niacinamide and Breast Neoplasms studies

nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.

Research Excerpts

Excerpt	Relevance	Reference
"We conducted an open-label, randomized, two-arm multi-center study to assess the efficacy and safety of paclitaxel versus paclitaxel + sorafenib in patients with locally advanced or metastatic HER2-negative breast cancer."	9.24	A randomized phase II study of paclitaxel alone versus paclitaxel plus sorafenib in second- and third-line treatment of patients with HER2-negative metastatic breast cancer (PASO). ( Decker, T; Göhler, T; Indorf, M; Nusch, A; Overkamp, F; Rösel, S; Sahlmann, J; Trarbach, T, 2017)
" In this randomized, double-blind, placebo-controlled phase III trial, we assessed first- or second-line capecitabine with sorafenib or placebo in patients with locally advanced/metastatic HER2-negative breast cancer resistant to a taxane and anthracycline and with known estrogen/progesterone receptor status."	9.24	RESILIENCE: Phase III Randomized, Double-Blind Trial Comparing Sorafenib With Capecitabine Versus Placebo With Capecitabine in Locally Advanced or Metastatic HER2-Negative Breast Cancer. ( Baselga, J; Bergh, J; Bermejo, B; Chan, A; Costa, F; Gómez, HL; Gómez, P; Gradishar, WJ; Huang, L; Hudis, CA; Maeda, P; Mángel, L; Meinhardt, G; Melichar, B; Nagai, SE; Rapoport, BL; Roché, H; Schwartzberg, LS; Zamagni, C; Zhang, J, 2017)
"The purposes of the present phase I/II trial were (1) to define tolerable doses of ixabepilone and sorafenib when used in combination and (2) to evaluate the efficacy and toxicity of this combination in the treatment of patients with human epidermal growth factor receptor-negative metastatic breast cancer (MBC)."	9.22	Sorafenib Plus Ixabepilone as First-Line Treatment of Metastatic HER2-Negative Breast Cancer: A Sarah Cannon Research Institute Phase I/II Trial. ( Dickson, N; Drosick, D; Earwood, C; Hainsworth, JD; Inhorn, R; Murphy, P; Yardley, DA, 2016)
"A pilot Phase II study adding sorafenib to endocrine therapy in 11 patients with metastatic estrogen receptor-positive breast cancer was conducted."	9.19	Impact of adding the multikinase inhibitor sorafenib to endocrine therapy in metastatic estrogen receptor-positive breast cancer. ( Black, EP; Karabakhtsian, RG; Massarweh, S; Moss, J; Napier, D; Romond, E; Slone, S; Wang, C; Weiss, H, 2014)
"We investigated the efficacy and toxicity of sorafenib, a multikinase inhibitor of vascular endothelial growth factor receptor tyrosine kinase, in combination with vinorelbine therapy in a phase I/II trial in patients with metastatic breast cancer."	9.19	Phase I/II trial of vinorelbine and sorafenib in metastatic breast cancer. ( Chow, W; Chung, C; Frankel, P; Hurria, A; Luu, T; Mortimer, J; Somlo, G, 2014)
"We conducted a phase 2b, randomised, double-blind, placebo-controlled screening trial to evaluate the addition of the multikinase inhibitor sorafenib (antiproliferative/antiangiogenic) to first-line paclitaxel for human epidermal growth factor receptor 2 (HER2)-negative locally recurrent/metastatic breast cancer."	9.17	A double-blind, randomised, placebo-controlled, phase 2b study evaluating sorafenib in combination with paclitaxel as a first-line therapy in patients with HER2-negative advanced breast cancer. ( Bondarde, S; Gradishar, WJ; Jain, M; Kaklamani, V; Lokanatha, D; Lokker, NA; Raina, V; Ro, SK; Sahoo, TP; Schwartzberg, L, 2013)
" A randomized phase 2b screening trial in human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer demonstrated a significant improvement in progression-free survival (PFS) when sorafenib was added to capecitabine versus placebo (median 6."	9.17	A phase 3 tRial comparing capecitabinE in combination with SorafenIb or pLacebo for treatment of locally advanced or metastatIc HER2-Negative breast CancEr (the RESILIENCE study): study protocol for a randomized controlled trial. ( Baselga, J; Costa, F; Gomez, H; Gradishar, WJ; Hudis, CA; Petrenciuc, O; Rapoport, B; Roche, H; Schwartzberg, LS; Shan, M, 2013)
" We evaluated the efficacy and safety of dual angiogenesis blockade with bevacizumab and sorafenib in patients with metastatic breast cancer."	9.17	A phase II study of combined VEGF inhibitor (bevacizumab+sorafenib) in patients with metastatic breast cancer: Hoosier Oncology Group Study BRE06-109. ( Burkhardt, C; Johnson, C; Miller, KD; Mina, LA; Yu, M; Zon, R, 2013)
"We assessed adding the multikinase inhibitor sorafenib to gemcitabine or capecitabine in patients with advanced breast cancer whose disease progressed during/after bevacizumab."	9.17	Sorafenib or placebo with either gemcitabine or capecitabine in patients with HER-2-negative advanced breast cancer that progressed during or after bevacizumab. ( Beck, JT; Bell-McGuinn, K; Eisenberg, P; Emanuelson, R; Hermann, RC; Hudis, CA; Isaacs, C; Kaklamani, V; Keaton, M; Kirshner, JJ; Levine, E; Lokker, NA; Makari-Judson, G; Medgyesy, DC; Qamar, R; Ro, SK; Rugo, HS; Schwartzberg, LS; Starr, A; Stepanski, EJ; Tauer, KW; Wang, W, 2013)
" A randomized, double-blind, placebo-controlled phase IIB trial assessed sorafenib with capecitabine for locally advanced or metastatic human epidermal growth factor receptor 2 (HER2) -negative breast cancer."	9.16	Sorafenib in combination with capecitabine: an oral regimen for patients with HER2-negative locally advanced or metastatic breast cancer. ( Baselga, J; Bermejo, B; Ciruelos, EM; Costa, F; de Moraes, AA; Del Giglio, A; Durán, MÁ; Espié, M; Filho, SC; Garicochea, B; Gil Gil, M; Gómez, P; Hoff, PM; Kwon Ro, S; Li, S; Llombart, A; Mathias, C; Morales, J; Ojeda, B; Pinczowski, H; Ribeiro, RA; Roché, H; Segalla, JG; Van Eyll, B, 2012)
"The purpose of this study was to investigate the safety, tolerability, and pharmacokinetics of motesanib when combined with docetaxel or paclitaxel in patients with metastatic breast cancer."	9.16	Phase 1b dose-finding study of motesanib with docetaxel or paclitaxel in patients with metastatic breast cancer. ( Adewoye, AH; Chan, A; De Boer, RH; Kaufman, PA; Koczwara, B; Kotasek, D; Mainwaring, P; Melara, R; Sikorski, R; White, S; Ye, Y, 2012)
"To examine the safety of sorafenib combined with standard adjuvant treatment in patients with node-positive or otherwise high-risk breast cancer."	9.15	A pilot study of adjuvant doxorubicin and cyclophosphamide followed by paclitaxel and sorafenib in women with node-positive or high-risk early-stage breast cancer. ( Burris, HA; Greco, FA; Hainsworth, JD; Kommor, M; Molthrop, DC; Peacock, N; Spigel, DR; Vazquez, ER; Yardley, DA, 2011)
"Between Dec 1, 2006, and July 4, 2008, patients with untreated HER2-negative metastatic breast cancer were randomly assigned (using a randomisation list created by personnel not associated with the study) in a 1:1:1 ratio to paclitaxel (90 mg/m(2) on days 1, 8, and 15 every 3 weeks) plus either masked motesanib 125 mg orally once per day (n=91), masked placebo orally once per day (n=94), or open-label bevacizumab 10 mg/kg intravenously on days 1 and 15 of each 28-day cycle (n=97), after stratification according to adjuvant or neoadjuvant chemotherapy (taxane-containing regimens vs other regimens vs none), number of metastatic sites (<3 vs ≥3), and hormone receptor status (positive vs negative)."	9.15	Motesanib, or open-label bevacizumab, in combination with paclitaxel, as first-line treatment for HER2-negative locally recurrent or metastatic breast cancer: a phase 2, randomised, double-blind, placebo-controlled study. ( Adewoye, H; Adrover, E; Alba, E; Almel, S; Baños, A; Cabaribere, D; Crown, J; Eiermann, W; Hei, YJ; Hurvitz, S; Jagiełło-Gruszfeld, A; Kennedy, MJ; Lang, I; Latreille, J; Lemmerick, Y; Lindsay, MA; Mackey, JR; Martin, M; Moroose, R; Munoz, M; Pienkowski, T; Pinter, T; Priou, F; Provencher, L; Ramos, M; Roche, H; Rolski, J; Rupin, M; Snyder, R, 2011)
"We evaluated the use of sorafenib to overcome resistance to aromatase inhibitors (AIs) in patients with metastatic breast cancer who had disease recurrence or progression while on AIs."	9.15	Phase I/II study of sorafenib with anastrozole in patients with hormone receptor positive aromatase inhibitor resistant metastatic breast cancer. ( Chung, GG; Cohen, P; Creswell, K; Eng-Wong, J; Herbolsheimer, P; Isaacs, C; Liu, MC; Novielli, A; Ottaviano, Y; Slack, R; Smith, KL; Warren, R; Wilkinson, M, 2011)
"We conducted a cooperative group phase II study to assess antitumor activity and toxicity of sorafenib in patients with metastatic breast cancer (MBC) who had received prior treatment for their disease."	9.14	Phase II trial of sorafenib in patients with metastatic breast cancer previously exposed to anthracyclines or taxanes: North Central Cancer Treatment Group and Mayo Clinic Trial N0336. ( Fitch, TR; Flynn, PJ; Hillman, DW; Lingle, WL; Moreno-Aspitia, A; Morton, RF; Perez, EA; Rowland, KM; Wiesenfeld, M, 2009)
"This trial was conducted to assess the efficacy and safety of sorafenib in patients with metastatic breast cancer."	9.14	Phase II multicenter, uncontrolled trial of sorafenib in patients with metastatic breast cancer. ( Bergamini, L; Bianchi, G; Gianni, L; Laferriere, N; Lathia, C; Loibl, S; Peña, C; Raab, G; Salvagni, S; Siena, S; Zamagni, C, 2009)
"Sorafenib is a clinically useful multiple kinase inhibitor for the treatment of kidney cancer, liver cancer and acute myelocytic leukemia, while it has shown weak efficacy in suppressing breast cancer."	8.12	Potential synthetic lethality for breast cancer: A selective sirtuin 2 inhibitor combined with a multiple kinase inhibitor sorafenib. ( Guan, XY; Li, GB; Ma, X; Song, C; Wang, HL; Yang, LL; Yu, YM, 2022)
"We studied the relation between the polymorphism of P-glycoprotein (P-gp) and of breast cancer resistance protein (BCRP), encoded by ABCB1 and ABCG2 genes, respectively, and the pharmacokinetic variability and clinical response during the treatment with sorafenib of hepatocellular carcinoma."	7.85	Correlation between clinical response to sorafenib in hepatocellular carcinoma treatment and polymorphisms of P-glycoprotein (ABCB1) and of breast cancer resistance protein (ABCG2): monocentric study. ( Bonhomme-Faivre, L; Cailliez, V; Farinotti, R; Mhiri, A; Noé, G; Paule, B; Saffroy, R; Tandia, M, 2017)
"To assess whether the combination of letrozole, metronomic cyclophosphamide and sorafenib (LCS) is well tolerated and shows activity in primary breast cancer (BC)."	7.81	Combination of letrozole, metronomic cyclophosphamide and sorafenib is well-tolerated and shows activity in patients with primary breast cancer. ( Aguggini, S; Allevi, G; Andreis, D; Bazzola, L; Berruti, A; Bertoni, R; Bottini, A; Ferrozzi, F; Foroni, C; Fox, SB; Gatter, K; Generali, D; Giardini, R; Harris, AL; Martinotti, M; Milani, M; Petronini, PG; R Cappelletti, M; Reynolds, AR; Strina, C; Turley, H; Venturini, S; Zanoni, V, 2015)
"Tamoxifen‑resistant breast cancer is a major clinical problem and new treatment strategies are highly warranted."	7.80	Sorafenib and nilotinib resensitize tamoxifen resistant breast cancer cells to tamoxifen treatment via estrogen receptor α. ( Lykkesfeldt, AE; Pedersen, AM; Thrane, S; Yde, CW, 2014)
" The present study shows that both sorafenib and lapatinib alone are effective in the treatment of breast cancer."	7.80	Investigation of antitumor effects of sorafenib and lapatinib alone and in combination on MCF-7 breast cancer cells. ( Altun, A; Altun, GG; Babacan, N; Bahceci, A; Kacan, SB; Kacan, T; Sarac, B; Seker, MM, 2014)
"The multi-kinase inhibitor sorafenib is used for the treatment of renal and hepatic carcinomas and is undergoing evaluation for treatment of breast cancer in combination with other agents."	7.79	Anti-proliferative actions of N'-desmethylsorafenib in human breast cancer cells. ( Bourget, K; Cui, PH; Gillani, TB; Murray, M; Rawling, T; Wang, XS; Zhou, F, 2013)
"Novel sorafenib analogues SC-1 and SC-43 induce apoptosis through SHP-1 dependent STAT3 inactivation and demonstrate greater potency than sorafenib in human breast cancer cells."	7.79	Novel sorafenib analogues induce apoptosis through SHP-1 dependent STAT3 inactivation in human breast cancer cells. ( Chang, KC; Chen, KF; Chu, PY; Liu, CY; Shiau, CW; Su, JC; Tai, WT; Tseng, LM, 2013)
