end of infusion (CEOI) of Avelumab is reported. (NCT01772004)
Timeframe: At Day 1, 15, 29, 43, 85, 127 and 169
| Intervention | Microgram per milliliter (Mean) | ||
|---|---|---|---|
| Day 1 | Day 43 | Day 85 | |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 241 | 240 | 237 |
Serum concentration at end of infusion (CEOI) of Avelumab is reported. (NCT01772004)
Timeframe: At Day 1, 15, 29, 43, 85, 127 and 169
| Intervention | Microgram per milliliter (Mean) | |||
|---|---|---|---|---|
| Day 1 | Day 43 | Day 85 | Day 169 | |
| Efficacy Expansion Cohort: HNSCC | 212 | 249 | 255 | 245 |
| Efficacy Expansion Cohort: Ovarian Cancer | 247 | 268 | 263 | 233 |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 224 | 241 | 247 | 313 |
| Primary Expansion Cohort: NSCLC, First Line | 246 | 250 | 266 | 304 |
| Secondary Expansion Cohort: Renal Cell Carcinoma (Second Line) | 239 | 255 | 252 | 235 |
Serum concentration at end of infusion (CEOI) of Avelumab is reported. (NCT01772004)
Timeframe: At Day 1, 15, 29, 43, 85, 127 and 169
| Intervention | Microgram per milliliter (Mean) | ||||||
|---|---|---|---|---|---|---|---|
| Day 1 | Day 15 | Day 29 | Day 43 | Day 85 | Day 127 | Day 169 | |
| Secondary Expansion Cohort: Colorectal Cancer | 272 | 297 | 287 | 306 | 216 | 269 | 272 |
| Secondary Expansion Cohort: Castrate-resistant Prostate Cancer | 343 | 305 | 291 | 294 | 348 | 339 | 287 |
Confirmed BOR was determined according to RECIST 1.1 and as adjudicated by an Independent Endpoint Review Committee (IERC) and defined as best response of any of complete response (CR), partial response (PR), stable disease (SD) and progressive disease (PD) recorded from date of randomization until disease progression/recurrence (taking smallest measurement recorded since start of treatment as reference). CR: Disappearance of all evidence of target/non-target lesions. PR: At least 30% reduction from baseline in sum of longest diameter (SLD) of all lesions. SD: Neither sufficient increase to qualify for PD nor sufficient shrinkage to qualify for PR. PD: at least a 20% increase in SLD, taking as reference smallest SLD recorded from baseline/appearance of 1 or more new lesions and unequivocal progression of non-target lesions. (NCT01772004)
Timeframe: GC/GEJC, Third Line Efficacy Expansion: Baseline up to Day 871
| Intervention | Participants (Count of Participants) | |||||
|---|---|---|---|---|---|---|
| Complete response (CR) | Partial response (PR) | Stable disease (SD) | Progressive disease (PD) | Non-CR/Non-PD | Non-evaluable | |
| Efficacy Expansion Cohort: GC/GEJC, Third Line | 2 | 5 | 24 | 72 | 5 | 24 |
Confirmed BOR was determined according to RECIST 1.1 and as adjudicated by an Independent Endpoint Review Committee (IERC) and defined as best response of any of complete response (CR), partial response (PR), stable disease (SD) and progressive disease (PD) recorded from date of randomization until disease progression/recurrence (taking smallest measurement recorded since start of treatment as reference). CR: Disappearance of all evidence of target/non-target lesions. PR: At least 30%reduction from baseline in sum of longest diameter (SLD) of all lesions. SD: Neither sufficient increase to qualify for PD nor sufficient shrinkage to qualify for PR. PD: at least a 20% increase in SLD, taking as reference smallest SLD recorded from baseline/appearance of 1or more new lesions and unequivocal progression of non-target lesions. (NCT01772004)
Timeframe: HNSCC Efficacy Expansion: Baseline up to Day 1072
| Intervention | Participants (Count of Participants) | |||||
|---|---|---|---|---|---|---|
| Complete response (CR) | Partial response (PR) | Stable disease (SD) | Progressive disease (PD) | Non-CR/Non-PD | Non-evaluable | |
| Efficacy Expansion Cohort: HNSCC | 2 | 12 | 46 | 67 | 1 | 25 |
