entinostat has been researched along with Breast Neoplasms in 37 studies
Breast Neoplasms: Tumors or cancer of the human BREAST.
| Excerpt | Relevance | Reference |
|---|---|---|
| "We aimed to confirm the efficacy and safety of the oral histone deacetylase inhibitor entinostat in Japanese patients with hormone receptor-positive advanced/recurrent breast cancer and to explore potential biomarkers." | 9.69 | Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial. ( Aruga, T; Iwasa, T; Iwata, H; Kaneda, A; Kaneko, K; Kawabata, A; Kobayashi, K; Lee, MJ; Masuda, N; Nakamura, R; Nishimura, Y; Saji, S; Seike, T; Tamura, K; Tokunaga, E; Trepel, JB; Tsurutani, J; Yamamoto, Y; Yamashita, T; Yonemori, K; Yuno, A, 2023) |
| "Entinostat is an oral inhibitor of class I histone deacetylases intended for endocrine therapy-resistant patients with hormone receptor-positive (HR+) advanced or metastatic breast cancer (BC)." | 9.41 | Phase 1 trial of entinostat as monotherapy and combined with exemestane in Japanese patients with hormone receptor-positive advanced breast cancer. ( Iwata, H; Kimura, R; Lee, MJ; Masuda, N; Nishimura, Y; Saji, S; Sawaki, M; Shimomura, A; Tamura, K; Trepel, J; Yasojima, H; Yuno, A, 2021) |
| "Previous clinical trials have demonstrated that entinostat in combination with exemestane had good tolerability and significant clinical efficacy in patients with advanced hormone receptor positive (HR+) and HER2 negative (HER2-) metastatic breast cancer (MBC) in the USA." | 9.41 | Phase I Study and Pilot Efficacy Analysis of Entinostat, a Novel Histone Deacetylase Inhibitor, in Chinese Postmenopausal Women with Hormone Receptor-Positive Metastatic Breast Cancer. ( Guan, J; Hao, J; Jing, J; Li, H; Li, Q; Li, W; Lu, L; Mu, Y; Ouyang, Q; Wang, J; Wang, X; Xu, B; Yu, G; Zhang, Q; Zhou, L, 2021) |
| "Endocrine therapy resistance in advanced breast cancer remains a significant clinical problem that may be overcome with the use of histone deacetylase inhibitors such as entinostat." | 9.41 | E2112: Randomized Phase III Trial of Endocrine Therapy Plus Entinostat or Placebo in Hormone Receptor-Positive Advanced Breast Cancer. A Trial of the ECOG-ACRIN Cancer Research Group. ( Brown-Glaberman, UA; Budd, GT; Burkard, ME; Connolly, RM; Faller, BA; Kaufman, PA; Lee, MJ; Levine, EG; Miller, KD; Onitilo, AA; Piekarz, RL; Royce, ME; Smith, KL; Sparano, JA; Thomas, A; Trepel, JB; Winn, JS; Wolff, AC; Zhao, F, 2021) |
| "This study identified the MTD of the entinostat, lapatinib, and trastuzumab combination that provided acceptable tolerability and anti-tumour activity in heavily pre-treated patients with HER2+ metastatic breast cancer, supporting a confirmatory trial." | 9.30 | A phase Ib study of entinostat plus lapatinib with or without trastuzumab in patients with HER2-positive metastatic breast cancer that progressed during trastuzumab treatment. ( Alvarez, R; Barcenas, CH; Booser, DJ; Brewster, AM; Brown, PH; Davis, DW; Giordano, SH; Ibrahim, NK; Iwase, T; Jackson, SA; Lee, J; Lim, B; Moscow, JA; Moulder, SL; Murthy, RK; Piekarz, R; Shen, Y; Tripathy, D; Ueno, NT; Valero, V; Willey, JS; Wu, J, 2019) |
| "Entinostat is an oral isoform selective histone deacetylase inhibitor that targets resistance to hormonal therapies in estrogen receptor-positive (ER+) breast cancer." | 9.17 | Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata ( Cruickshank, S; Ismail-Khan, RR; Klein, PM; Lee, MJ; Lichinitser, M; Melichar, B; Miller, KD; Munster, PN; Trepel, JB; Yardley, DA, 2013) |