"In this study, we investigated the effects and the underlying molecular mechanisms of the multi-kinase inhibitor sorafenib in a panel of breast cancer cell lines."	7.79	Effects of sorafenib on energy metabolism in breast cancer cells: role of AMPK-mTORC1 signaling. ( Alfieri, RR; Bonelli, MA; Caffarra, C; Cavazzoni, A; Fumarola, C; Galetti, M; Galvani, E; Generali, D; La Monica, S; Petronini, PG, 2013)
" We investigated whether the Src/Abl kinase inhibitor dasatinib displays synergy with other agents in molecularly heterogeneous breast cancer cell lines."	7.78	Dasatinib synergizes with both cytotoxic and signal transduction inhibitors in heterogeneous breast cancer cell lines--lessons for design of combination targeted therapy. ( Corey, SJ; Park, BJ; Whichard, ZL, 2012)
"In this study we investigated sorafenib tosylate and paclitaxel as single and combination therapies regarding their effects on tumour growth and vasculature as well as their potency to inhibit osteolysis in experimental breast cancer bone metastases."	7.77	Sorafenib tosylate and paclitaxel induce anti-angiogenic, anti-tumour and anti-resorptive effects in experimental breast cancer bone metastases. ( Bäuerle, T; Komljenovic, D; Merz, M; Semmler, W; Zwick, S, 2011)
" In this study we demonstrated the preclinical therapeutic efficacy of combining the aromatase inhibitor letrozole with the multi-kinase inhibitor sorafenib in aromatase-expressing breast cancer cell lines."	7.76	Synergistic activity of letrozole and sorafenib on breast cancer cells. ( Alfieri, RR; Belletti, S; Bonelli, MA; Bottini, A; Cavazzoni, A; Dowsett, M; Evans, DB; Fox, SB; Fumarola, C; Galetti, M; Gatti, R; Generali, D; Harris, AL; La Monica, S; Martin, LA; Petronini, PG, 2010)
"Sorafenib has also been studied in combination with other agents."	6.55	Sorafenib for the treatment of breast cancer. ( Amadori, D; Andreis, D; Bravaccini, S; Bronte, G; Cecconetto, L; Donati, C; Farolfi, A; Fedeli, A; Maltoni, R; Rocca, A; Schirone, A; Serra, P, 2017)
"Sorafenib is an oral multikinase inhibitor with anti-angiogenic and anti-proliferative activity that is indicated for use in hepatocellular and renal cell carcinomas."	6.48	Sorafenib in locally advanced or metastatic breast cancer. ( Gradishar, WJ, 2012)
"Sorafenib has both antiangiogenic and antiproliferative activities and is indicated for patients with unresectable hepatocellular and advanced renal cell carcinoma."	6.47	Clinical presentation and management of hand-foot skin reaction associated with sorafenib in combination with cytotoxic chemotherapy: experience in breast cancer. ( Gomez, P; Lacouture, ME, 2011)
"Sorafenib is an oral multikinase inhibitor that inhibits tumor growth and proliferation by interfering with several receptor tyrosine kinases involved in the pathogenesis and perpetuation of malignant breast cancer cells."	6.46	Clinical overview of sorafenib in breast cancer. ( Moreno-Aspitia, A, 2010)
" Moreover, imetelstat alone and in combination with trastuzumab reduced the CSC fraction and inhibited CSC functional ability, as shown by decreased mammosphere counts and invasive potential."	5.42	The telomerase inhibitor imetelstat alone, and in combination with trastuzumab, decreases the cancer stem cell population and self-renewal of HER2+ breast cancer cells. ( Herbert, BS; Koziel, JE, 2015)
"The study was performed on three breast cancer cell lines (BRC-230, MCF-7 and SkBr3)."	5.36	Tyrosine kinase inhibitors gefitinib, lapatinib and sorafenib induce rapid functional alterations in breast cancer cells. ( Amadori, D; Brigliadori, G; Carloni, S; Fabbri, F; Silvestrini, R; Ulivi, P; Zoli, W, 2010)
"Carbogen breathing was started 5 min prior to treatment and continued during it."	5.29	Short communication: the addition of carbogen and nicotinamide to a palliative fractionation schedule for locally advanced breast cancer. ( Dische, S; Pigott, K; Saunders, MI, 1995)
" In this randomized, double-blind, placebo-controlled phase III trial, we assessed first- or second-line capecitabine with sorafenib or placebo in patients with locally advanced/metastatic HER2-negative breast cancer resistant to a taxane and anthracycline and with known estrogen/progesterone receptor status."	5.24	RESILIENCE: Phase III Randomized, Double-Blind Trial Comparing Sorafenib With Capecitabine Versus Placebo With Capecitabine in Locally Advanced or Metastatic HER2-Negative Breast Cancer. ( Baselga, J; Bergh, J; Bermejo, B; Chan, A; Costa, F; Gómez, HL; Gómez, P; Gradishar, WJ; Huang, L; Hudis, CA; Maeda, P; Mángel, L; Meinhardt, G; Melichar, B; Nagai, SE; Rapoport, BL; Roché, H; Schwartzberg, LS; Zamagni, C; Zhang, J, 2017)
"We conducted an open-label, randomized, two-arm multi-center study to assess the efficacy and safety of paclitaxel versus paclitaxel + sorafenib in patients with locally advanced or metastatic HER2-negative breast cancer."	5.24	A randomized phase II study of paclitaxel alone versus paclitaxel plus sorafenib in second- and third-line treatment of patients with HER2-negative metastatic breast cancer (PASO). ( Decker, T; Göhler, T; Indorf, M; Nusch, A; Overkamp, F; Rösel, S; Sahlmann, J; Trarbach, T, 2017)
"The purposes of the present phase I/II trial were (1) to define tolerable doses of ixabepilone and sorafenib when used in combination and (2) to evaluate the efficacy and toxicity of this combination in the treatment of patients with human epidermal growth factor receptor-negative metastatic breast cancer (MBC)."	5.22	Sorafenib Plus Ixabepilone as First-Line Treatment of Metastatic HER2-Negative Breast Cancer: A Sarah Cannon Research Institute Phase I/II Trial. ( Dickson, N; Drosick, D; Earwood, C; Hainsworth, JD; Inhorn, R; Murphy, P; Yardley, DA, 2016)
"We investigated the efficacy and toxicity of sorafenib, a multikinase inhibitor of vascular endothelial growth factor receptor tyrosine kinase, in combination with vinorelbine therapy in a phase I/II trial in patients with metastatic breast cancer."	5.19	Phase I/II trial of vinorelbine and sorafenib in metastatic breast cancer. ( Chow, W; Chung, C; Frankel, P; Hurria, A; Luu, T; Mortimer, J; Somlo, G, 2014)
"A pilot Phase II study adding sorafenib to endocrine therapy in 11 patients with metastatic estrogen receptor-positive breast cancer was conducted."	5.19	Impact of adding the multikinase inhibitor sorafenib to endocrine therapy in metastatic estrogen receptor-positive breast cancer. ( Black, EP; Karabakhtsian, RG; Massarweh, S; Moss, J; Napier, D; Romond, E; Slone, S; Wang, C; Weiss, H, 2014)
" We evaluated the efficacy and safety of dual angiogenesis blockade with bevacizumab and sorafenib in patients with metastatic breast cancer."	5.17	A phase II study of combined VEGF inhibitor (bevacizumab+sorafenib) in patients with metastatic breast cancer: Hoosier Oncology Group Study BRE06-109. ( Burkhardt, C; Johnson, C; Miller, KD; Mina, LA; Yu, M; Zon, R, 2013)
"We assessed adding the multikinase inhibitor sorafenib to gemcitabine or capecitabine in patients with advanced breast cancer whose disease progressed during/after bevacizumab."	5.17	Sorafenib or placebo with either gemcitabine or capecitabine in patients with HER-2-negative advanced breast cancer that progressed during or after bevacizumab. ( Beck, JT; Bell-McGuinn, K; Eisenberg, P; Emanuelson, R; Hermann, RC; Hudis, CA; Isaacs, C; Kaklamani, V; Keaton, M; Kirshner, JJ; Levine, E; Lokker, NA; Makari-Judson, G; Medgyesy, DC; Qamar, R; Ro, SK; Rugo, HS; Schwartzberg, LS; Starr, A; Stepanski, EJ; Tauer, KW; Wang, W, 2013)
" A randomized phase 2b screening trial in human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer demonstrated a significant improvement in progression-free survival (PFS) when sorafenib was added to capecitabine versus placebo (median 6."	5.17	A phase 3 tRial comparing capecitabinE in combination with SorafenIb or pLacebo for treatment of locally advanced or metastatIc HER2-Negative breast CancEr (the RESILIENCE study): study protocol for a randomized controlled trial. ( Baselga, J; Costa, F; Gomez, H; Gradishar, WJ; Hudis, CA; Petrenciuc, O; Rapoport, B; Roche, H; Schwartzberg, LS; Shan, M, 2013)
"We conducted a phase 2b, randomised, double-blind, placebo-controlled screening trial to evaluate the addition of the multikinase inhibitor sorafenib (antiproliferative/antiangiogenic) to first-line paclitaxel for human epidermal growth factor receptor 2 (HER2)-negative locally recurrent/metastatic breast cancer."	5.17	A double-blind, randomised, placebo-controlled, phase 2b study evaluating sorafenib in combination with paclitaxel as a first-line therapy in patients with HER2-negative advanced breast cancer. ( Bondarde, S; Gradishar, WJ; Jain, M; Kaklamani, V; Lokanatha, D; Lokker, NA; Raina, V; Ro, SK; Sahoo, TP; Schwartzberg, L, 2013)
"The purpose of this study was to investigate the safety, tolerability, and pharmacokinetics of motesanib when combined with docetaxel or paclitaxel in patients with metastatic breast cancer."	5.16	Phase 1b dose-finding study of motesanib with docetaxel or paclitaxel in patients with metastatic breast cancer. ( Adewoye, AH; Chan, A; De Boer, RH; Kaufman, PA; Koczwara, B; Kotasek, D; Mainwaring, P; Melara, R; Sikorski, R; White, S; Ye, Y, 2012)
" A randomized, double-blind, placebo-controlled phase IIB trial assessed sorafenib with capecitabine for locally advanced or metastatic human epidermal growth factor receptor 2 (HER2) -negative breast cancer."	5.16	Sorafenib in combination with capecitabine: an oral regimen for patients with HER2-negative locally advanced or metastatic breast cancer. ( Baselga, J; Bermejo, B; Ciruelos, EM; Costa, F; de Moraes, AA; Del Giglio, A; Durán, MÁ; Espié, M; Filho, SC; Garicochea, B; Gil Gil, M; Gómez, P; Hoff, PM; Kwon Ro, S; Li, S; Llombart, A; Mathias, C; Morales, J; Ojeda, B; Pinczowski, H; Ribeiro, RA; Roché, H; Segalla, JG; Van Eyll, B, 2012)
"To examine the safety of sorafenib combined with standard adjuvant treatment in patients with node-positive or otherwise high-risk breast cancer."	5.15	A pilot study of adjuvant doxorubicin and cyclophosphamide followed by paclitaxel and sorafenib in women with node-positive or high-risk early-stage breast cancer. ( Burris, HA; Greco, FA; Hainsworth, JD; Kommor, M; Molthrop, DC; Peacock, N; Spigel, DR; Vazquez, ER; Yardley, DA, 2011)
"We evaluated the use of sorafenib to overcome resistance to aromatase inhibitors (AIs) in patients with metastatic breast cancer who had disease recurrence or progression while on AIs."	5.15	Phase I/II study of sorafenib with anastrozole in patients with hormone receptor positive aromatase inhibitor resistant metastatic breast cancer. ( Chung, GG; Cohen, P; Creswell, K; Eng-Wong, J; Herbolsheimer, P; Isaacs, C; Liu, MC; Novielli, A; Ottaviano, Y; Slack, R; Smith, KL; Warren, R; Wilkinson, M, 2011)
"Between Dec 1, 2006, and July 4, 2008, patients with untreated HER2-negative metastatic breast cancer were randomly assigned (using a randomisation list created by personnel not associated with the study) in a 1:1:1 ratio to paclitaxel (90 mg/m(2) on days 1, 8, and 15 every 3 weeks) plus either masked motesanib 125 mg orally once per day (n=91), masked placebo orally once per day (n=94), or open-label bevacizumab 10 mg/kg intravenously on days 1 and 15 of each 28-day cycle (n=97), after stratification according to adjuvant or neoadjuvant chemotherapy (taxane-containing regimens vs other regimens vs none), number of metastatic sites (<3 vs ≥3), and hormone receptor status (positive vs negative)."	5.15	Motesanib, or open-label bevacizumab, in combination with paclitaxel, as first-line treatment for HER2-negative locally recurrent or metastatic breast cancer: a phase 2, randomised, double-blind, placebo-controlled study. ( Adewoye, H; Adrover, E; Alba, E; Almel, S; Baños, A; Cabaribere, D; Crown, J; Eiermann, W; Hei, YJ; Hurvitz, S; Jagiełło-Gruszfeld, A; Kennedy, MJ; Lang, I; Latreille, J; Lemmerick, Y; Lindsay, MA; Mackey, JR; Martin, M; Moroose, R; Munoz, M; Pienkowski, T; Pinter, T; Priou, F; Provencher, L; Ramos, M; Roche, H; Rolski, J; Rupin, M; Snyder, R, 2011)
"We conducted a cooperative group phase II study to assess antitumor activity and toxicity of sorafenib in patients with metastatic breast cancer (MBC) who had received prior treatment for their disease."	5.14	Phase II trial of sorafenib in patients with metastatic breast cancer previously exposed to anthracyclines or taxanes: North Central Cancer Treatment Group and Mayo Clinic Trial N0336. ( Fitch, TR; Flynn, PJ; Hillman, DW; Lingle, WL; Moreno-Aspitia, A; Morton, RF; Perez, EA; Rowland, KM; Wiesenfeld, M, 2009)