Confirmed BOR was determined according to RECIST 1.1 and as adjudicated by an Independent Endpoint Review Committee (IERC) and defined as best response of any of complete response (CR), partial response (PR), stable disease (SD) and progressive disease (PD) recorded from date of randomization until disease progression/recurrence (taking smallest measurement recorded since start of treatment as reference). CR: Disappearance of all evidence of target/non-target lesions. PR: At least 30%reduction from baseline in sum of longest diameter (SLD) of all lesions. SD: Neither sufficient increase to qualify for PD nor sufficient shrinkage to qualify for PR. PD: at least a 20% increase in SLD, taking as reference smallest SLD recorded from baseline/appearance of 1or more new lesions and unequivocal progression of non-target lesions. (NCT01772004)
Timeframe: Ovarian Cancer Efficacy Expansion: Baseline up to Day 620
| Intervention | Participants (Count of Participants) | |||||
|---|---|---|---|---|---|---|
| Complete response (CR) | Partial response (PR) | Stable disease (SD) | Progressive disease (PD) | Non-CR/Non-PD | Non-evaluable | |
| Efficacy Expansion Cohort: Ovarian Cancer | 3 | 1 | 41 | 39 | 3 | 16 |
Confirmed BOR was determined according to RECIST 1.1 and as adjudicated by an Independent Endpoint Review Committee (IERC) and defined as best response of any of complete response (CR), partial response (PR), stable disease (SD) and progressive disease (PD) recorded from date of randomization until disease progression/recurrence (taking smallest measurement recorded since start of treatment as reference). CR: Disappearance of all evidence of target/non-target lesions. PR: At least 30% reduction from baseline in sum of longest diameter (SLD) of all lesions. SD: Neither sufficient increase to qualify for PD nor sufficient shrinkage to qualify for PR. PD: at least a 20% increase in SLD, taking as reference smallest SLD recorded from baseline/appearance of 1 or more new lesions and unequivocal progression of non-target lesions. (NCT01772004)
Timeframe: Urothelial Carcinoma Efficacy Expansion: Baseline up to Day 931
| Intervention | Participants (Count of Participants) | |||||
|---|---|---|---|---|---|---|
| Complete response (CR) | Partial response (PR) | Stable disease (SD) | Progressive disease (PD) | Non-CR/Non-PD | Non-evaluable | |
| Efficacy Expansion Cohort: Urothelial Carcinoma | 6 | 26 | 51 | 77 | 1 | 37 |
The response criteria evaluation was carried out according to Response Evaluation Criteria in Solid Tumors (RECIST) 1.1. CR and PR did not need to be confirmed by a subsequent tumor assessment due to blinded central assessment. CR: Disappearance of all target lesions since baseline; PR: At least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum of diameters; SD: Neither sufficient increase to qualify for PD nor sufficient shrinkage to qualify for PR and PD: at least a 20% increase in SLD, taking as reference smallest SLD recorded from baseline/appearance of 1or more new lesions and unequivocal progression of non-target lesions. Number of participants with unconfirmed response at week 13 according to response evaluation criteria in solid tumors (RECIST) version 1.1 were reported. (NCT01772004)
Timeframe: Week 13
| Intervention | Participants (Count of Participants) | ||||
|---|---|---|---|---|---|
| Unconfirmed Complete Response | Unconfirmed Partial Response | Unconfirmed Stable Disease | Unconfirmed Progressive Disease | Non-evaluable | |
| Primary Expansion Cohort: GC/GEJC Non Progressed | 2 | 5 | 44 | 31 | 8 |
| Primary Expansion Cohort: GC/GEJC Progressed | 0 | 6 | 11 | 37 | 6 |
| Primary Expansion Cohort: Metastatic Breast Cancer | 1 | 7 | 38 | 107 | 15 |
| Primary Expansion Cohort: NSCLC, First Line | 1 | 24 | 54 | 28 | 49 |
| Primary Expansion Cohort: NSCLC, Post-platinum Doublet | 2 | 28 | 62 | 68 | 24 |
23 reviews available for 1-anilino-8-naphthalenesulfonate and Disease Exacerbation
| Article | Year |
|---|---|
Genetic contributions to NAFLD: leveraging shared genetics to uncover systems biology.
Topics: 17-Hydroxysteroid Dehydrogenases; Acyltransferases; Adaptor Proteins, Signal Transducing; Carcinoma, | 2020 |
Molecular Mechanisms: Connections between Nonalcoholic Fatty Liver Disease, Steatohepatitis and Hepatocellular Carcinoma.
Topics: 17-Hydroxysteroid Dehydrogenases; Animals; Apoptosis; Carcinoma, Hepatocellular; Diet, High-Fat; Dis | 2020 |
Drilling for Oil: Tumor-Surrounding Adipocytes Fueling Cancer.