| "Based on promising phase II data, the histone deacetylase inhibitor entinostat is in phase III trials for patients with metastatic estrogen receptor-positive breast cancer." | 7.88 | Identification of Jun loss promotes resistance to histone deacetylase inhibitor entinostat through Myc signaling in luminal breast cancer. ( Darr, DB; Fan, C; Hollern, DP; Mott, KR; Perou, CM; Tanioka, M, 2018) |
| "We reported that the class I HDAC inhibitor entinostat induced apoptosis in erbB2-overexpressing breast cancer cells via downregulation of erbB2 and erbB3." | 7.79 | Functional cooperation of miR-125a, miR-125b, and miR-205 in entinostat-induced downregulation of erbB2/erbB3 and apoptosis in breast cancer cells. ( Huang, J; Lee, CK; Liu, B; Lyu, H; Tan, J; Wang, J; Wang, S, 2013) |
| "Adding entinostat to exemestane improves survival in women with ER(+) advanced breast cancer." | 7.79 | Entinostat plus exemestane has activity in ER+ advanced breast cancer. ( , 2013) |
| "We aimed to confirm the efficacy and safety of the oral histone deacetylase inhibitor entinostat in Japanese patients with hormone receptor-positive advanced/recurrent breast cancer and to explore potential biomarkers." | 5.69 | Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial. ( Aruga, T; Iwasa, T; Iwata, H; Kaneda, A; Kaneko, K; Kawabata, A; Kobayashi, K; Lee, MJ; Masuda, N; Nakamura, R; Nishimura, Y; Saji, S; Seike, T; Tamura, K; Tokunaga, E; Trepel, JB; Tsurutani, J; Yamamoto, Y; Yamashita, T; Yonemori, K; Yuno, A, 2023) |
| "Entinostat is a synthetic benzamide derivative histone deacetylase (HDAC) inhibitor, which potently and selectively inhibits class I and IV HDAC enzymes." | 5.46 | Entinostat: a promising treatment option for patients with advanced breast cancer. ( Connolly, RM; Piekarz, R; Rudek, MA, 2017) |
| "Entinostat is an oral inhibitor of class I histone deacetylases intended for endocrine therapy-resistant patients with hormone receptor-positive (HR+) advanced or metastatic breast cancer (BC)." | 5.41 | Phase 1 trial of entinostat as monotherapy and combined with exemestane in Japanese patients with hormone receptor-positive advanced breast cancer. ( Iwata, H; Kimura, R; Lee, MJ; Masuda, N; Nishimura, Y; Saji, S; Sawaki, M; Shimomura, A; Tamura, K; Trepel, J; Yasojima, H; Yuno, A, 2021) |
| "Previous clinical trials have demonstrated that entinostat in combination with exemestane had good tolerability and significant clinical efficacy in patients with advanced hormone receptor positive (HR+) and HER2 negative (HER2-) metastatic breast cancer (MBC) in the USA." | 5.41 | Phase I Study and Pilot Efficacy Analysis of Entinostat, a Novel Histone Deacetylase Inhibitor, in Chinese Postmenopausal Women with Hormone Receptor-Positive Metastatic Breast Cancer. ( Guan, J; Hao, J; Jing, J; Li, H; Li, Q; Li, W; Lu, L; Mu, Y; Ouyang, Q; Wang, J; Wang, X; Xu, B; Yu, G; Zhang, Q; Zhou, L, 2021) |
| "Endocrine therapy resistance in advanced breast cancer remains a significant clinical problem that may be overcome with the use of histone deacetylase inhibitors such as entinostat." | 5.41 | E2112: Randomized Phase III Trial of Endocrine Therapy Plus Entinostat or Placebo in Hormone Receptor-Positive Advanced Breast Cancer. A Trial of the ECOG-ACRIN Cancer Research Group. ( Brown-Glaberman, UA; Budd, GT; Burkard, ME; Connolly, RM; Faller, BA; Kaufman, PA; Lee, MJ; Levine, EG; Miller, KD; Onitilo, AA; Piekarz, RL; Royce, ME; Smith, KL; Sparano, JA; Thomas, A; Trepel, JB; Winn, JS; Wolff, AC; Zhao, F, 2021) |
| "Loss of ERα in breast cancer correlates with poor prognosis, increased recurrence rates, and higher incidence of metastasis." | 5.40 | Histone deacetylase inhibitor entinostat reverses epithelial to mesenchymal transition of breast cancer cells by reversing the repression of E-cadherin. ( Gau, Y; Sabnis, G; Shah, P, 2014) |