"This trial was conducted to assess the efficacy and safety of sorafenib in patients with metastatic breast cancer."	5.14	Phase II multicenter, uncontrolled trial of sorafenib in patients with metastatic breast cancer. ( Bergamini, L; Bianchi, G; Gianni, L; Laferriere, N; Lathia, C; Loibl, S; Peña, C; Raab, G; Salvagni, S; Siena, S; Zamagni, C, 2009)
"Sorafenib is a clinically useful multiple kinase inhibitor for the treatment of kidney cancer, liver cancer and acute myelocytic leukemia, while it has shown weak efficacy in suppressing breast cancer."	4.12	Potential synthetic lethality for breast cancer: A selective sirtuin 2 inhibitor combined with a multiple kinase inhibitor sorafenib. ( Guan, XY; Li, GB; Ma, X; Song, C; Wang, HL; Yang, LL; Yu, YM, 2022)
" The highest cellular uptake was observed in MCF-7 breast tumor cells treated with 99mTc-(tricine)-HYNIC-Lys-FROP as compared to other cell lines (lung, ovarian, T47D breast cancer cell lines)."	3.88	( Abedi, SM; Ahmadpour, S; Hosseinimehr, SJ; Noaparast, Z, 2018)
"We studied the relation between the polymorphism of P-glycoprotein (P-gp) and of breast cancer resistance protein (BCRP), encoded by ABCB1 and ABCG2 genes, respectively, and the pharmacokinetic variability and clinical response during the treatment with sorafenib of hepatocellular carcinoma."	3.85	Correlation between clinical response to sorafenib in hepatocellular carcinoma treatment and polymorphisms of P-glycoprotein (ABCB1) and of breast cancer resistance protein (ABCG2): monocentric study. ( Bonhomme-Faivre, L; Cailliez, V; Farinotti, R; Mhiri, A; Noé, G; Paule, B; Saffroy, R; Tandia, M, 2017)
"To assess whether the combination of letrozole, metronomic cyclophosphamide and sorafenib (LCS) is well tolerated and shows activity in primary breast cancer (BC)."	3.81	Combination of letrozole, metronomic cyclophosphamide and sorafenib is well-tolerated and shows activity in patients with primary breast cancer. ( Aguggini, S; Allevi, G; Andreis, D; Bazzola, L; Berruti, A; Bertoni, R; Bottini, A; Ferrozzi, F; Foroni, C; Fox, SB; Gatter, K; Generali, D; Giardini, R; Harris, AL; Martinotti, M; Milani, M; Petronini, PG; R Cappelletti, M; Reynolds, AR; Strina, C; Turley, H; Venturini, S; Zanoni, V, 2015)
"Tamoxifen‑resistant breast cancer is a major clinical problem and new treatment strategies are highly warranted."	3.80	Sorafenib and nilotinib resensitize tamoxifen resistant breast cancer cells to tamoxifen treatment via estrogen receptor α. ( Lykkesfeldt, AE; Pedersen, AM; Thrane, S; Yde, CW, 2014)
" The present study shows that both sorafenib and lapatinib alone are effective in the treatment of breast cancer."	3.80	Investigation of antitumor effects of sorafenib and lapatinib alone and in combination on MCF-7 breast cancer cells. ( Altun, A; Altun, GG; Babacan, N; Bahceci, A; Kacan, SB; Kacan, T; Sarac, B; Seker, MM, 2014)
" Here we confirm that bafilomycin A1 (BafA1), a selective vATPase inhibitor, significantly increased death of breast cancer cells in a hypoxia and Bnip3-dependent manner and significantly reduced tumor growth in MCF7 and MDA-MB-231 mouse xenografts."	3.80	Inhibition of the vacuolar ATPase induces Bnip3-dependent death of cancer cells and a reduction in tumor burden and metastasis. ( Graham, RM; Thompson, JW; Webster, KA, 2014)
"In this study, we investigated the effects and the underlying molecular mechanisms of the multi-kinase inhibitor sorafenib in a panel of breast cancer cell lines."	3.79	Effects of sorafenib on energy metabolism in breast cancer cells: role of AMPK-mTORC1 signaling. ( Alfieri, RR; Bonelli, MA; Caffarra, C; Cavazzoni, A; Fumarola, C; Galetti, M; Galvani, E; Generali, D; La Monica, S; Petronini, PG, 2013)
"Novel sorafenib analogues SC-1 and SC-43 induce apoptosis through SHP-1 dependent STAT3 inactivation and demonstrate greater potency than sorafenib in human breast cancer cells."	3.79	Novel sorafenib analogues induce apoptosis through SHP-1 dependent STAT3 inactivation in human breast cancer cells. ( Chang, KC; Chen, KF; Chu, PY; Liu, CY; Shiau, CW; Su, JC; Tai, WT; Tseng, LM, 2013)
"The multi-kinase inhibitor sorafenib is used for the treatment of renal and hepatic carcinomas and is undergoing evaluation for treatment of breast cancer in combination with other agents."	3.79	Anti-proliferative actions of N'-desmethylsorafenib in human breast cancer cells. ( Bourget, K; Cui, PH; Gillani, TB; Murray, M; Rawling, T; Wang, XS; Zhou, F, 2013)
" We investigated whether the Src/Abl kinase inhibitor dasatinib displays synergy with other agents in molecularly heterogeneous breast cancer cell lines."	3.78	Dasatinib synergizes with both cytotoxic and signal transduction inhibitors in heterogeneous breast cancer cell lines--lessons for design of combination targeted therapy. ( Corey, SJ; Park, BJ; Whichard, ZL, 2012)
"In this study we investigated sorafenib tosylate and paclitaxel as single and combination therapies regarding their effects on tumour growth and vasculature as well as their potency to inhibit osteolysis in experimental breast cancer bone metastases."	3.77	Sorafenib tosylate and paclitaxel induce anti-angiogenic, anti-tumour and anti-resorptive effects in experimental breast cancer bone metastases. ( Bäuerle, T; Komljenovic, D; Merz, M; Semmler, W; Zwick, S, 2011)
" In this study we demonstrated the preclinical therapeutic efficacy of combining the aromatase inhibitor letrozole with the multi-kinase inhibitor sorafenib in aromatase-expressing breast cancer cell lines."	3.76	Synergistic activity of letrozole and sorafenib on breast cancer cells. ( Alfieri, RR; Belletti, S; Bonelli, MA; Bottini, A; Cavazzoni, A; Dowsett, M; Evans, DB; Fox, SB; Fumarola, C; Galetti, M; Gatti, R; Generali, D; Harris, AL; La Monica, S; Martin, LA; Petronini, PG, 2010)
"EVESOR is a multiparameter dose-escalation phase I trial investigating different doses and dosing schedules, with the final objective of generating data for modeling and simulation."	3.30	Clinical results of the EVESOR trial, a multiparameter phase I trial of everolimus and sorafenib combination in solid tumors. ( Augu-Denechere, D; Bonnin, N; Calattini, S; Colomban, O; Fontaine, J; Freyer, G; Guitton, J; Lopez, J; Maillet, D; Payen, L; Peron, J; Puszkiel, A; Schwiertz, V; Tartas, S; Tod, M; Varnier, R; You, B, 2023)
"Sorafenib has also been studied in combination with other agents."	2.55	Sorafenib for the treatment of breast cancer. ( Amadori, D; Andreis, D; Bravaccini, S; Bronte, G; Cecconetto, L; Donati, C; Farolfi, A; Fedeli, A; Maltoni, R; Rocca, A; Schirone, A; Serra, P, 2017)
"Sorafenib is an oral multikinase inhibitor with anti-angiogenic and anti-proliferative activity that is indicated for use in hepatocellular and renal cell carcinomas."	2.48	Sorafenib in locally advanced or metastatic breast cancer. ( Gradishar, WJ, 2012)
"Treatment of breast cancer (BC) has changed over the last decade with the advent of targeted therapies."	2.47	Predicting and preventing cardiotoxicity in the era of breast cancer targeted therapies. Novel molecular tools for clinical issues. ( Catalano, O; De Giuli, L; Della Porta, MG; Eleuteri, E; Riccardi, A; Tondini, C; Zambelli, A, 2011)
"Sorafenib has both antiangiogenic and antiproliferative activities and is indicated for patients with unresectable hepatocellular and advanced renal cell carcinoma."	2.47	Clinical presentation and management of hand-foot skin reaction associated with sorafenib in combination with cytotoxic chemotherapy: experience in breast cancer. ( Gomez, P; Lacouture, ME, 2011)
"Sorafenib is an oral multikinase inhibitor that inhibits tumor growth and proliferation by interfering with several receptor tyrosine kinases involved in the pathogenesis and perpetuation of malignant breast cancer cells."	2.46	Clinical overview of sorafenib in breast cancer. ( Moreno-Aspitia, A, 2010)
"A 64-year-old woman with metastatic breast cancer on follow-up had suspicious recurrent brain metastases."	1.56	18F-PSMA 1007 Uptake in Brain Metastases From Breast Cancer. ( Alfeeli, M; Fathallah, W; Marafi, F; Sasikumar, A, 2020)
"Breast cancer is one of the leading causes of cancer deaths in female worldwide."	1.51	Nicotinamide Overcomes Doxorubicin Resistance of Breast Cancer Cells through Deregulating SIRT1/Akt Pathway. ( Dai, K; Guo, Y; Jin, X; Wei, Y; Xu, Q; Zhou, J, 2019)
"Sorafenib treatment had no effect on tumor growth in a 4T1 mouse model of breast cancer, but induced M2 macrophage polarization in tumors."	1.43	Inhibition of tumor growth and metastasis by photoimmunotherapy targeting tumor-associated macrophage in a sorafenib-resistant tumor model. ( Cai, Y; Gao, D; Gao, L; Jia, B; Lai, J; Liu, H; Liu, Z; Wang, F; Zhang, C, 2016)
"Identical data to that in breast cancer were obtained in NSCLC tumors using the ERBB1/2/4 inhibitor afatinib."	1.43	[Pemetrexed + Sorafenib] lethality is increased by inhibition of ERBB1/2/3-PI3K-NFκB compensatory survival signaling. ( Boone, DL; Booth, L; Chuckalovcak, J; Dent, P; Koromilas, AE; McGuire, WP; Poklepovic, A; Roberts, JL; Stringer, DK; Tavallai, M, 2016)
" Moreover, imetelstat alone and in combination with trastuzumab reduced the CSC fraction and inhibited CSC functional ability, as shown by decreased mammosphere counts and invasive potential."	1.42	The telomerase inhibitor imetelstat alone, and in combination with trastuzumab, decreases the cancer stem cell population and self-renewal of HER2+ breast cancer cells. ( Herbert, BS; Koziel, JE, 2015)
"Nine of 11 breast cancer cell lines tested were sensitive to nanomolar levels of TAI-95 (GI(50) = 14."	1.40	Activity of a novel Hec1-targeted anticancer compound against breast cancer cell lines in vitro and in vivo. ( Chang, CC; Chang, JM; Chuang, SH; Huang, JJ; Huang, LY; Kao, KJ; Lau, GM; Lau, JY; Lee, YS; Lin, HS; Liu, CW; Tsai, PY, 2014)
"Considering the crucial role of EMT in breast cancer metastasis, a better understanding of this process may provide new therapeutic options."	1.39	Comparative proteome profiling of breast tumor cell lines by gel electrophoresis and mass spectrometry reveals an epithelial mesenchymal transition associated protein signature. ( Acierno, R; Alberti, S; del Boccio, P; Giannelli, G; Maffia, M; Pieragostino, D; Sacchetta, P; Salzet, M; Simeone, P; Tinelli, A; Toto, C; Vergara, D, 2013)
"Approximately 27% of breast cancers express high LMW-E protein levels, which significantly correlates with poor survival."	1.38	LMW-E/CDK2 deregulates acinar morphogenesis, induces tumorigenesis, and associates with the activated b-Raf-ERK1/2-mTOR pathway in breast cancer patients. ( Akli, S; Duong, MT; Hunt, KK; Keyomarsi, K; Liu, W; Lu, Y; Mills, GB; Wei, C; Wingate, HF; Yi, M, 2012)
"The study was performed on three breast cancer cell lines (BRC-230, MCF-7 and SkBr3)."	1.36	Tyrosine kinase inhibitors gefitinib, lapatinib and sorafenib induce rapid functional alterations in breast cancer cells. ( Amadori, D; Brigliadori, G; Carloni, S; Fabbri, F; Silvestrini, R; Ulivi, P; Zoli, W, 2010)
"When breast and pancreatic cancer cell lines were treated with imetelstat in vitro, telomerase activity in the bulk tumor cells and CSC subpopulations were inhibited."	1.36	The telomerase inhibitor imetelstat depletes cancer stem cells in breast and pancreatic cancer cell lines. ( Bassett, E; Buseman, CM; Go, NF; Harley, C; Joseph, I; Pattamatta, P; Shay, JW; Tressler, R; Wright, WE, 2010)
"Patients with renal cell and breast carcinoma metastases to the brain were identified from the prospective database at the Penn State Hershey Medical Center and Penn State Cancer Institute."	1.35	Brain magnetic resonance imaging changes after sorafenib and sunitinib chemotherapy in patients with advanced renal cell and breast carcinoma. ( Hill, KL; Lipson, AC; Sheehan, JM, 2009)
"Carbogen breathing was started 5 min prior to treatment and continued during it."	1.29	Short communication: the addition of carbogen and nicotinamide to a palliative fractionation schedule for locally advanced breast cancer. ( Dische, S; Pigott, K; Saunders, MI, 1995)
"As the conservative management of breast cancer is now widely adopted, oncologists and physicians should be aware of such rare side effects due to radiation therapy."	1.29	Bullous pemphigoid induced by radiation therapy. ( Amanti, C; Di Paola, M; Folliero, G; Tombolini, V; Zurlo, A, 1995)