Topics: Adipocytes; Disease Progression; Energy Metabolism; Extracellular Vesicles; Fatty Acids, Nonesterifi | 2020 |
Involvement of the exocrine pancreas during COVID-19 infection and possible pathogenetic hypothesis: a concise review.
Topics: COVID-19; Disease Progression; Humans; Hyperamylasemia; Lipase; Pancreas, Exocrine; Pancreatitis; SA | 2020 |
The genetic backgrounds in nonalcoholic fatty liver disease.
Topics: Adaptor Proteins, Signal Transducing; Disease Progression; Genetic Background; Humans; Lipase; Membr | 2018 |
The relationship between obesity and the severity of non-alcoholic fatty liver disease: systematic review and meta-analysis.
Topics: Adult; Aged; Disease Progression; Genetic Predisposition to Disease; Humans; Lipase; Membrane Protei | 2018 |
Genetics of alcoholic liver disease and non-alcoholic steatohepatitis.
Topics: Acyltransferases; Disease Progression; Genetic Association Studies; Genetic Predisposition to Diseas | 2018 |
Novel multi-target directed ligand-based strategies for reducing neuroinflammation in Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Anti-Inflammatory Agents; Cathepsin B; Dinoprosto | 2018 |
Non-alcoholic fatty liver disease: causes, diagnosis, cardiometabolic consequences, and treatment strategies.
Topics: Antioxidants; Bariatric Surgery; Carcinoma, Hepatocellular; Cardiovascular Diseases; Diabetes Mellit | 2019 |
Non-alcoholic fatty liver disease: causes, diagnosis, cardiometabolic consequences, and treatment strategies.
Topics: Antioxidants; Bariatric Surgery; Carcinoma, Hepatocellular; Cardiovascular Diseases; Diabetes Mellit | 2019 |
Non-alcoholic fatty liver disease: causes, diagnosis, cardiometabolic consequences, and treatment strategies.
Topics: Antioxidants; Bariatric Surgery; Carcinoma, Hepatocellular; Cardiovascular Diseases; Diabetes Mellit | 2019 |
Non-alcoholic fatty liver disease: causes, diagnosis, cardiometabolic consequences, and treatment strategies.
Topics: Antioxidants; Bariatric Surgery; Carcinoma, Hepatocellular; Cardiovascular Diseases; Diabetes Mellit | 2019 |
Genetics of Nonalcoholic Fatty Liver Disease: A 2018 Update.
Topics: Apolipoproteins B; Disease Progression; Gene-Environment Interaction; Humans; Insulin Resistance; Li | 2018 |
The genetics of NAFLD.
Topics: Disease Progression; Epigenomics; Fatty Liver; Genome-Wide Association Study; Humans; Lipase; Membra | 2013 |
PNPLA3 I148M polymorphism and progressive liver disease.
Topics: Carcinoma, Hepatocellular; Cholangitis, Sclerosing; Disease Progression; Fatty Liver; Fatty Liver, A | 2013 |
The effect of PNPLA3 on fibrosis progression and development of hepatocellular carcinoma: a meta-analysis.
Topics: Carcinoma, Hepatocellular; Disease Progression; Genetic Predisposition to Disease; Humans; Lipase; L | 2014 |
Role of metabolic lipases and lipolytic metabolites in the pathogenesis of NAFLD.
Topics: Animals; Disease Progression; Humans; Lipase; Lipolysis; Liver; Non-alcoholic Fatty Liver Disease; R | 2014 |
Challenges and Management of Liver Cirrhosis: Practical Issues in the Therapy of Patients with Cirrhosis due to NAFLD and NASH.
Topics: Anticholesteremic Agents; Antioxidants; Bariatric Surgery; Carcinoma, Hepatocellular; Disease Progre | 2015 |
Impact of IL28B, ITPA and PNPLA3 genetic variants on therapeutic outcome and progression of hepatitis C virus infection.
Topics: Disease Progression; Genetic Variation; Hepacivirus; Hepatitis C; Humans; Interferons; Interleukins; | 2015 |
The Genetics of Nonalcoholic Fatty Liver Disease: Spotlight on PNPLA3 and TM6SF2.
Topics: Animals; Disease Progression; Genetic Association Studies; Genetic Markers; Genetic Predisposition t | 2015 |
Genetics of Alcoholic Liver Disease.
Topics: Alcohol Drinking; Alcoholism; Carcinoma, Hepatocellular; Disease Progression; Ethanol; Fatty Liver, | 2015 |
Hepatocellular carcinoma in patients with non-alcoholic fatty liver disease.