| "This study identified the MTD of the entinostat, lapatinib, and trastuzumab combination that provided acceptable tolerability and anti-tumour activity in heavily pre-treated patients with HER2+ metastatic breast cancer, supporting a confirmatory trial." | 5.30 | A phase Ib study of entinostat plus lapatinib with or without trastuzumab in patients with HER2-positive metastatic breast cancer that progressed during trastuzumab treatment. ( Alvarez, R; Barcenas, CH; Booser, DJ; Brewster, AM; Brown, PH; Davis, DW; Giordano, SH; Ibrahim, NK; Iwase, T; Jackson, SA; Lee, J; Lim, B; Moscow, JA; Moulder, SL; Murthy, RK; Piekarz, R; Shen, Y; Tripathy, D; Ueno, NT; Valero, V; Willey, JS; Wu, J, 2019) |
| "Entinostat is an oral isoform selective histone deacetylase inhibitor that targets resistance to hormonal therapies in estrogen receptor-positive (ER+) breast cancer." | 5.17 | Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata ( Cruickshank, S; Ismail-Khan, RR; Klein, PM; Lee, MJ; Lichinitser, M; Melichar, B; Miller, KD; Munster, PN; Trepel, JB; Yardley, DA, 2013) |
| "Based on promising phase II data, the histone deacetylase inhibitor entinostat is in phase III trials for patients with metastatic estrogen receptor-positive breast cancer." | 3.88 | Identification of Jun loss promotes resistance to histone deacetylase inhibitor entinostat through Myc signaling in luminal breast cancer. ( Darr, DB; Fan, C; Hollern, DP; Mott, KR; Perou, CM; Tanioka, M, 2018) |
| "We reported that the class I HDAC inhibitor entinostat induced apoptosis in erbB2-overexpressing breast cancer cells via downregulation of erbB2 and erbB3." | 3.79 | Functional cooperation of miR-125a, miR-125b, and miR-205 in entinostat-induced downregulation of erbB2/erbB3 and apoptosis in breast cancer cells. ( Huang, J; Lee, CK; Liu, B; Lyu, H; Tan, J; Wang, J; Wang, S, 2013) |
| "Adding entinostat to exemestane improves survival in women with ER(+) advanced breast cancer." | 3.79 | Entinostat plus exemestane has activity in ER+ advanced breast cancer. ( , 2013) |
| "Entinostat is a synthetic benzamide derivative histone deacetylase (HDAC) inhibitor, which potently and selectively inhibits class I and IV HDAC enzymes." | 1.46 | Entinostat: a promising treatment option for patients with advanced breast cancer. ( Connolly, RM; Piekarz, R; Rudek, MA, 2017) |
| "A previous methylome study on breast cancer tissues detected inverse correlation between RECK CpG methylation (in an intron-1 region) and relapse-free survival." | 1.43 | Pattern of RECK CpG methylation as a potential marker for predicting breast cancer prognosis and drug-sensitivity. ( Iwaisako, K; Kawashima, M; Kawata, Y; Kurebayashi, J; Nishimura, T; Noda, M; Shi, G; Toi, M; Yoshida, Y; Yoshikawa, K; Yuki, K, 2016) |
| "Loss of ERα in breast cancer correlates with poor prognosis, increased recurrence rates, and higher incidence of metastasis." | 1.40 | Histone deacetylase inhibitor entinostat reverses epithelial to mesenchymal transition of breast cancer cells by reversing the repression of E-cadherin. ( Gau, Y; Sabnis, G; Shah, P, 2014) |
| "In addition, approximately 25% of breast cancers do not express the estrogen receptor (ERα) and consequently, are innately resistant to endocrine therapy." | 1.37 | Aromatase inhibitors and xenograft studies. ( Brodie, AM; Chumsri, S; Howes, T; Sabnis, GJ, 2011) |