Research

Studies (91)

Authors

Clinical Trials (11)

Trial Overview

Trial Outcomes

Disease Control Rate (DCR) by Central Review

Timeframe	Studies, this research(%)	All Research%
pre-1990	6 (6.59)	18.7374
1990's	2 (2.20)	18.2507
2000's	9 (9.89)	29.6817
2010's	70 (76.92)	24.3611
2020's	4 (4.40)	2.80

Authors	Studies
Wang, HL	1
Ma, X	2
Guan, XY	1
Song, C	1
Li, GB	1
Yu, YM	1
Yang, LL	1
Varnier, R	1
Puszkiel, A	1
Tod, M	1
Calattini, S	1
Payen, L	1
Lopez, J	1
Guitton, J	1
Schwiertz, V	1
Fontaine, J	1
Peron, J	1
Maillet, D	1
Tartas, S	1
Bonnin, N	1
Colomban, O	1
Augu-Denechere, D	1
Freyer, G	1
You, B	1
Cui, H	1
Ren, X	1
Dai, L	1
Chang, L	1
Liu, D	1
Zhai, Z	1
Kang, H	1
Marafi, F	1
Sasikumar, A	1
Alfeeli, M	1
Fathallah, W	1
Bronte, G	1
Andreis, D	2
Bravaccini, S	1
Maltoni, R	1
Cecconetto, L	1
Schirone, A	1
Farolfi, A	1
Fedeli, A	1
Serra, P	1
Donati, C	1
Amadori, D	2
Rocca, A	1
Decker, T	1
Overkamp, F	1
Rösel, S	1
Nusch, A	1
Göhler, T	1
Indorf, M	1
Sahlmann, J	1
Trarbach, T	1
Baselga, J	3
Zamagni, C	2
Gómez, P	3
Bermejo, B	2
Nagai, SE	1
Melichar, B	1
Chan, A	2
Mángel, L	1
Bergh, J	2
Costa, F	3
Gómez, HL	1
Gradishar, WJ	4
Hudis, CA	3
Rapoport, BL	1
Roché, H	4
Maeda, P	1
Huang, L	1
Meinhardt, G	1
Zhang, J	1
Schwartzberg, LS	3
Ahmadpour, S	1
Noaparast, Z	1
Abedi, SM	1
Hosseinimehr, SJ	1
Wei, Y	2
Guo, Y	1
Zhou, J	1
Dai, K	1
Xu, Q	1
Jin, X	1
Tauer, KW	1
Hermann, RC	1
Makari-Judson, G	1
Isaacs, C	2
Beck, JT	1
Kaklamani, V	3
Stepanski, EJ	1
Rugo, HS	1
Wang, W	1
Bell-McGuinn, K	1
Kirshner, JJ	1
Eisenberg, P	1
Emanuelson, R	1
Keaton, M	1
Levine, E	1
Medgyesy, DC	1
Qamar, R	1
Starr, A	1
Ro, SK	2
Lokker, NA	2
Cui, PH	1
Rawling, T	1
Gillani, TB	1
Bourget, K	1
Wang, XS	1
Zhou, F	1
Murray, M	1
Mina, LA	1
Yu, M	1
Johnson, C	1
Burkhardt, C	1
Miller, KD	1
Zon, R	1
Gomez, H	1
Rapoport, B	1
Petrenciuc, O	1
Shan, M	1
Nagaria, TS	1
Williams, JL	1
Leduc, C	1
Squire, JA	1
Greer, PA	1
Sangrar, W	1
Liu, CY	1
Tseng, LM	1
Su, JC	1
Chang, KC	1
Chu, PY	1
Tai, WT	1
Shiau, CW	1
Chen, KF	1
Fumarola, C	2
Caffarra, C	1
La Monica, S	2
Galetti, M	2
Alfieri, RR	2
Cavazzoni, A	2
Galvani, E	1
Generali, D	3
Petronini, PG	3
Bonelli, MA	2
Jafary, H	1
Ahmadian, S	1
Soleimani, M	1
Luu, T	1
Frankel, P	1
Chung, C	1
Chow, W	1
Mortimer, J	1
Hurria, A	1
Somlo, G	1
Santolla, MF	1
De Francesco, EM	1
Lappano, R	1
Rosano, C	1
Abonante, S	1
Maggiolini, M	1
Huang, LY	1
Chang, CC	1
Lee, YS	1
Chang, JM	1
Huang, JJ	1
Chuang, SH	1
Kao, KJ	1
Lau, GM	1
Tsai, PY	1
Liu, CW	1
Lin, HS	1
Lau, JY	1
Nguyen, TV	1
Sleiman, M	1
Moriarty, T	1
Herrick, WG	1
Peyton, SR	1
Graham, RM	1
Thompson, JW	1
Webster, KA	1
Kacan, T	1
Altun, A	1
Altun, GG	1
Kacan, SB	1
Sarac, B	1
Seker, MM	1
Bahceci, A	1
Babacan, N	1
Massarweh, S	1
Moss, J	1
Wang, C	1
Romond, E	1
Slone, S	1
Weiss, H	1
Karabakhtsian, RG	1
Napier, D	1
Black, EP	1
Hicks, M	1
Hu, Q	1
Macrae, E	1
DeWille, J	1
Pedersen, AM	1
Thrane, S	1
Lykkesfeldt, AE	1
Yde, CW	1
Bazzola, L	1
Foroni, C	1
Zanoni, V	1
R Cappelletti, M	1
Allevi, G	1
Aguggini, S	1
Strina, C	1
Milani, M	1
Venturini, S	1
Ferrozzi, F	1
Giardini, R	1
Bertoni, R	1
Turley, H	1
Gatter, K	1
Fox, SB	2
Harris, AL	2
Martinotti, M	1
Berruti, A	1
Bottini, A	2
Reynolds, AR	1
Domínguez-Gómez, G	1
Díaz-Chávez, J	1
Chávez-Blanco, A	1
Gonzalez-Fierro, A	1
Jiménez-Salazar, JE	1
Damián-Matsumura, P	1
Gómez-Quiroz, LE	1
Dueñas-González, A	1
Koziel, JE	1
Herbert, BS	1
Correia, A	1
Shahbazi, MA	1
Mäkilä, E	1
Almeida, S	1
Salonen, J	1
Hirvonen, J	1
Santos, HA	1
Kim, SY	1
Park, SE	1
Shim, SM	1
Park, S	1
Kim, KK	1
Jeong, SY	1
Choi, EK	1
Hwang, JJ	1
Jin, DH	1
Chung, CD	1
Kim, I	1
Zhang, C	1
Gao, L	1
Cai, Y	1
Liu, H	1
Gao, D	1
Lai, J	1
Jia, B	1
Wang, F	1
Liu, Z	1
Yardley, DA	2
Dickson, N	1
Drosick, D	1
Earwood, C	1
Inhorn, R	1
Murphy, P	1
Hainsworth, JD	2
Booth, L	1
Roberts, JL	1
Tavallai, M	1
Chuckalovcak, J	1
Stringer, DK	1
Koromilas, AE	1
Boone, DL	1
McGuire, WP	1
Poklepovic, A	2
Dent, P	2
Salavert, F	1
Hidago, MR	1
Amadoz, A	1
Çubuk, C	1
Medina, I	1
Crespo, D	1
Carbonell-Caballero, J	1
Dopazo, J	1
Gu, Y	2
Helenius, M	1
Väänänen, K	1
Bulanova, D	1
Saarela, J	1
Sokolenko, A	1
Martens, J	1
Imyanitov, E	1
Kuznetsov, S	1
Shah, AA	1
Ito, A	1
Nakata, A	1
Yoshida, M	1
Mondal, A	1
Bennett, LL	1
Ferrario, C	1
Strepponi, I	1
Esfahani, K	1
Charamis, H	1
Langleben, A	1
Scarpi, E	1
Nanni, O	1
Miller, WH	1
Panasci, LC	1
Park, EY	1
Woo, Y	1
Kim, SJ	1
Kim, DH	1
Lee, EK	1
De, U	1
Kim, KS	1
Lee, J	1
Jung, JH	1
Ha, KT	1
Choi, WS	1
Kim, IS	1
Lee, BM	1
Yoon, S	1
Moon, HR	1
Kim, HS	1
Sui, J	1
Cui, Y	1
Cai, H	1
Bian, S	1
Xu, Z	1
Zhou, L	1
Sun, Y	1
Liang, J	1
Fan, Y	1
Zhang, X	1
Tandia, M	1
Mhiri, A	1
Paule, B	1
Saffroy, R	1
Cailliez, V	1
Noé, G	1
Farinotti, R	1
Bonhomme-Faivre, L	1
Tran, MA	1
Smith, CD	1
Kester, M	1
Robertson, GP	1
Ding, Q	1
Huo, L	1
Yang, JY	2
Xia, W	2
Liao, Y	1
Chang, CJ	2
Yang, Y	1
Lai, CC	1
Lee, DF	1
Yen, CJ	1
Chen, YJ	1
Hsu, JM	2
Kuo, HP	1
Lin, CY	1
Tsai, FJ	1
Li, LY	1
Tsai, CH	1
Hung, MC	2
Moreno-Aspitia, A	2
Morton, RF	1
Hillman, DW	1
Lingle, WL	1
Rowland, KM	1
Wiesenfeld, M	1
Flynn, PJ	1
Fitch, TR	1
Perez, EA	1
Li, Y	1
Xu, R	1
Zhang, XM	1
Li, DD	1
He, QY	1
Hill, KL	1
Lipson, AC	1
Sheehan, JM	1
Bianchi, G	1
Loibl, S	1
Salvagni, S	1
Raab, G	1
Siena, S	1
Laferriere, N	1
Peña, C	1
Lathia, C	1
Bergamini, L	1
Gianni, L	1
Gusani, NJ	1
Jiang, Y	1
Kimchi, ET	1
Staveley-O'Carroll, KF	1
Cheng, H	1
Ajani, JA	1
Yao, Y	1
Li, H	1
Davidson, NE	1
Zhou, Q	1
Gatti, R	1
Belletti, S	1
Evans, DB	1
Dowsett, M	1
Martin, LA	1
Puca, R	1
Nardinocchi, L	1
Starace, G	1
Rechavi, G	1
Sacchi, A	1
Givol, D	1
D'Orazi, G	1
Carloni, S	1
Fabbri, F	1
Brigliadori, G	1
Ulivi, P	1
Silvestrini, R	1
Zoli, W	1
Wallach, I	1
Jaitly, N	1
Lilien, R	1
Merz, M	1
Komljenovic, D	1
Zwick, S	1
Semmler, W	1
Bäuerle, T	1
Herbolsheimer, P	1
Liu, MC	1
Wilkinson, M	1
Ottaviano, Y	1
Chung, GG	1
Warren, R	1
Eng-Wong, J	1
Cohen, P	1
Smith, KL	1
Creswell, K	1
Novielli, A	1
Slack, R	1
Joseph, I	1
Tressler, R	1
Bassett, E	1
Harley, C	1
Buseman, CM	1
Pattamatta, P	1
Wright, WE	1
Shay, JW	1
Go, NF	1
Nielsen, DL	1
Andersson, M	1
Andersen, JL	1
Kamby, C	1
Kashuro, VA	1
Glushkov, SI	1
Zheregelia, SN	1
Zambelli, A	1
Della Porta, MG	1
Eleuteri, E	1
De Giuli, L	1
Catalano, O	1
Tondini, C	1
Riccardi, A	1
Valabrega, G	1
Capellero, S	1
Cavalloni, G	1
Zaccarello, G	1
Petrelli, A	1
Migliardi, G	1
Milani, A	1
Peraldo-Neia, C	1
Gammaitoni, L	1
Sapino, A	1
Pecchioni, C	1
Moggio, A	1
Giordano, S	1
Aglietta, M	1
Montemurro, F	1
Chen, CT	1
Xie, X	1
Chao, CH	1
Woodward, WA	1
Hortobagyi, GN	1
Buzdar, AU	1
Martin, M	1
Pinter, T	1
Crown, J	1
Kennedy, MJ	1
Provencher, L	1
Priou, F	1
Eiermann, W	1
Adrover, E	1
Lang, I	1
Ramos, M	1
Latreille, J	1
Jagiełło-Gruszfeld, A	1