Topics: Adiponectin; Carcinoma, Hepatocellular; Disease Progression; Humans; Immune System; Inflammation; Li | 2016 |
What's unique about acute pancreatitis in children: risk factors, diagnosis and management.
Topics: Abdominal Pain; Acute Disease; Amylases; Antioxidants; Carrier Proteins; Child; Cholangiopancreatogr | 2017 |
Genetic determinants of susceptibility and severity in nonalcoholic fatty liver disease.
Topics: Animals; Cytokines; Disease Progression; Fatty Liver; Female; Genetic Predisposition to Disease; Gen | 2011 |
The impact of human gene polymorphisms on HCV infection and disease outcome.
Topics: Antiviral Agents; Disease Progression; Genetic Predisposition to Disease; Genotype; Hepacivirus; Hep | 2011 |
Heparan sulfate: a complex polymer charged with biological activity.
Topics: Chromosome Aberrations; Cytokines; Disease Progression; Extracellular Matrix; Fibroblast Growth Fact | 2005 |
3 trials available for 1-anilino-8-naphthalenesulfonate and Disease Exacerbation
80 other studies available for 1-anilino-8-naphthalenesulfonate and Disease Exacerbation
| Article | Year |
|---|---|
Should PNPLA3 polymorphism be performed in clinical practice in patients with NAFLD to predict the risk of disease progression?
Topics: Disease Progression; Genetic Predisposition to Disease; Genotype; Humans; Lipase; Non-alcoholic Fatt | 2022 |
Identification of novel immune-related targets mediating disease progression in acute pancreatitis.
Topics: Acute Disease; Amylases; Animals; Anti-Inflammatory Agents; Ceruletide; Disease Models, Animal; Dise | 2022 |
Association between PNPLA3[G]/I148M variant, steatosis and fibrosis stage in hepatitis C virus - genetic matters.
Topics: Antiviral Agents; Disease Progression; Fatty Liver; Female; Hepatitis C, Chronic; Humans; Interferon | 2019 |
Risk factors for histological progression of non-alcoholic steatohepatitis analyzed from repeated biopsy cases.
Topics: Adult; Aged; Aged, 80 and over; Alanine Transaminase; Alleles; Biomarkers; Biopsy; Disease Progressi | 2020 |
Liver transcriptomics highlights interleukin-32 as novel NAFLD-related cytokine and candidate biomarker.
Topics: Adult; Biomarkers; Disease Progression; Drug Discovery; Female; Gene Expression Profiling; Genetic P | 2020 |
The PNPLA3 rs738409 GG genotype is associated with poorer prognosis in 239 patients with autoimmune hepatitis.
Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Disease Progression; Female; Follow-Up Studies; Ge | 2020 |
Validating candidate biomarkers for different stages of non-alcoholic fatty liver disease.
Topics: Adult; Biomarkers; Case-Control Studies; Disease Progression; Enzyme-Linked Immunosorbent Assay; Fem | 2020 |
Topics: Acute Coronary Syndrome; Adolescent; Adsorption; Adult; Aged; Animals; Aspergillus; Aspergillus oryz | 2021 |
Identification of a Metabolic, Transcriptomic, and Molecular Signature of Patatin-Like Phospholipase Domain Containing 3-Mediated Acceleration of Steatohepatitis.
Topics: Animals; Diet, High-Fat; Diet, Western; Disease Models, Animal; Disease Progression; Gene Expression | 2021 |
Characterization of the Relationship Between the Expression of Aspartate β-Hydroxylase and the Pathological Characteristics of Breast Cancer.
Topics: Acyltransferases; Adult; Aged; Atlases as Topic; Breast Neoplasms; Calcium-Binding Proteins; Carcino | 2020 |
Discordant hepatic fatty acid oxidation and triglyceride hydrolysis leads to liver disease.
Topics: Animals; Carnitine O-Palmitoyltransferase; Disease Progression; Fatty Acids; Female; Hydrolysis; Lip | 2021 |
Serum concentrations of canine pancreatic lipase immunoreactivity and C-reactive protein for monitoring disease progression in dogs with acute pancreatitis.
Topics: Acute Disease; Animals; C-Reactive Protein; Disease Progression; Dog Diseases; Dogs; Lipase; Pancrea | 2021 |
New Discriminant Method for Identifying the Aggressive Disease Phenotype of Non-alcoholic Fatty Liver Disease.
Topics: Adult; Age Factors; Aged; Biopsy; Body Mass Index; Disease Progression; Female; Fibrosis; Genotype; | 2017 |
Disease progression: Divergent paths.