| "More importantly, breast cancer T47D cells in which Sp1 was knocked down or Sp1-knockout mouse embryonic stem cells were resistant to the combined treatments." | 1.35 | Sp1-mediated TRAIL induction in chemosensitization. ( Philipsen, S; Wei, WZ; Wu, GS; Xu, J; Zhou, JY, 2008) |
| "Breast cancer is a highly heterogeneous disease with distinct histologic subtypes." | 1.35 | HDAC inhibitor SNDX-275 induces apoptosis in erbB2-overexpressing breast cancer cells via down-regulation of erbB3 expression. ( Gao, L; Huang, X; Lee, CK; Liu, B; Ordentlich, P; Wang, S, 2009) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 7 (18.92) | 29.6817 |
| 2010's | 22 (59.46) | 24.3611 |
| 2020's | 8 (21.62) | 2.80 |
| Authors | Studies |
|---|---|
| Frey, RR | 1 |
| Wada, CK | 1 |
| Garland, RB | 1 |
| Curtin, ML | 1 |
| Michaelides, MR | 1 |
| Li, J | 1 |
| Pease, LJ | 1 |
| Glaser, KB | 2 |
| Marcotte, PA | 1 |
| Bouska, JJ | 1 |
| Murphy, SS | 1 |
| Davidsen, SK | 2 |
| Casero, RA | 1 |
| Woster, PM | 1 |
| Mendoza-Sanchez, R | 1 |
| Cotnoir-White, D | 1 |
| Kulpa, J | 1 |
| Jutras, I | 1 |
| Pottel, J | 1 |
| Moitessier, N | 1 |
| Mader, S | 1 |
| Gleason, JL | 1 |
| Masuda, N | 4 |
| Tamura, K | 4 |
| Yasojima, H | 1 |
| Shimomura, A | 1 |
| Sawaki, M | 1 |
| Lee, MJ | 6 |
| Yuno, A | 4 |
| Trepel, J | 1 |
| Kimura, R | 1 |
| Nishimura, Y | 4 |
| Saji, S | 4 |
| Iwata, H | 4 |
| Mezni, E | 1 |
| Sabatier, R | 1 |
| Goncalves, A | 1 |
| Vicier, C | 1 |
| Sidiropoulos, DN | 1 |
| Rafie, CI | 1 |
| Jang, JK | 1 |
| Castanon, S | 1 |
| Baugh, AG | 1 |
| Gonzalez, E | 1 |
| Christmas, BJ | 1 |
| Narumi, VH | 1 |
| Davis-Marcisak, EF | 1 |
| Sharma, G | 1 |
| Bigelow, E | 1 |
| Vaghasia, A | 1 |
| Gupta, A | 1 |
| Skaist, A | 1 |
| Considine, M | 1 |
| Wheelan, SJ | 1 |
| Ganesan, SK | 1 |
| Yu, M | 1 |
| Yegnasubramanian, S | 1 |
| Stearns, V | 1 |
| Connolly, RM | 3 |
| Gaykalova, DA | 1 |
| Kagohara, LT | 1 |
| Jaffee, EM | 1 |
| Fertig, EJ | 1 |
| Roussos Torres, ET | 1 |
| Nakamura, R | 3 |
| Yamashita, T | 3 |
| Yamamoto, Y | 3 |
| Kobayashi, K | 3 |
| Tsurutani, J | 3 |
| Iwasa, T | 3 |
| Yonemori, K | 3 |
| Aruga, T | 3 |
| Tokunaga, E | 3 |
| Kaneko, K | 3 |
| Kawabata, A | 3 |
| Seike, T | 3 |
| Kaneda, A | 3 |
| Trepel, JB | 7 |
| McCaw, TR | 1 |
| Li, M | 1 |
| Starenki, D | 1 |
| Liu, M | 1 |
| Cooper, SJ | 1 |
| Arend, RC | 1 |
| Forero, A | 1 |
| Buchsbaum, DJ | 1 |
| Randall, TD | 1 |
| Lee, CH | 1 |
| Kang, YN | 1 |
| Ho, CL | 1 |
| Lin, C | 1 |
| Chen, PH | 1 |
| Wu, YY | 1 |
| Huang, TC | 1 |
| Wang, J | 3 |
| Zhang, Q | 1 |
| Li, Q | 2 |
| Mu, Y | 1 |
| Jing, J | 1 |
| Li, H | 1 |
| Li, W | 1 |
| Yu, G | 1 |
| Wang, X | 1 |
| Ouyang, Q | 1 |
| Hao, J | 1 |
| Lu, L | 1 |
| Zhou, L | 1 |
| Guan, J | 1 |
| Xu, B | 1 |
| Zhao, F | 1 |
| Miller, KD | 2 |
| Piekarz, RL | 1 |
| Smith, KL | 1 |
| Brown-Glaberman, UA | 1 |
| Winn, JS | 1 |
| Faller, BA | 1 |
| Onitilo, AA | 1 |
| Burkard, ME | 1 |
| Budd, GT | 1 |
| Levine, EG | 1 |
| Royce, ME | 1 |
| Kaufman, PA | 1 |
| Thomas, A | 1 |
| Wolff, AC | 1 |
| Sparano, JA | 1 |
| Hicks, KC | 1 |
| Chariou, PL | 1 |
| Ozawa, Y | 1 |
| Minnar, CM | 1 |
| Knudson, KM | 1 |
| Meyer, TJ | 1 |
| Bian, J | 1 |
| Cam, M | 1 |
| Schlom, J | 1 |
| Gameiro, SR | 2 |
| Rudek, MA | 1 |
| Piekarz, R | 2 |
| Liu, CY | 1 |
| Wu, CY | 1 |
| Petrossian, K | 1 |
| Huang, TT | 1 |
| Tseng, LM | 1 |
| Chen, S | 1 |
| Trapani, D | 1 |
| Esposito, A | 1 |
| Criscitiello, C | 1 |
| Mazzarella, L | 1 |
| Locatelli, M | 1 |
| Minchella, I | 1 |
| Minucci, S | 1 |
| Curigliano, G | 1 |
| Tanioka, M | 1 |
| Mott, KR | 1 |
| Hollern, DP | 1 |
| Fan, C | 1 |
| Darr, DB | 1 |
| Perou, CM | 1 |
| Lim, B | 1 |
| Murthy, RK | 1 |
| Lee, J | 2 |
| Jackson, SA | 1 |