Trial	Phase	Enrollment	Study Type	Start Date	Status
Randomised Phase II Study of Paclitaxel Alone Versus Paclitaxel Plus Sorafenib in Second- or Third-line Treatment of Patients With Metastatic Breast Cancer[NCT01320111]	Phase 2	59 participants (Actual)	Interventional	2010-07-01	Completed
A Phase III Randomized, Double Blind, Placebo-controlled Trial Comparing Capecitabine Plus Sorafenib Versus Capecitabine Plus Placebo in the Treatment of Locally Advanced or Metastatic HER2-Negative Breast Cancer[NCT01234337]	Phase 3	537 participants (Actual)	Interventional	2011-02-21	Completed
A Double-Blind, Randomized Phase 2b Study of Sorafenib Compared to Placebo When Administered in Combination With Chemotherapy for Patients With Locally Advanced or MBC That Has Progressed During or After Bevacizumab Therapy[NCT00493636]	Phase 2	160 participants (Actual)	Interventional	2007-06-30	Completed
A Phase II Study of Combined VEGF Inhibitor (Bevacizumab + Sorafenib) in Patients With Metastatic Breast Cancer: Hoosier Oncology Group BRE06-109[NCT00632541]	Phase 2	18 participants (Actual)	Interventional	2007-10-31	Terminated (stopped due to Significant Toxicities Experienced)
Phase I/II Vinorelbine and Sorafenib as Salvage Therapy in Metastatic Breast Cancer[NCT00828074]	Phase 1/Phase 2	46 participants (Actual)	Interventional	2008-11-30	Completed
A Phase II Study of Adding the Multikinase Inhibitor Sorafenib (Nexavar) to Existing Endocrine Therapy in Patients With Advanced Breast Cancer[NCT00525161]	Phase 2	11 participants (Actual)	Interventional	2007-10-31	Terminated (stopped due to Slow accrual and loss of funding)
A Phase IB/II Trial of Combination of Vinorelbine With Sorafenib (BAY 43-9006) as First-Line Treatment in Patients With Metastatic Breast Cancer[NCT00764972]	Phase 1/Phase 2	36 participants (Anticipated)	Interventional	2007-10-31	Recruiting
A Phase II Multicenter Uncontrolled Trial of BAY43-9006 in Subjects With Metastatic Breast Cancer.[NCT00101400]	Phase 2	54 participants (Actual)	Interventional	2004-02-29	Completed
A Randomized Phase 2 Trial of Double-Blind, Placebo Controlled AMG 706 in Combination With Paclitaxel, or Open-Label Bevacizumab in Combination With Paclitaxel, as First Line Therapy in Women With HER2 Negative Locally Recurrent or Metastatic Breast Cance[NCT00356681]	Phase 2	282 participants (Actual)	Interventional	2006-12-31	Terminated (stopped due to Sponsor decision to close study)
A Pilot Study of Adjuvant Doxorubicin and Cyclophosphamide Followed by Paclitaxel Plus Sorafenib in Women With Node Positive or High-Risk Early Stage Breast Cancer[NCT00544167]		45 participants (Actual)	Interventional	2007-05-31	Completed
An Open-label, Dose-finding Study to Evaluate the Safety of AMG 706 in Combination With Paclitaxel or Docetaxel as Treatment for Locally Recurrent or Metastatic Breast Cancer[NCT00322400]	Phase 1	46 participants (Actual)	Interventional	2006-03-31	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

DCR was defined as the proportion of participants whose best response was CR, PR, stable disease (SD) or Non-CR/Non-PD. Per RECIST version 1.1, CR=all target lesions disappeared, any pathological lymph node, target/non-target, a reduction in short axis to <10 mm. PR=at least 30% decrease in the sum of diameters of target lesions taking as reference baseline sum diameters. PD=at least 20% increase in the sum of diameters of the target lesions, taking as a reference smallest sum on study. Appearance of new lesions and unequivocal progression of existing non-target lesions. SD=neither sufficient shrinkage qualified for PR nor sufficient increase qualified for PD, taking smallest sum of diameters as a reference. Non-CR/Non-PD=persistence of 1/more non-target lesion(s) and/or maintenance of tumor marker level above normal limits. DCR=CR+PR+SD or Non-CR/Non-PD. CR and PR confirmed by another scan at least 4 weeks later. SD and Non-CR/Non-PD documented at least 6 weeks after randomization. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years later or until disease radiological progression

Duration of Response (DOR) by Central Reader

Intervention	percentage (%) of participants (Number)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	60.5
Placebo + Capecitabine	58.3

DOR was defined as the time from date of first response (CR or PR) to the date when PD is first documented, or to the date of death, whichever occurred first according to RECIST version 1.1. CR=all target lesions disappeared, and any pathological lymph node, whether target or non-target, had a reduction in short axis to <10 mm. If any residual lesion was present, cyto-histology was made available to unequivocally document benignity. PR=at least 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. Participants still having CR or PR and have not died at the time of analysis were censored at their last date of tumor evaluation. DOR defined for confirmed responders only (that is, CR or PR). 'NA' indicates that value could not be estimated due to censored data. Median and 95% CIs were computed using Kaplan-Meier estimates. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years later or until disease radiological progression

Objective Response Rate (ORR) by Central Review

Intervention	days (Median)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	313
Placebo + Capecitabine	290

ORR was defined as the best tumor response (Complete Response [CR] or Partial Response [PR]) observed during treatment or within 30 days after termination of study treatment, assessed according to the RECIST version 1.1. CR=all target lesions disappeared, and any pathological lymph node, whether target or non-target, had a reduction in short axis to <10 mm. If any residual lesion was present, cyto-histology was made available to unequivocally document benignity. PR=at least 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. ORR=CR+PR. CR and PR were confirmed by another scan at least 4 weeks later. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years later or until disease radiological progression

Overall Survival (OS)

Intervention	Percentage (%) of participants (Number)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	13.5
Placebo + Capecitabine	15.5

OS was defined as the time from date of randomization to death due to any cause. Participants still alive at the time of analysis were censored at their last known alive date. Median and other 95% CIs computed using Kaplan-Meier estimates. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years later

Patient Reported Outcomes: Euroqol-5 Dimensions (EQ-5D) - Index Score

Intervention	days (Median)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	575
Placebo + Capecitabine	616

The EQ-5D was a generic Quality of life (QoL) based instrument validated in cancer populations. EQ-5D questionnaire contained a 5-item descriptive system of health states (mobility, self-care, usual activities, pain/discomfort, anxiety/depression) and visual analogue scale (VAS). A single HRQoL score ranging from -0.59 to 1 was generated from standard scoring algorithm developed by the EuroQoL was the EQ-5D index score, higher scores represent better health status. A change of at least 0.10 to 0.12 points was considered clinically meaningful. The results on the ANCOVA of time-adjusted AUC for the EQ-5D - Index Score were reported. The time-adjusted AUC was calculated by dividing the AUC by duration (in days) over the period of interest, and reported as 'scores on a scale'. (NCT01234337)
Timeframe: Day 1 of Cycles 1, 3, 5, 7, 9, 11, 13, 16, 19, 22, 25, 28, and EOT (21 days after last dose of study drug)

Patient Reported Outcomes: Euroqol-5 Dimensions (EQ-5D) - Visual Analogue Scale (VAS) Score

Intervention	Scores on a scale (Least Squares Mean)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	0.665
Placebo + Capecitabine	0.69

The EQ-5D was a generic QoL preference based instrument and has been validated in the cancer populations. VAS was generated from 0 (worst imaginable health state) to 100 (best imaginable health state). This VAS score was referred to as the EQ-5D self-reported health status score. The results on ANCOVA of time-adjusted AUC were reported. The time-adjusted AUC was calculated by dividing the AUC by duration (in days) over the period of interest, and reported as 'scores on a scale'. (NCT01234337)
Timeframe: Day 1 of Cycles 1, 3, 5, 7, 9, 11, 13, 16, 19, 22, 25, 28, and EOT (21 days after last dose of study drug)

Patient Reported Outcomes: Functional Assessment of Cancer Therapy-Breast Symptom Index (8 Item) (FBSI-8)

Intervention	Scores on a scale (Least Squares Mean)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	67.532
Placebo + Capecitabine	69.228

The FBSI-8 was an 8-item questionnaire. Participants responded to each item using a 5-point Likert-type scale ranging from 0 (not at all) to 4 (very much). A total scale score was calculated (range from 0 to 32), with higher scores indicating low symptomatology and reflecting a better Health-Related Quality of Life (HRQoL). The results on the analysis of covariance (ANCOVA) of time-adjusted area under curve (AUC) for the FBSI-8 score were reported. The time-adjusted AUC was calculated by dividing the AUC by duration (in days) over the period of interest, and reported as 'scores on a scale'. (NCT01234337)
Timeframe: Day 1 of Cycles 1, 3, 5, 7, 9, 11, 13, 16, 19, 22, 25, 28, 31, 34, 37, and end of treatment (EOT, 21 days after last dose of study drug)

Progression-free Survival (PFS) Assessed by the Independent Review Panel According to Response Evaluation Criteria for Solid Tumors (RECIST) 1.1

Intervention	Scores on a scale (Least Squares Mean)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	20.915
Placebo + Capecitabine	21.356

PFS was defined as the time from date of randomization to disease progression, radiological or death due to any cause, whichever occurs first. Per RECIST version 1.1, progressive disease was determined when there was at least 20% increase in the sum of diameters of the target lesions, taking as a reference the smallest sum on study (this included the baseline sum if that was the smallest sum on trial). In addition to a relative increase of 20%, the sum had demonstrated an absolute increase of at least 5 mm. Appearance of new lesions and unequivocal progression of existing non-target lesions was also interpreted as progressive disease. Participants without progression or death at the time of analysis were censored at their last date of evaluable tumor evaluation. Median and other 95% confidence intervals (CIs) computed using Kaplan-Meier estimates. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years or until disease radiological progression

Time to Progression (TTP) by Central Review

Intervention	days (Median)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	166
Placebo + Capecitabine	165