Topics: Age Factors; Body Mass Index; Disease Progression; Epigenesis, Genetic; Genetic Predisposition to Di | 2017 |
Genetic variants in PNPLA3 and TM6SF2 predispose to the development of hepatocellular carcinoma in individuals with alcohol-related cirrhosis.
Topics: Acyltransferases; Aged; Carcinoma, Hepatocellular; Case-Control Studies; Disease Progression; Europe | 2018 |
PNPLA3 rs738409 polymorphism is associated with liver fibrosis progression in patients with chronic hepatitis C: A repeated measures study.
Topics: Adult; Disease Progression; Disease Susceptibility; Elasticity Imaging Techniques; Female; Genetic A | 2018 |
Combining Genetic Variants to Improve Risk Prediction for NAFLD and Its Progression to Cirrhosis: A Proof of Concept Study.
Topics: Adult; Aged; Case-Control Studies; Disease Progression; Gene Frequency; Genetic Loci; Genotype; Huma | 2018 |
Utilization of adipocyte-derived lipids and enhanced intracellular trafficking of fatty acids contribute to breast cancer progression.
Topics: 3T3-L1 Cells; Adipocytes; Animals; Biological Transport; Breast Neoplasms; Cell Communication; Disea | 2018 |
Atglistatin ameliorates functional decline in heart failure via adipocyte-specific inhibition of adipose triglyceride lipase.
Topics: Adipocytes; Animals; Disease Models, Animal; Disease Progression; Enzyme Inhibitors; Heart Failure; | 2018 |
Neutral lipid storage disease with myopathy and dropped head syndrome. Report of a new variant susceptible of treatment with late diagnosis.
Topics: Delayed Diagnosis; Disease Progression; Female; Humans; Lipase; Lipid Metabolism, Inborn Errors; Mid | 2018 |
Protective Effects of Calcitonin Gene-Related Peptide-Mediated p38 Mitogen-Activated Protein Kinase Pathway on Severe Acute Pancreatitis in Rats.
Topics: Acute Disease; Amylases; Animals; Calcitonin Gene-Related Peptide; Cytokines; Disease Progression; E | 2019 |
Genetic determinants of steatosis and fibrosis progression in paediatric non-alcoholic fatty liver disease.
Topics: Adaptor Proteins, Signal Transducing; Adolescent; Age Factors; Case-Control Studies; Child; Disease | 2019 |
Promoting genetics in non-alcoholic fatty liver disease: Combined risk score through polymorphisms and clinical variables.
Topics: Disease Progression; Genetic Predisposition to Disease; Humans; Lipase; Liver; Membrane Proteins; No | 2018 |
LIPG-promoted lipid storage mediates adaptation to oxidative stress in breast cancer.
Topics: Breast Neoplasms; Cell Line, Tumor; Disease Progression; Disease-Free Survival; Female; Humans; Lipa | 2019 |
GWAS and enrichment analyses of non-alcoholic fatty liver disease identify new trait-associated genes and pathways across eMERGE Network.
Topics: Adult; Aged; Body Mass Index; Case-Control Studies; Community Networks; Disease Progression; Electro | 2019 |
Patatin-like phospholipase domain-containing 3 I148M affects liver steatosis in patients with chronic hepatitis B.
Topics: Adult; Alcoholism; Cohort Studies; Disease Progression; Fatty Liver; Female; Genetic Predisposition | 2013 |
[Genotyping in progressive age-related macular degeneration].
Topics: Biomarkers; Bruch Membrane; Cholesterol, HDL; Complement Factor H; Complement Inactivating Agents; D | 2012 |
Dual regulation of adipose triglyceride lipase by pigment epithelium-derived factor: a novel mechanistic insight into progressive obesity.
Topics: 3T3-L1 Cells; Adipocytes; Adipose Tissue; Animals; Body Weight; Diet, High-Fat; Disease Progression; | 2013 |
Orlistat, an under-recognised cause of progressive renal impairment.
Topics: Acute Kidney Injury; Aged; Anti-Obesity Agents; Diabetes Mellitus, Type 2; Disease Progression; Esse | 2013 |
Donor PNPLA3 rs738409 genotype affects fibrosis progression in liver transplantation for hepatitis C.
Topics: Biopsy; Cohort Studies; Disease Progression; Female; Follow-Up Studies; Genotype; Hepatitis C; Human | 2014 |
Impact of hyperglycemia and acute pancreatitis on the receptor for advanced glycation endproducts.