| Iwase, T | 1 |
| Davis, DW | 1 |
| Willey, JS | 1 |
| Wu, J | 1 |
| Shen, Y | 1 |
| Tripathy, D | 1 |
| Alvarez, R | 1 |
| Ibrahim, NK | 1 |
| Brewster, AM | 1 |
| Barcenas, CH | 1 |
| Brown, PH | 1 |
| Giordano, SH | 1 |
| Moulder, SL | 1 |
| Booser, DJ | 1 |
| Moscow, JA | 1 |
| Valero, V | 1 |
| Ueno, NT | 2 |
| Caslini, C | 1 |
| Hong, S | 1 |
| Ban, YJ | 1 |
| Chen, XS | 1 |
| Ince, TA | 1 |
| Wang, S | 3 |
| Huang, J | 1 |
| Lyu, H | 1 |
| Lee, CK | 3 |
| Tan, J | 1 |
| Liu, B | 3 |
| Yardley, DA | 1 |
| Ismail-Khan, RR | 1 |
| Melichar, B | 1 |
| Lichinitser, M | 1 |
| Munster, PN | 1 |
| Klein, PM | 1 |
| Cruickshank, S | 1 |
| Shah, P | 2 |
| Gau, Y | 1 |
| Sabnis, G | 1 |
| Bartholomeusz, C | 1 |
| Mansour, O | 1 |
| Humphries, J | 1 |
| Hortobagyi, GN | 1 |
| Ordentlich, P | 2 |
| Ji, Z | 1 |
| Su, J | 1 |
| Liu, C | 1 |
| Wang, H | 1 |
| Huang, D | 1 |
| Zhou, X | 1 |
| Ou, O | 1 |
| Huppi, K | 1 |
| Chakka, S | 1 |
| Gehlhaus, K | 1 |
| Dubois, W | 1 |
| Patel, J | 1 |
| Chen, J | 1 |
| Mackiewicz, M | 1 |
| Jones, TL | 1 |
| Pitt, JJ | 1 |
| Martin, SE | 1 |
| Goldsmith, P | 1 |
| Simmons, JK | 1 |
| Mock, BA | 1 |
| Caplen, NJ | 1 |
| Schech, AJ | 1 |
| Yu, S | 1 |
| Sabnis, GJ | 2 |
| Goloubeva, O | 1 |
| Rosenblatt, P | 1 |
| Kazi, A | 1 |
| Chumsri, S | 2 |
| Brodie, A | 1 |
| Nidhyanandan, S | 1 |
| Boreddy, TS | 1 |
| Chandrasekhar, KB | 1 |
| Reddy, ND | 1 |
| Kulkarni, NM | 1 |
| Narayanan, S | 1 |
| Malamas, AS | 1 |
| Tsang, KY | 1 |
| Ferrone, S | 1 |
| Hodge, JW | 1 |
| Shi, G | 1 |
| Yoshida, Y | 1 |
| Yuki, K | 1 |
| Nishimura, T | 1 |
| Kawata, Y | 1 |
| Kawashima, M | 1 |
| Iwaisako, K | 1 |
| Yoshikawa, K | 1 |
| Kurebayashi, J | 1 |
| Toi, M | 1 |
| Noda, M | 1 |
| Xu, J | 1 |
| Zhou, JY | 1 |
| Wei, WZ | 1 |
| Philipsen, S | 1 |
| Wu, GS | 1 |
| Huang, X | 2 |
| Gao, L | 1 |
| Srivastava, RK | 1 |
| Kurzrock, R | 1 |
| Shankar, S | 1 |
| Howes, T | 1 |
| Brodie, AM | 1 |
| Yang, X | 1 |
| Staver, MJ | 1 |
| Waring, JF | 1 |
| Stender, J | 1 |
| Ulrich, RG | 1 |
| Lee, BI | 2 |
| Park, SH | 2 |
| Kim, JW | 1 |
| Sausville, EA | 2 |
| Kim, HT | 1 |
| Nakanishi, O | 2 |
| Kim, SJ | 2 |
| Lee, SR | 1 |
| Kim, BC | 1 |
| Cho, EA | 1 |
| Patel, SP | 1 |
| Kang, HB | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Phase 1 Study of KHK2375 in Subjects With Advanced or Recurrent Breast Cancer[NCT02623751] | Phase 1 | 15 participants (Actual) | Interventional | 2015-11-30 | Completed | ||
| Study of KHK2375 in Subjects With Advanced or Recurrent Breast Cancer[NCT03291886] | Phase 2 | 133 participants (Actual) | Interventional | 2017-09-22 | Completed | ||
| A Phase I and Pharmacokinetic Study to Evaluate Histone Deacetylase Inhibitor, Entinostat in Chinese Postmenopausal Women Patients With Locally Recurrent or Metastatic Breast Cancer[NCT02833155] | Phase 1 | 19 participants (Actual) | Interventional | 2016-08-29 | Completed | ||
| A Randomized Phase III Trial of Endocrine Therapy Plus Entinostat/Placebo in Patients With Hormone Receptor-Positive Advanced Breast Cancer[NCT02115282] | Phase 3 | 608 participants (Actual) | Interventional | 2014-03-29 | Active, not recruiting | ||
| A Phase 2, Randomized, Double-Blind, Multicenter Study of Exemestane With and Without SNDX-275 in Postmenopausal Women With Locally Recurrent or Metastatic Estrogen Receptor-Positive Breast Cancer, Progressing on Treatment With a Non-Steroidal Aromatase I[NCT00676663] | Phase 2 | 130 participants (Actual) | Interventional | 2008-06-13 | Completed | ||