TTP was defined as the time from date of randomization to disease radiological progression by central review. Per RECIST version 1.1, progressive disease was determined when there was at least 20% increase in the sum of diameters of the target lesions, taking as a reference the smallest sum on study (this included the baseline sum if that was the smallest sum on trial). In addition to a relative increase of 20%, the sum had demonstrated an absolute increase of at least 5 mm. Appearance of new lesions and unequivocal progression of existing non-target lesions was also interpreted as progressive disease. Participants without progression or death at the time of analysis were censored at their last date of evaluable tumor evaluation. Median and other 95% confidence intervals (CIs) computed using Kaplan-Meier estimates. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years later or until disease radiological progression

Area Under Curve From Time Zero to Last Quantifiable Concentration (AUC[0-tlast]) of Capecitabine and 5-fluorouracil

Intervention	days (Median)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	168
Placebo + Capecitabine	165

AUC(0-tlast) is defined as AUC from time 0 to the last data point, calculated up by linear trapezoidal rule, down by logarithmic trapezoidal rule. Geometric mean and percentage geometric coefficient of variation (%CV) were reported. In the listed categories below, 'N' signifies the number of evaluable participants for the drug administered. (NCT01234337)
Timeframe: Pre-dose and 0.5, 1, 2, and 4 hours after capecitabine dosing at Cycle 2, Day 14

Maximum Observed Drug Concentration (Cmax) of Capecitabine and 5-fluorouracil

Intervention	milligram*hour per liter (Geometric Mean)
	Capecitabine	5-fluorouracil
Placebo + Capecitabine	5.13	0.557
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	7.12	0.621

Maximum observed drug concentration, directly taken from analytical data. Geometric mean and percentage geometric coefficient of variation (%CV) were reported. In the listed categories below, 'N' signifies the number of evaluable participants for the drug administered. (NCT01234337)
Timeframe: Pre-dose and 0.5, 1, 2, and 4 hours after capecitabine dosing at Cycle 2, Day 14

Number of Participants With Treatment-emergent Grade 3 and 4 Laboratory Abnormalities

Intervention	milligram per liter (Geometric Mean)
	Capecitabine	5-fluorouracil
Placebo + Capecitabine	4.68	0.382
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	6.05	0.434

Hematological (anemia, hemoglobin, international normalized ratio [INR], lymphocyte, neutrophil, platelet, white blood cell [WBC]), biochemical (ALT [alanine aminotransferase], AST [aspartate aminotransferase], GGT [gamma-glutamyl-transferase], lipase, hypoalbuminemia, hypocalcemia, hyperglycemia, hyperuricemia) evaluations were done. Common terminology criteria for adverse events (CTCAE) version 4-Grade 3: Severe or medically significant; hospitalization or prolongation of hospitalization and CTCAE version 4-Grade 4: life-threatening consequences; urgent intervention were indicated. (NCT01234337)
Timeframe: From the start of study treatment up to 30 days after the last dose

Duration of Overall Response

Intervention	Participants (Number)
	Anemia (grade 3)	Hemoglobin increased (grade 3)	INR increased (grade 3)	Lymphocyte count decreased (grade 3)	Neutrophil count decreased (grade 3)	Platelet count decreased (grade 3)	WBC decreased (grade 3)	ALT increased (grade 3)	AST increased (grade 3)	Alkaline phosphatase increased (grade 3)	Bilirubin increased (grade 3)	GGT increased (grade 3)	Lipase increased (grade 3)	Serum amylase increased (grade 3)	Hypoalbuminemia (grade 3)	Hypocalcemia (grade 3)	Hypokalemia (grade 3)	Hyponatremia (grade 3)	Hypophosphatemia (grade 3)	Hyperglycemia (grade 3)	Lymphocyte count decreased (grade 4)	Neutrophil count decreased (grade 4)	Platelet count decreased (grade 4)	WBC decreased (grade 4)	ALT increased (grade 4)	GGT increased (grade 4)	Lipase increased (grade 4)	Hypokalemia (grade 4)	Hyponatremia (grade 4)	Hypophosphatemia (grade 4)	Hyperuricemia (grade 4)
Placebo + Capecitabine	7	3	9	17	19	2	13	5	5	13	1	21	12	4	2	6	11	7	15	10	2	7	7	3	0	2	1	4	0	0	0
Sorafenib (Nexavar, BAY43-9006) + Capecitabine	12	0	9	20	11	6	15	4	10	12	9	22	19	8	4	9	20	9	47	9	3	7	1	2	3	6	5	2	4	5	5

Duration of overall response was calculated as the time (days) from first documentation of CR or PR (whichever status is recorded first) until the first date that recurrent or progressive disease (PD) or death is objectively documented. Response was evaluated via changes from baseline in radiological tumor measurements using RECIST version 1.0 guidelines, where complete response (CR) is the disappearance of all target lesions; partial response (PR) is >=30% decrease in the sum of the longest diameter (LD) of target lesions; Stable Disease (SD) is neither sufficient shrinkage in sum of LD of target lesions to be PR nor increase of >=20%; Progressive Disease (PD) is the increase in existing lesions or new lesions. (NCT00493636)
Timeframe: Period measured from the first documentation of complete or partial response (whichever status is recorded first) until the first date that recurrent or progressive disease or death is objectively documented.

Overall Response Rate

Intervention	Days (Median)
A (Sorafenib + Gemcitabine or Capecitabine)	94
B (Placebo + Gemcitabine or Capecitabine)	147

Overall response rate was defined as the proportion of participants experiencing complete response (CR) and partial response (PR) as best overall response. Response was evaluated via changes from baseline in radiological tumor measurements using RECIST version 1.0 guidelines, where complete response (CR) is the disappearance of all target lesions; partial response (PR) is >=30% decrease in the sum of the longest diameter (LD) of target lesions; Stable Disease (SD) is neither sufficient shrinkage in sum of LD of target lesions to be PR nor increase of >=20%; Progressive Disease (PD) is the increase in existing lesions or new lesions. (NCT00493636)
Timeframe: The overall tumor burden at baseline will be compared with subsequent measurements up to the date of first documented disease progression or the date of death due to any cause, if before progression, assessed up to 39 months.

Overall Survival

Intervention	percentage of participants (Number)
A (Sorafenib + Gemcitabine or Capecitabine)	19.8
B (Placebo + Gemcitabine or Capecitabine)	12.7

(NCT00493636)
Timeframe: From the date of randomization to date of death due to any cause, assessed up to 56 months.

Progression Free Survival

Intervention	Days (Median)
A (Sorafenib + Gemcitabine or Capecitabine)	407
B (Placebo + Gemcitabine or Capecitabine)	348

(NCT00493636)
Timeframe: From the date of randomization to date of first documented disease progression (i.e., the date on which a radiologic procedure or clinical evaluation was performed) or the date of death due to any cause, if before progression, assessed up to 39 months.

Time to Progression

Intervention	Days (Median)
A (Sorafenib + Gemcitabine or Capecitabine)	103
B (Placebo + Gemcitabine or Capecitabine)	81

(NCT00493636)
Timeframe: Calculated as the time (days) from date of randomization to date of first observed disease progression (radiological or clinical, whichever is earlier), assessed up to 39 months.

Progression-Free Survival

Intervention	Days (Median)
A (Sorafenib + Gemcitabine or Capecitabine)	111
B (Placebo + Gemcitabine or Capecitabine)	82

The primary objective was to assess the Progression-Free Survival of sorafenib combined with bevacizumab in patients with metastatic breast cancer. Progression is defined by RECIST as a 20% increase in the sum of the longest diameters of target measurable lesions over the smallest sum observed (over baseline if no decrease during therapy) or by the appearance of a new lesion. (NCT00632541)
Timeframe: From the start of the treatment until the criteria for disease progression is met (or death occurs) maximum of 24 months

Number of Participants With at Least One Dose Limiting Toxicity in Phase I

Intervention	months (Median)
Single Arm A	2.8

Dose Limiting Toxicity (DLT) defined as any treatment-related grade 3 or greater non-hematologic toxicity (excluding alopecia, controllable nausea and vomiting, and serum triglycerides < 1,500 mg/dL which recover within 1 week), grade 4 or greater thrombocytopenia, grade 4 or greater febrile neutropenia requiring hospitalization, or treatment delay of > 2 weeks as a result of unresolved toxicity during the first cycle of therapy. (NCT00828074)
Timeframe: 4 weeks from start of treatment, up to 2 years

Objective Response Rate

Intervention	participants with DLTs (Number)
Phase I: Dose Level 1 - Vinorelbine at 20mg/m^2	0
Phase I: Dose Level 2 - Vinorelbine at 25mg/m^2	3

Overall Survival

Intervention	percentage of participants (Number)
Dose Level II - Vinorelbine 20 mg/m^2	10

Estimated using the product-limit method of Kaplan and Meier. (NCT00828074)
Timeframe: Until death from any cause, up to 5 years.

Progression-free Survival

Intervention	Months (Median)
Dose Level II - Vinorelbine 20 mg/m^2	15.4

Estimated using the product-limit method of Kaplan and Meier. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT00828074)
Timeframe: Until disease progression, up to 5 years.

Progression-free Survival Rate at 4 Months

Intervention	Months (Median)
Dose Level II - Vinorelbine 20 mg/m^2	4.1

Estimated using the product-limit method of Kaplan and Meier.Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT00828074)
Timeframe: 4 months following the last course of treatment

Recommended Phase II Dose

Intervention	percentage of participants (Number)
Dose Level II - Vinorelbine I.V. 20 mg/m^2	44

The maximum tolerated dose (MTD) of Vinorelbine is based on toxicities observed during the first cycle and is defined as the highest dose tested in which fewer than 33% of patients experience an attributable DLT to the study drug, when at least 6 patients are treated at that dose and are evaluable for toxicity. Dose escalations proceeded according to a standard 3+3 design. (NCT00828074)
Timeframe: 4 weeks from start of treatment, up to 2 years

Toxicity Profile

Intervention	mg/m^2 (Number)
Phase I	20

Number of Participants with Treatment-Related Grade 3 & 4 Toxicities for Sorafenib and Vinorelbine Combination (NCT00828074)
Timeframe: 28 days following the last course of treatment

Clinical Benefit Rate

Intervention	participants (Number)
	Anemia	Leukopenia	Neutropenia	Thrombocytopenia	Alkalosis	Cellulitis	Cough	Diarrhea	Fatigue	Genital abscess	Hand-foot toxicity	Hiccups	High glucose level	Hypertension	Hypokalemia	Hyponatremia	Infection (NOS)	Low phosphate	Pulmonary embolus	Myalgia	Pain (NOS)	Phlebitis	Sensory neuropathy	Somnolence	Transaminases/alkaline	Urinary tract infection
Phase I & II	2	16	16	1	1	1	1	3	5	1	7	1	1	3	1	2	1	3	1	1	3	1	1	1	1	1

Clinical benefit rate is defined as complete response, partial response, or stable disease (CR/PR/SD) as measured by Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for a minimum of at least 24 weeks. (NCT00525161)
Timeframe: 24 weeks

Time to Progression

Response Rate

Intervention	percentage of participants (Number)
Sorafenib & Endocrine Therapy	50

Intervention	months (Median)
Sorafenib & Endocrine Therapy	6.1

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. Patients were followed monthly for clinical and toxicity evaluation. Disease response by RECIST criteria v1.0 was assessed after 3 months by appropriate scans and these were obtained every 2 months thereafter until progression. (NCT00525161)
Timeframe: 12 weeks after treatment & 8 weeks after initial documentation of response

Number of Subjects With Stable Disease up to Cycle 4

Intervention	participants (Number)
	Stable Disease	Progression
Sorafenib & Endocrine Therapy	7	3

Number of subjects who had not responded to treatment but had stable disease up to cycle 4. (NCT00101400)
Timeframe: Until 30 days after termination of active therapy

Overall Response Duration

Intervention	participants (Number)
Sorafenib (Nexavar, BAY43-9006)	12

Overall response duration was defined only for subjects achieving confirmed objective response (PR or CR). It was measured from start of treatment to the date when progressive disease was first objectively documented. (NCT00101400)
Timeframe: Time from PR or CR to progression

Survival Time

Intervention	days (Number)
Sorafenib (Nexavar, BAY43-9006)	256

After the end of treatment visit (30 days after the last dose), the subjects were monitored every 3 months for survival (visits/phone calls). (NCT00101400)
Timeframe: Start of treatment to death

Time to Objective Response

Intervention	days (Median)
Sorafenib (Nexavar, BAY43-9006)	259

Defined only for subjects achieving objective tumor response from start of treatment to the date when confirmed PR or CR was first documented according to the Modified WHO Tumor Response Criteria. (NCT00101400)
Timeframe: Until objective response occurs