Topics: Animals; Diabetes Mellitus, Experimental; Disease Progression; Hyperglycemia; Lipase; MAP Kinase Sig | 2013 |
Species- and dose-specific pancreatic responses and progression in single- and repeat-dose studies with GI181771X: a novel cholecystokinin 1 receptor agonist in mice, rats, and monkeys.
Topics: Amylases; Animals; Benzodiazepines; Disease Models, Animal; Disease Progression; Dose-Response Relat | 2014 |
Modified Xiaochaihu Decoction () prevents the progression of chronic pancreatitis in rats possibly by inhibiting transforming growth factor-β1/Sma- and mad-related proteins signaling pathway.
Topics: Amylases; Animals; Base Sequence; Blood Glucose; Body Weight; Chronic Disease; Disease Progression; | 2013 |
Carriage of the PNPLA3 rs738409 C >G polymorphism confers an increased risk of non-alcoholic fatty liver disease associated hepatocellular carcinoma.
Topics: Adult; Aged; Carcinoma, Hepatocellular; Case-Control Studies; Cohort Studies; Disease Progression; F | 2014 |
Targeted next-generation sequencing and fine linkage disequilibrium mapping reveals association of PNPLA3 and PARVB with the severity of nonalcoholic fatty liver disease.
Topics: Actinin; Adult; Aged; Biopsy; Case-Control Studies; Chromosome Mapping; Disease Progression; Female; | 2014 |
Revisiting liver disease progression in HIV/HCV-coinfected patients: the influence of vitamin D, insulin resistance, immune status, IL28B and PNPLA3.
Topics: Adult; Coinfection; Disease Progression; Female; Genotype; Hepatitis C; Hepatitis C, Chronic; HIV; H | 2015 |
Interaction between PNPLA3 I148M variant and age at infection in determining fibrosis progression in chronic hepatitis C.
Topics: Adolescent; Adult; Age Factors; Aged; Disease Progression; Fatty Liver; Gene Frequency; Genetic Pred | 2014 |
Patatin-Like Phospholipase Domain-Containing 3 I148M Variant Is Associated with Liver Steatosis and Fat Distribution in Chronic Hepatitis B.
Topics: Abdominal Fat; Adult; Aged; Anthropometry; Body Mass Index; Chi-Square Distribution; Cohort Studies; | 2015 |
Genetic Polymorphisms of IL28B and PNPLA3 Are Predictive for HCV Related Rapid Fibrosis Progression and Identify Patients Who Require Urgent Antiviral Treatment with New Regimens.
Topics: Aged; Antiviral Agents; Disease Progression; Fatty Liver; Female; Genome-Wide Association Study; Gen | 2015 |
PNPLA3 148M Carriers with Inflammatory Bowel Diseases Have Higher Susceptibility to Hepatic Steatosis and Higher Liver Enzymes.
Topics: Alanine Transaminase; Alleles; Aspartate Aminotransferases; Biomarkers; Cohort Studies; Disease Prog | 2016 |
Retinoic Acid Ameliorates Pancreatic Fibrosis and Inhibits the Activation of Pancreatic Stellate Cells in Mice with Experimental Chronic Pancreatitis via Suppressing the Wnt/β-Catenin Signaling Pathway.
Topics: Actins; Active Transport, Cell Nucleus; Animals; Apoptosis; Axin Protein; Cells, Cultured; Ceruletid | 2015 |
The Impact of PNPLA3 rs738409 SNP on Liver Fibrosis Progression, Portal Hypertension and Hepatic Steatosis in HIV/HCV Coinfection.
Topics: Adult; Age Factors; Alleles; Biopsy; Cohort Studies; Coinfection; Cross-Sectional Studies; Disease P | 2015 |
Impact of Donor and Recipient Single Nucleotide Polymorphisms in Living Liver Donor Transplantation for Hepatitis C.
Topics: Cohort Studies; Disease Progression; Female; Genotype; Hepacivirus; Hepatitis C; Humans; Lipase; Liv | 2015 |
Association of PNPLA3 Polymorphism with Hepatocellular Carcinoma Development and Prognosis in Viral and Non-Viral Chronic Liver Diseases.
Topics: Aged; Carcinoma, Hepatocellular; Case-Control Studies; Disease Progression; Fatty Liver, Alcoholic; | 2015 |
Perfusion-CT--Can We Predict Acute Pancreatitis Outcome within the First 24 Hours from the Onset of Symptoms?