| A Phase I Study of Entinostat in Combination With Enzalutamide for Treatment of Patients With Castration-Resistant Prostate Cancer[NCT03829930] | Phase 1 | 6 participants (Actual) | Interventional | 2019-05-01 | Terminated (stopped due to Sponsor discontinued the drug) | ||
| IGHID 11424 - A Pilot Trial of the Effect of Vorinostat and AGS-004 on Persistent HIV-1 Infection (The VOR VAX Study)[NCT02707900] | Phase 1 | 6 participants (Actual) | Interventional | 2016-03-31 | Terminated (stopped due to Manufacturing of the AGS-004 HIV vaccine by Argos could no longer be provided.) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Peripheral blood samples (PBMCs) were collected prior to therapy and on Days 8 and 15 of cycle 1, for assessment of lysine acetylation, using an assay developed by the Trepel Laboratory, NCI/NIH. CD45 blood mononuclear cells were measured. Patients with lysine acetylation change of 1.5 folds or higher were compared to patients with lysine acetylation change of less than 1.5 folds. (NCT02115282)
Timeframe: Disease assessed at baseline, then every 12 weeks until treatment discontinuation, then every 3 months within 2 years from study entry, every 6 months between 2-5 years and annually between 6-10 years from study entry, until first disease progression
| Intervention | months (Median) |
|---|---|
| Arm A (Exemestane, Entinostat)- Lysine Acetylation Change>=1.5 Fold | 2.8 |
| Arm A (Exemestane, Entinostat)- Lysine Acetylation Change<1.5 Fold | 2.7 |
Objective response rate was defined as number of patients with complete response (CR) or partial response (PR) divided by all randomized patients. Responses were evaluated using the revised Response Evaluation Criteria in Solid Tumors (RECIST) guideline. CR was defined as disappearance of all target and non-target lesions. PR was defined as at least a 30% decrease in the sum of the diameters of target lesions (taking as reference the baseline sum diameters), and/or persistence of one or more non-target lesion(s). (NCT02115282)
Timeframe: Assessed at baseline, then every 12 weeks until treatment discontinuation, then every 3 months within 2 years from study entry, every 6 months between 2-5 years and annually between 6-10 years from study entry, until first disease progression
| Intervention | percentage of participants (Number) |
|---|---|
| Arm A (Exemestane, Entinostat) | 4.6 |
| Arm B (Exemestane, Placebo) | 4.3 |
Overall survival (OS) was defined to be time from randomization to death from any cause. Cases who were still alive were censored at the date last known alive. (NCT02115282)
Timeframe: Assessed every 3 months within 2 years from study entry, every 6 months between 2-5 years and annually between 6-10 years from study entry, until death
| Intervention | months (Median) |
|---|---|
| Arm A (Exemestane, Entinostat) | 23.4 |
| Arm B (Exemestane, Placebo) | 21.7 |
Diarrhea was measured by Functional Assessment of Chronic Illness Therapy for Patients With Diarrhea (FACIT-Diarrhea) subscale form, which had 11 items, all items were rated on a 5-point Likert scale from 0 to 4. FACIT-Diarrhea subscale score was calculated based on the scoring manual, subscale score ranges from 0 to 44, and higher score indicates less diarrhea. The primary comparison of patient-reported diarrhea between treatment arms was based on the end of cycle 3 assessment. (NCT02115282)
Timeframe: Assessed at baseline and end of cycle 3
| Intervention | units on a scale (Mean) |
|---|---|
| Arm A (Exemestane, Entinostat) | 38.8 |
| Arm B (Exemestane, Placebo) | 41.5 |