Time to Progression

Intervention	days (Number)
Sorafenib (Nexavar, BAY43-9006)	145

Time from start of treatment until progression was first documented. (NCT00101400)
Timeframe: Until progression occurs

Number of Subjects With Response (Complete or Partial)

Intervention	days (Median)
Sorafenib (Nexavar, BAY43-9006)	58

Number of subjects with metastatic breast cancer treated with single agent BAY43-9006 who had best overall response assessed as complete response (CR) or partial response (PR) as per Modified World Health Organization (WHO) Tumor Response Criteria. (NCT00101400)
Timeframe: Until 30 days after termination of active therapy

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Sorafenib for the treatment of breast cancer. Expert opinion on pharmacotherapy, 2017, Volume: 18, Issue:6 Topics: Antineoplastic Combined Chemotherapy Protocols; Bevacizumab; Breast Neoplasms; Capecitabine; Disease	2017
Clinical overview of sorafenib in breast cancer. Future oncology (London, England), 2010, Volume: 6, Issue:5 Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Breast Neoplasms; Clinical Trials as Topic; Femal	2010
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Sorafenib in locally advanced or metastatic breast cancer. Expert opinion on investigational drugs, 2012, Volume: 21, Issue:8 Topics: Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates	2012
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A randomized phase II study of paclitaxel alone versus paclitaxel plus sorafenib in second- and third-line treatment of patients with HER2-negative metastatic breast cancer (PASO). BMC cancer, 2017, Jul-25, Volume: 17, Issue:1 Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Disease-Free Survival; Femal	2017
RESILIENCE: Phase III Randomized, Double-Blind Trial Comparing Sorafenib With Capecitabine Versus Placebo With Capecitabine in Locally Advanced or Metastatic HER2-Negative Breast Cancer. Clinical breast cancer, 2017, Volume: 17, Issue:8 Topics: Administration, Oral; Aged; Anthracyclines; Antineoplastic Combined Chemotherapy Protocols; Breast N	2017
Sorafenib or placebo with either gemcitabine or capecitabine in patients with HER-2-negative advanced breast cancer that progressed during or after bevacizumab. Clinical cancer research : an official journal of the American Association for Cancer Research, 2013, May-15, Volume: 19, Issue:10 Topics: Adult; Aged; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Protocols; Beva	2013
A phase II study of combined VEGF inhibitor (bevacizumab+sorafenib) in patients with metastatic breast cancer: Hoosier Oncology Group Study BRE06-109. Investigational new drugs, 2013, Volume: 31, Issue:5 Topics: Adult; Aged; Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Che	2013
A phase 3 tRial comparing capecitabinE in combination with SorafenIb or pLacebo for treatment of locally advanced or metastatIc HER2-Negative breast CancEr (the RESILIENCE study): study protocol for a randomized controlled trial. Trials, 2013, Jul-22, Volume: 14 Topics: Administration, Oral; Algorithms; Angiogenesis Inhibitors; Antineoplastic Combined Chemotherapy Prot	2013
Phase I/II trial of vinorelbine and sorafenib in metastatic breast cancer. Clinical breast cancer, 2014, Volume: 14, Issue:2 Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Female; Follow-Up Stu	2014
Impact of adding the multikinase inhibitor sorafenib to endocrine therapy in metastatic estrogen receptor-positive breast cancer. Future oncology (London, England), 2014, Volume: 10, Issue:15 Topics: Adult; Aged; Antineoplastic Agents, Hormonal; Biomarkers, Tumor; Bone Neoplasms; Brain Neoplasms; Br	2014
Sorafenib Plus Ixabepilone as First-Line Treatment of Metastatic HER2-Negative Breast Cancer: A Sarah Cannon Research Institute Phase I/II Trial. Clinical breast cancer, 2016, Volume: 16, Issue:3 Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Di	2016
Phase I/II Trial of Sorafenib in Combination with Vinorelbine as First-Line Chemotherapy for Metastatic Breast Cancer. PloS one, 2016, Volume: 11, Issue:12 Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Drug Administration S	2016
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Phase II multicenter, uncontrolled trial of sorafenib in patients with metastatic breast cancer. Anti-cancer drugs, 2009, Volume: 20, Issue:7 Topics: Adult; Aged; Antineoplastic Agents; Benzenesulfonates; Biomarkers, Tumor; Breast Neoplasms; ErbB Rec	2009
New pharmacological developments in the treatment of hepatocellular cancer. Drugs, 2009, Volume: 69, Issue:18 Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Breast Neo	2009
Phase I/II study of sorafenib with anastrozole in patients with hormone receptor positive aromatase inhibitor resistant metastatic breast cancer. Breast cancer research and treatment, 2011, Volume: 125, Issue:1 Topics: Adult; Aged; Anastrozole; Antineoplastic Combined Chemotherapy Protocols; Aromatase Inhibitors; Benz	2011
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A pilot study of adjuvant doxorubicin and cyclophosphamide followed by paclitaxel and sorafenib in women with node-positive or high-risk early-stage breast cancer. Clinical advances in hematology & oncology : H&O, 2011, Volume: 9, Issue:4 Topics: Adult; Aged; Antineoplastic Agents; Benzenesulfonates; Breast Neoplasms; Chemotherapy, Adjuvant; Cyc	2011
Sorafenib in combination with capecitabine: an oral regimen for patients with HER2-negative locally advanced or metastatic breast cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2012, May-01, Volume: 30, Issue:13 Topics: Administration, Oral; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates	2012
Phase 1b dose-finding study of motesanib with docetaxel or paclitaxel in patients with metastatic breast cancer. Breast cancer research and treatment, 2012, Volume: 135, Issue:1 Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Di	2012
A double-blind, randomised, placebo-controlled, phase 2b study evaluating sorafenib in combination with paclitaxel as a first-line therapy in patients with HER2-negative advanced breast cancer. European journal of cancer (Oxford, England : 1990), 2013, Volume: 49, Issue:2 Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Disease-Free Survival; Double-Blin	2013