Topics: Adult; Aged; Aged, 80 and over; Amylases; Disease Progression; Early Diagnosis; Female; Humans; Lipa | 2016 |
Association of PNPLA3 rs738409 and TM6SF2 rs58542926 with health services utilization in a population-based study.
Topics: Adult; Aged; Disease Progression; Female; Genotype; Germany; Health Services; Humans; Lipase; Male; | 2016 |
Impact of EGF, IL28B, and PNPLA3 polymorphisms on the outcome of allograft hepatitis C: a multicenter study.
Topics: Adult; Allografts; Antiviral Agents; Carcinoma, Hepatocellular; Cohort Studies; Disease Progression; | 2016 |
[Relationship between changes of increased amylase or lipase levels and pancreas injury in critically ill children].
Topics: Amylases; Blood Urea Nitrogen; Calcitonin; Child; Child, Preschool; Creatinine; Critical Illness; Di | 2016 |
The PNPLA3 Genetic Variant rs738409 Influences the Progression to Cirrhosis in HIV/Hepatitis C Virus Coinfected Patients.
Topics: Adult; Alleles; Coinfection; Cross-Sectional Studies; Disease Progression; Elasticity Imaging Techni | 2016 |
Serum Lipase as Clinical Laboratory Index for Chronic Renal Failure Diagnosis.
Topics: Adult; Aged; Aged, 80 and over; Amylases; Biomarkers; Case-Control Studies; Clinical Enzyme Tests; C | 2016 |
Putative role of endothelial lipase in dialysis patients with hypoalbuminemia and inflammation.
Topics: Aged; Atherosclerosis; Cholesterol, HDL; Disease Progression; Female; Humans; Hypoalbuminemia; Infla | 2008 |
The effect of synacthen on acute necrotizing pancreatitis in rats.
Topics: Adrenal Insufficiency; Amylases; Animals; Cosyntropin; Cytokines; Disease Models, Animal; Disease Pr | 2008 |
Reduced hepatic expression of adipose tissue triglyceride lipase and CGI-58 may contribute to the development of non-alcoholic fatty liver disease in patients with insulin resistance.
Topics: 1-Acylglycerol-3-Phosphate O-Acyltransferase; Adipose Tissue; Biomarkers; Disease Progression; Fatty | 2008 |
Gene polymorphisms in APOE, NOS3, and LIPC genes may be risk factors for cardiac adverse events after primary CABG.
Topics: Apolipoproteins E; Cohort Studies; Coronary Artery Bypass; Disease Progression; Female; Genetic Pred | 2009 |
[Management of chronic pancreatitis].
Topics: Amylases; Analgesics; Cholangiopancreatography, Endoscopic Retrograde; Combined Modality Therapy; Di | 2010 |
PNPLA3 variants specifically confer increased risk for histologic nonalcoholic fatty liver disease but not metabolic disease.
Topics: Adult; Alleles; Biopsy; Case-Control Studies; Disease Progression; Fatty Liver; Female; Genetic Pred | 2010 |
The association of genetic variability in patatin-like phospholipase domain-containing protein 3 (PNPLA3) with histological severity of nonalcoholic fatty liver disease.
Topics: Adolescent; Adult; Aged; Alleles; Biopsy; Case-Control Studies; Child; Chromosomes, Human, Pair 10; | 2010 |
Emerging genes associated with the progression of nonalcoholic fatty liver disease.
Topics: Alleles; Biopsy; Disease Progression; Fatty Liver; Genetic Predisposition to Disease; Humans; Lipase | 2010 |
Role of hormonal axis, growth hormone - IGF-1, in the therapeutic effect of ghrelin in the course of cerulein-induced acute pancreatitis.
Topics: Amylases; Animals; Ceruletide; Disease Progression; Ghrelin; Growth Hormone; Hypophysectomy; Insulin | 2010 |
Deficiency of liver adipose triglyceride lipase in mice causes progressive hepatic steatosis.
Topics: Alanine Transaminase; Animals; Cytoplasm; Disease Models, Animal; Disease Progression; Energy Metabo | 2011 |
Impact of patatin-like phospholipase-3 (rs738409 C>G) polymorphism on fibrosis progression and steatosis in chronic hepatitis C.
Topics: Adult; Aged; Antiviral Agents; Belgium; Cross-Sectional Studies; Disease Progression; Fatty Liver; F | 2011 |
The common I148 M variant of PNPLA3 does not predict fibrosis progression after liver transplantation for hepatitis C.
Topics: Cohort Studies; Disease Progression; End Stage Liver Disease; Female; Genetic Markers; Graft Rejecti | 2011 |
HIV-1 disease progression is associated with bile-salt stimulated lipase (BSSL) gene polymorphism.