Fatigue was measured by PROMIS Fatigue short form, it had 7 items and all items were rated on a 5-point Likert scale from 1 to 5. The PROMIS Fatigue total score and T score were calculated based on the scoring manual. The total score ranges from 7 to 35, the T score ranges from 29.4 to 83.2, higher scores indicate more fatigue. The PROMIS Fatigue T score was used for arm comparison. The primary comparison of patient-reported fatigue between treatment arms was based on the end of cycle 3 assessment. (NCT02115282)
Timeframe: Assessed at baseline and end of cycle 3
| Intervention | T-score (Mean) |
|---|---|
| Arm A (Exemestane, Entinostat) | 55.5 |
| Arm B (Exemestane, Placebo) | 54.1 |
Health-related quality of life (HRQL) was measured using Functional Assessment of Cancer Therapy - General (FACT-G). The primary endpoint for HRQL was the FACT-G Trial Outcome Index (TOI) which was an aggregate score of 5 items from the FACT-G-Physical subscale (GP2, GP3, GP4, GP6, and GP7) and 6 items from the FACT-G-Functional subscale (GF1, GF2, GF3, GF4, GF6, and GF7). All items were rated on a 5-point Likert scale from 0 to 4. FACT-G TOI subscale score was calculated based on the scoring manual, subscale score ranges from 0 to 44, and higher scores indicate better quality of life. The primary comparison of HRQL between treatment arms was based on the end of cycle 3 assessment. (NCT02115282)
Timeframe: Assessed at baseline and end of cycle 3
| Intervention | units on a scale (Mean) |
|---|---|
| Arm A (Exemestane, Entinostat) | 20.5 |
| Arm B (Exemestane, Placebo) | 20.9 |
Nausea and anorexia were measured by The Functional Assessment of Anorexia/Cachexia Treatment (FAACT)-additional concerns, which had 12 items, all items were rated on a 5-point Likert scale from 0 to 4. FAACT-additional concerns subscale score was calculated based on scoring manual. Subscale score ranges from 0 to 48, and higher scores indicate less nausea and anorexia. The primary comparison of patient-reported nausea and anorexia between treatment arms was based on the end of cycle 3 assessment. (NCT02115282)
Timeframe: Assessed at baseline and end of cycle 3
| Intervention | units on a scale (Mean) |
|---|---|
| Arm A (Exemestane, Entinostat) | 35.8 |
| Arm B (Exemestane, Placebo) | 37.0 |
Progression-free survival (PFS) was defined to be time from randomization to the earliest documented disease progression as defined by the RECIST criteria, new primary breast cancer, or death without progression. Disease assessment was to continue until disease progression, even after non-protocol anti-cancer therapy was started. Cases with incomplete follow up or without adequate disease evaluations were censored at the date last documented to be free of progression, regardless of whether non-protocol anti-cancer therapy was started or not. Disease progression was based on central review, and defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. In addition, the appearance of one or more new lesions was also considered progression. Kaplan-Meier method was used to estimate PFS rate. (NCT02115282)
Timeframe: Assessed at baseline, then every 12 weeks until treatment discontinuation, then every 3 months within 2 years from study entry, every 6 months between 2-5 years and annually between 6-10 years from study entry, until first disease progression
| Intervention | months (Median) |
|---|---|
| Arm A (Exemestane, Entinostat) | 3.3 |
| Arm B (Exemestane, Placebo) | 3.1 |