Article	Year
Potential synthetic lethality for breast cancer: A selective sirtuin 2 inhibitor combined with a multiple kinase inhibitor sorafenib. Pharmacological research, 2022, Volume: 177 Topics: Antineoplastic Agents; Apoptosis; Breast Neoplasms; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor	2022
Comprehensive analysis of nicotinamide metabolism-related signature for predicting prognosis and immunotherapy response in breast cancer. Frontiers in immunology, 2023, Volume: 14 Topics: Breast; Breast Neoplasms; Female; Humans; Immunotherapy; Niacinamide; Prognosis; Tumor Microenvironm	2023
18F-PSMA 1007 Uptake in Brain Metastases From Breast Cancer. Clinical nuclear medicine, 2020, Volume: 45, Issue:2 Topics: Biological Transport; Brain Neoplasms; Breast Neoplasms; Female; Humans; Middle Aged; Niacinamide; O	2020
Anti-cancer agents in medicinal chemistry, 2018, Volume: 18, Issue:9 Topics: Animals; Breast Neoplasms; Cell Line, Tumor; Chelating Agents; Female; Glycine; Humans; Hydrazines;	2018
Nicotinamide Overcomes Doxorubicin Resistance of Breast Cancer Cells through Deregulating SIRT1/Akt Pathway. Anti-cancer agents in medicinal chemistry, 2019, Volume: 19, Issue:5 Topics: Antibiotics, Antineoplastic; Apoptosis; Breast Neoplasms; Cell Proliferation; Doxorubicin; Female; H	2019
Anti-proliferative actions of N'-desmethylsorafenib in human breast cancer cells. Biochemical pharmacology, 2013, Aug-01, Volume: 86, Issue:3 Topics: Antineoplastic Agents; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Female; Humans; MAP K	2013
Flavopiridol synergizes with sorafenib to induce cytotoxicity and potentiate antitumorigenic activity in EGFR/HER-2 and mutant RAS/RAF breast cancer model systems. Neoplasia (New York, N.Y.), 2013, Volume: 15, Issue:8 Topics: Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Ce	2013
Novel sorafenib analogues induce apoptosis through SHP-1 dependent STAT3 inactivation in human breast cancer cells. Breast cancer research : BCR, 2013, Volume: 15, Issue:4 Topics: Antineoplastic Agents; Apoptosis; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell Survi	2013
Effects of sorafenib on energy metabolism in breast cancer cells: role of AMPK-mTORC1 signaling. Breast cancer research and treatment, 2013, Volume: 141, Issue:1 Topics: Adenosine Triphosphate; AMP-Activated Protein Kinases; Anilides; Antineoplastic Agents; Breast Neopl	2013
The enhanced apoptosis and antiproliferative response to combined treatment with valproate and nicotinamide in MCF-7 breast cancer cells. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014, Volume: 35, Issue:3 Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Blotting, Western; Breast Neoplasms; Cell	2014
Niacin activates the G protein estrogen receptor (GPER)-mediated signalling. Cellular signalling, 2014, Volume: 26, Issue:7 Topics: Breast Neoplasms; Cell Line, Tumor; Cell Movement; Cell Proliferation; ErbB Receptors; Extracellular	2014
Activity of a novel Hec1-targeted anticancer compound against breast cancer cell lines in vitro and in vivo. Molecular cancer therapeutics, 2014, Volume: 13, Issue:6 Topics: Animals; Antineoplastic Agents; Apoptosis; Breast Neoplasms; Cytoskeletal Proteins; Doxorubicin; Dru	2014
Sorafenib resistance and JNK signaling in carcinoma during extracellular matrix stiffening. Biomaterials, 2014, Volume: 35, Issue:22 Topics: Antineoplastic Agents; Biomechanical Phenomena; Breast; Breast Neoplasms; Carcinoma; Cell Line, Tumo	2014
Inhibition of the vacuolar ATPase induces Bnip3-dependent death of cancer cells and a reduction in tumor burden and metastasis. Oncotarget, 2014, Mar-15, Volume: 5, Issue:5 Topics: Animals; Antineoplastic Agents; Apoptosis; Breast Neoplasms; Butadienes; Cell Hypoxia; Enzyme Inhibi	2014
Investigation of antitumor effects of sorafenib and lapatinib alone and in combination on MCF-7 breast cancer cells. Asian Pacific journal of cancer prevention : APJCP, 2014, Volume: 15, Issue:7 Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Cell Line,	2014
JUNB promotes the survival of Flavopiridol treated human breast cancer cells. Biochemical and biophysical research communications, 2014, Jul-18, Volume: 450, Issue:1 Topics: Antineoplastic Agents; Breast Neoplasms; Cell Line, Tumor; Cell Survival; Drug Resistance, Neoplasm;	2014
Sorafenib and nilotinib resensitize tamoxifen resistant breast cancer cells to tamoxifen treatment via estrogen receptor α. International journal of oncology, 2014, Volume: 45, Issue:5 Topics: Breast Neoplasms; Cell Proliferation; Drug Resistance, Neoplasm; Estrogen Receptor alpha; Female; Ge	2014
Combination of letrozole, metronomic cyclophosphamide and sorafenib is well-tolerated and shows activity in patients with primary breast cancer. British journal of cancer, 2015, Jan-06, Volume: 112, Issue:1 Topics: Administration, Metronomic; Aged; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protoc	2015
Nicotinamide sensitizes human breast cancer cells to the cytotoxic effects of radiation and cisplatin. Oncology reports, 2015, Volume: 33, Issue:2 Topics: Apoptosis; BRCA1 Protein; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Cisplatin; DNA Dam	2015
The telomerase inhibitor imetelstat alone, and in combination with trastuzumab, decreases the cancer stem cell population and self-renewal of HER2+ breast cancer cells. Breast cancer research and treatment, 2015, Volume: 149, Issue:3 Topics: Animals; Antibodies, Monoclonal, Humanized; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation;	2015
Cyclodextrin-Modified Porous Silicon Nanoparticles for Efficient Sustained Drug Delivery and Proliferation Inhibition of Breast Cancer Cells. ACS applied materials & interfaces, 2015, Oct-21, Volume: 7, Issue:41 Topics: Animals; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell Survival; Cyclodextrins; Drug	2015
Bay 61-3606 Sensitizes TRAIL-Induced Apoptosis by Downregulating Mcl-1 in Breast Cancer Cells. PloS one, 2015, Volume: 10, Issue:12 Topics: Apoptosis; Breast Neoplasms; Caspases; Cell Line; Cell Line, Tumor; Cyclin-Dependent Kinases; DNA Fr	2015
Inhibition of tumor growth and metastasis by photoimmunotherapy targeting tumor-associated macrophage in a sorafenib-resistant tumor model. Biomaterials, 2016, Volume: 84 Topics: Animals; Breast Neoplasms; Cell Death; Cell Line, Tumor; Cell Proliferation; Disease Models, Animal;	2016
[Pemetrexed + Sorafenib] lethality is increased by inhibition of ERBB1/2/3-PI3K-NFκB compensatory survival signaling. Oncotarget, 2016, Apr-26, Volume: 7, Issue:17 Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Biomarkers, Tumor; Breast Neopla	2016
Actionable pathways: interactive discovery of therapeutic targets using signaling pathway models. Nucleic acids research, 2016, 07-08, Volume: 44, Issue:W1 Topics: Antineoplastic Agents; Breast Neoplasms; Computer Graphics; Computer Simulation; Drug Discovery; Gen	2016
BRCA1-deficient breast cancer cell lines are resistant to MEK inhibitors and show distinct sensitivities to 6-thioguanine. Scientific reports, 2016, 06-17, Volume: 6 Topics: Antimetabolites, Antineoplastic; Benzimidazoles; BRCA1 Protein; Breast Neoplasms; Cell Line, Tumor;	2016
Identification of a Selective SIRT2 Inhibitor and Its Anti-breast Cancer Activity. Biological & pharmaceutical bulletin, 2016, Volume: 39, Issue:10 Topics: Antineoplastic Agents; Breast Neoplasms; Cell Survival; Histone Deacetylase Inhibitors; Humans; MCF-	2016
Resveratrol enhances the efficacy of sorafenib mediated apoptosis in human breast cancer MCF7 cells through ROS, cell cycle inhibition, caspase 3 and PARP cleavage. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2016, Volume: 84 Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Breast Neoplasms; Caspase 3; Cell Cycle Checkpoints; C	2016
Anticancer Effects of a New SIRT Inhibitor, MHY2256, against Human Breast Cancer MCF-7 Cells via Regulation of MDM2-p53 Binding. International journal of biological sciences, 2016, Volume: 12, Issue:12 Topics: Acetylation; Antineoplastic Agents; Apoptosis; Autophagy; Breast Neoplasms; Cell Cycle Checkpoints;	2016
Synergistic chemotherapeutic effect of sorafenib-loaded pullulan-Dox conjugate nanoparticles against murine breast carcinoma. Nanoscale, 2017, Feb-23, Volume: 9, Issue:8 Topics: Animals; Antineoplastic Agents; Breast Neoplasms; Cell Line, Tumor; Doxorubicin; Drug Delivery Syste	2017
Correlation between clinical response to sorafenib in hepatocellular carcinoma treatment and polymorphisms of P-glycoprotein (ABCB1) and of breast cancer resistance protein (ABCG2): monocentric study. Cancer chemotherapy and pharmacology, 2017, Volume: 79, Issue:4 Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; ATP Binding Cassette Transporter, Subfamily B	2017
Combining nanoliposomal ceramide with sorafenib synergistically inhibits melanoma and breast cancer cell survival to decrease tumor development. Clinical cancer research : an official journal of the American Association for Cancer Research, 2008, Jun-01, Volume: 14, Issue:11 Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzenesulfonates; Blotting, Western; Bre	2008
Down-regulation of myeloid cell leukemia-1 through inhibiting Erk/Pin 1 pathway by sorafenib facilitates chemosensitization in breast cancer. Cancer research, 2008, Aug-01, Volume: 68, Issue:15 Topics: Antineoplastic Agents; Benzenesulfonates; Breast Neoplasms; Cell Line, Tumor; Down-Regulation; Human	2008
Quo vadis with targeted drugs in the 21st century? Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2009, Jan-01, Volume: 27, Issue:1 Topics: Antineoplastic Agents; Benzenesulfonates; Breast Neoplasms; ErbB Receptors; Female; Humans; Niacinam	2009
[Mechanism of apoptosis induced by SIRT1 deacetylase inhibitors in human breast cancer MCF-7 drug-resistant cells]. Yao xue xue bao = Acta pharmaceutica Sinica, 2008, Volume: 43, Issue:10 Topics: Apoptosis; Benzamides; Breast Neoplasms; Caspases; Cell Cycle; Cell Line, Tumor; Cell Proliferation;	2008
Brain magnetic resonance imaging changes after sorafenib and sunitinib chemotherapy in patients with advanced renal cell and breast carcinoma. Journal of neurosurgery, 2009, Volume: 111, Issue:3 Topics: Aged; Antineoplastic Agents; Benzenesulfonates; Brain; Brain Edema; Brain Neoplasms; Breast Neoplasm	2009
Inhibition of SIRT1 deacetylase suppresses estrogen receptor signaling. Carcinogenesis, 2010, Volume: 31, Issue:3 Topics: Animals; Benzamides; Breast Neoplasms; Cell Line, Tumor; Cells, Cultured; Estradiol; Estrogen Recept	2010
Synergistic activity of letrozole and sorafenib on breast cancer cells. Breast cancer research and treatment, 2010, Volume: 124, Issue:1 Topics: Adaptor Proteins, Signal Transducing; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apo	2010
Nox1 is involved in p53 deacetylation and suppression of its transcriptional activity and apoptosis. Free radical biology & medicine, 2010, May-15, Volume: 48, Issue:10 Topics: Acetylation; Apoptosis; Breast Neoplasms; Carcinoma; Carrier Proteins; Cell Line, Tumor; Cloning, Mo	2010
Tyrosine kinase inhibitors gefitinib, lapatinib and sorafenib induce rapid functional alterations in breast cancer cells. Current cancer drug targets, 2010, Volume: 10, Issue:4 Topics: Antineoplastic Agents; Apoptosis; Base Sequence; Benzenesulfonates; Breast Neoplasms; Calcium; Cell	2010
A structure-based approach for mapping adverse drug reactions to the perturbation of underlying biological pathways. PloS one, 2010, Aug-23, Volume: 5, Issue:8 Topics: Breast Neoplasms; Computational Biology; Databases, Factual; Diabetes Mellitus, Type 2; Drug-Related	2010
Sorafenib tosylate and paclitaxel induce anti-angiogenic, anti-tumour and anti-resorptive effects in experimental breast cancer bone metastases. European journal of cancer (Oxford, England : 1990), 2011, Volume: 47, Issue:2 Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates;	2011
The telomerase inhibitor imetelstat depletes cancer stem cells in breast and pancreatic cancer cell lines. Cancer research, 2010, Nov-15, Volume: 70, Issue:22 Topics: Animals; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell Survival; Flow Cytometry; Huma	2010
HER2-positive breast cancer cells resistant to trastuzumab and lapatinib lose reliance upon HER2 and are sensitive to the multitargeted kinase inhibitor sorafenib. Breast cancer research and treatment, 2011, Volume: 130, Issue:1 Topics: Animals; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Benzenesulfonates; Breast Neoplas	2011
EZH2 promotes expansion of breast tumor initiating cells through activation of RAF1-β-catenin signaling. Cancer cell, 2011, Jan-18, Volume: 19, Issue:1 Topics: Animals; Benzenesulfonates; Benzimidazoles; beta Catenin; Breast Neoplasms; Cell Hypoxia; Cell Line,	2011
Anti-angiogenic therapies in metastatic breast cancer-an unfulfilled dream. The Lancet. Oncology, 2011, Volume: 12, Issue:4 Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic C	2011
Pericyte depletion results in hypoxia-associated epithelial-to-mesenchymal transition and metastasis mediated by met signaling pathway. Cancer cell, 2012, Jan-17, Volume: 21, Issue:1 Topics: Animals; Antineoplastic Agents; Benzamides; Benzenesulfonates; Breast Neoplasms; Cell Hypoxia; Cell	2012
Dasatinib synergizes with both cytotoxic and signal transduction inhibitors in heterogeneous breast cancer cell lines--lessons for design of combination targeted therapy. Cancer letters, 2012, Jul-01, Volume: 320, Issue:1 Topics: Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Breast Neoplasms; Butadienes; Cel	2012
Insight into the cooperation of P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) at the blood-brain barrier: a case study examining sorafenib efflux clearance. Molecular pharmaceutics, 2012, Mar-05, Volume: 9, Issue:3 Topics: Animals; ATP Binding Cassette Transporter, Subfamily B; ATP Binding Cassette Transporter, Subfamily	2012
LMW-E/CDK2 deregulates acinar morphogenesis, induces tumorigenesis, and associates with the activated b-Raf-ERK1/2-mTOR pathway in breast cancer patients. PLoS genetics, 2012, Volume: 8, Issue:3 Topics: Acinar Cells; Animals; Benzenesulfonates; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Ce	2012
Dynamic reprogramming of the kinome in response to targeted MEK inhibition in triple-negative breast cancer. Cell, 2012, Apr-13, Volume: 149, Issue:2 Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Benzimidazoles; Breast Neoplasms; Disease Models,	2012
Sorafenib and pemetrexed toxicity in cancer cells is mediated via SRC-ERK signaling. Cancer biology & therapy, 2012, Volume: 13, Issue:9 Topics: Antineoplastic Agents; Autophagy; Benzenesulfonates; Breast Neoplasms; Cell Line, Tumor; Drug Synerg	2012
Targeting angiogenesis in metastatic breast cancer. The oncologist, 2012, Volume: 17, Issue:8 Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Pro	2012
Comparative proteome profiling of breast tumor cell lines by gel electrophoresis and mass spectrometry reveals an epithelial mesenchymal transition associated protein signature. Molecular bioSystems, 2013, Volume: 9, Issue:6 Topics: Antineoplastic Agents; Breast Neoplasms; Cell Adhesion; Cell Line, Tumor; Cell Movement; Cell Prolif	2013
The combination of sorafenib and radiation preferentially inhibits breast cancer stem cells by suppressing HIF-1α expression. Oncology reports, 2013, Volume: 29, Issue:3 Topics: Antineoplastic Agents; Breast Neoplasms; Cell Survival; Chemoradiotherapy; Female; Gene Expression;	2013
Inhibition of S6K1 enhances glucose deprivation-induced cell death via downregulation of anti-apoptotic proteins in MCF-7 breast cancer cells. Biochemical and biophysical research communications, 2013, Mar-01, Volume: 432, Issue:1 Topics: Apoptosis; Apoptosis Regulatory Proteins; Breast Neoplasms; Down-Regulation; Female; Gene Knockdown	2013
Nicotinamide in adenocarcinoma 755 and in the milk of mice carrying the agent of spontaneous mammary tumor. Experientia, 1957, Dec-15, Volume: 13, Issue:12 Topics: Adenocarcinoma; Animals; Breast Neoplasms; Humans; Mammary Neoplasms, Animal; Mice; Milk; Neoplasms,	1957
AUGMENTATION OF 6-AMINONICOTINAMIDE ANTAGONISM OF TUMOR GROWTH BY COMPOUNDS WITH ESTROGENIC ACTIVITY. Cancer research, 1964, Volume: 24 Topics: 6-Aminonicotinamide; Adenocarcinoma; Animals; Antineoplastic Agents; Breast Neoplasms; Cortisone; Di	1964
Short communication: the addition of carbogen and nicotinamide to a palliative fractionation schedule for locally advanced breast cancer. The British journal of radiology, 1995, Volume: 68, Issue:806 Topics: Aged; Aged, 80 and over; Breast Neoplasms; Carbon Dioxide; Female; Humans; Middle Aged; Niacinamide;	1995
Bullous pemphigoid induced by radiation therapy. Clinical oncology (Royal College of Radiologists (Great Britain)), 1995, Volume: 7, Issue:4 Topics: Anti-Bacterial Agents; Breast Neoplasms; Carcinoma, Ductal, Breast; Dermatologic Agents; Female; Hum	1995
Control of histone H1 dimer-poly(ADP-ribose) complex formation by poly(ADP-ribose) glycohydrolase. Experimental cell research, 1977, Volume: 106, Issue:2 Topics: Animals; Breast Neoplasms; Cell Line; Cell Nucleus; Female; Glycoside Hydrolases; Histones; Humans;	1977
The effect of gossypol and 6-aminonicotinamide on tumor cell metabolism: a 31P-magnetic resonance spectroscopic study. Biochemical and biophysical research communications, 1989, Oct-31, Volume: 164, Issue:2 Topics: 6-Aminonicotinamide; Breast Neoplasms; Cell Line; Female; Gossypol; Humans; Magnetic Resonance Spect	1989
The influence of adrenocortical hormones and vitamins upon tryptophan metabolism in man. Clinical science, 1968, Volume: 35, Issue:1 Topics: Adrenocorticotropic Hormone; Adult; Benzoates; Breast Neoplasms; Female; Humans; Hydrocortisone; Kyn	1968

Intervention	participants (Number)
	Complete response (CR)	Partial response (PR)	Stable disease (SD)	Progressive disease (PD)	Not evaluated
Sorafenib (Nexavar, BAY43-9006)	0	1	20	31	2

niacinamide and Breast Neoplasms

Research Excerpts

Research

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Disease Control Rate (DCR) by Central Review

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Patient Reported Outcomes: Euroqol-5 Dimensions (EQ-5D) - Visual Analogue Scale (VAS) Score

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