Topics: Alleles; CD4 Lymphocyte Count; Disease Progression; Genotype; HIV Infections; HIV Seropositivity; HI | 2012 |
Patatin-like phospholipase domain containing-3 gene I148M polymorphism, steatosis, and liver damage in hereditary hemochromatosis.
Topics: Adult; Biomarkers; Biopsy; Chi-Square Distribution; Disease Progression; Fatty Liver; Female; Gene F | 2012 |
Genome-wide association study identifies variants associated with progression of liver fibrosis from HCV infection.
Topics: Adult; Apoptosis; c-Mer Tyrosine Kinase; Disease Progression; Eye Proteins; Female; Genome-Wide Asso | 2012 |
Genetic polymorphism in cyclooxygenase-2 promoter affects hepatic inflammation and fibrosis in patients with chronic hepatitis C.
Topics: Asian People; Cyclooxygenase 2; Disease Progression; Female; Genetic Predisposition to Disease; Hepa | 2012 |
PNPLA3, a genetic marker of progressive liver disease, still hiding its metabolic function?
Topics: Disease Progression; Fatty Liver; Genetic Markers; Humans; Lipase; Membrane Proteins; Non-alcoholic | 2013 |
Influence of leptin administration on the course of acute ischemic pancreatitis.
Topics: Amylases; Animals; Disease Progression; DNA; Interleukin-1; Interleukin-10; Ischemia; Leptin; Lipase | 2002 |
Exocrine pancreatic insufficiency as an end stage of pancreatitis in four dogs.
Topics: Amylases; Animals; Case-Control Studies; Chronic Disease; Disease Progression; Dog Diseases; Dogs; E | 2003 |
Effect of early administration of exogenous basic fibroblast growth factor on acute edematous pancreatitis in rats.
Topics: Amylases; Animals; Ceruletide; Disease Progression; DNA; Edema; Fibroblast Growth Factor 2; Immunohi | 2006 |
CETP (cholesteryl ester transfer protein) promoter -1337 C>T polymorphism protects against coronary atherosclerosis in Japanese patients with heterozygous familial hypercholesterolaemia.
Topics: Adult; Aged; Aged, 80 and over; Cholesterol Ester Transfer Proteins; Coronary Artery Disease; Diseas | 2006 |
Rapidly progressive renal failure associated with successful pharmacotherapy for obesity.
Topics: Acute Kidney Injury; Anti-Obesity Agents; Biopsy; Disease Progression; Female; Follow-Up Studies; Gl | 2007 |
Rapidly progressive renal failure associated with successful pharmacotherapy for obesity.
Topics: Acute Kidney Injury; Anti-Obesity Agents; Biopsy; Cohort Studies; Disease Progression; Follow-Up Stu | 2007 |
[Acute pancreatitis: what is really important in diagnosis and therapy].
Topics: Aged; Amylases; Critical Care; Disease Progression; Fatal Outcome; Female; Humans; Lipase; Pancreas; | 2007 |
Acute elevation of plasma PLTP activity strongly increases pre-existing atherosclerosis.
Topics: Animals; Apolipoproteins B; Atherosclerosis; Cholesterol, Dietary; Collagen; Disease Models, Animal; | 2008 |
Hyperlipaemia intensifies the course of acute oedematous and acute necrotising pancreatitis in the rat.
Topics: Acute Disease; Amylases; Animals; Cholesterol; Disease Models, Animal; Disease Progression; Edema; H | 1996 |
Progressive pan-colonic fibrosis secondary to oral administration of pancreatic enzymes.
Topics: Child; Colon; Constriction, Pathologic; Cystic Fibrosis; Disease Progression; Fibrosis; Humans; Inte | 1998 |
T cell-mediated exocrine pancreatic damage in major histocompatibility complex class II-deficient mice.
Topics: Amylases; Animals; Blood Glucose; Digestive System; Disease Progression; Histocompatibility Antigens | 1998 |
Serum pancreatic enzymes in human immunodeficiency virus-infected children. A collaborative study of the Italian Society of Pediatric Gastroenterology and Hepatology.
Topics: Adolescent; AIDS-Related Opportunistic Infections; Amylases; CD4-Positive T-Lymphocytes; Child; Chil | 1998 |
Ethanol administration delays recovery from acute pancreatitis induced by exocrine hyperstimulation.
Topics: Acute Disease; Amylases; Animals; Calcium; Central Nervous System Depressants; Ceruletide; Disease P | 1998 |