Time-to-treatment deterioration (TTD) was defined as time from randomization to disease progression or death or worsening of symptoms, whichever occurred first. Disease progression was assessed per RECIST v1.1. Symptoms deterioration was measured by 6 items (GP1, GP2, GP4, GF7, B1, P2, scored 0-24) from the 8-item FACT-Breast Symptom Index (FBSI). Symptom deterioration was defined as two consecutive available decreases of at least 3 points from baseline using the 6-item FBSI in this trial, and the second visit time was used as the time of symptom deterioration in this case, unless it was the final score, for which one decrease was sufficient. Kaplan-Meier method was used to estimate the median TTD and TTD rate at a certain time point. Symptoms were assessed every cycle for the first six months after randomization, every two cycles between 6 months and 1 year. It then were assessed based on the same schedule for tumor assessments until disease progression as specified below. (NCT02115282)
Timeframe: Disease assessed at baseline, then every 12 weeks until treatment discontinuation, then every 3 months within 2 years from study entry, every 6 months between 2-5 years and annually between 6-10 years from study entry, until first disease progression
| Intervention | months (Median) |
|---|---|
| Arm A (Exemestane, Entinostat) | 2.9 |
| Arm B (Exemestane, Placebo) | 2.9 |
CBR is defined as the percentage of participants with overall response (CR + PR) plus stable disease (SD) for 6 months as assessed by the investigator based on RECIST, version 1.0. CR is defined as the disappearance of all target lesions. PR is defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD. SD is defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started. (NCT00676663)
Timeframe: From date of randomization to discontinuation due to disease progression or intolerable AE up to primary completion date (Median follow-up 6 months)
| Intervention | percentage of participants (Number) |
|---|---|
| Exemestane 25 mg + Placebo | 25.8 |
| Exemestane 25 mg + Entinostat 5 mg | 26.6 |
ORR is defined as the percentage of participants with response during treatment classified as complete response (CR) or partial response (PR), as assessed by the investigator based on Response Evaluation Criteria in Solid Tumors (RECIST), version 1.0. CR is defined as the disappearance of all target lesions. PR is defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD. (NCT00676663)
Timeframe: From date of randomization to discontinuation due to disease progression or intolerable Adverse Event (AE) up to primary completion date (Median follow-up 6 months)
| Intervention | percentage of participants (Number) |
|---|---|
| Exemestane 25 mg + Placebo | 4.6 |
| Exemestane 25 mg + Entinostat 5 mg | 4.7 |
OS was defined as the number of months elapsed between the date of randomization and the date of death (whatever the cause). (NCT00676663)
Timeframe: First dose of study drug to end of study (Median follow-up 24 months in the EE arm and 26.4 months in the EP arm)
| Intervention | months (Median) |
|---|---|
| Exemestane 25 mg + Placebo (EP) | 19.84 |
| Exemestane 25 mg + Entinostat 5 mg (EE) | 28.13 |
PFS is defined as the number of months from the date of randomization to the earlier of progressive disease (PD) or death due to any cause. (NCT00676663)
Timeframe: From date of randomization to discontinuation due to disease progression or death up to primary completion date (Median follow-up 6 months)
| Intervention | months (Median) |
|---|---|
| Exemestane 25 mg + Placebo | 2.27 |
| Exemestane 25 mg + Entinostat 5 mg | 4.28 |
"An AE is defined as any untoward medical occurrence in a patient or clinical investigation patient administered a pharmaceutical product and that does not necessarily have a causal relationship with this treatment. Worsening of a pre-existing medical condition was considered an AE if there was either an increase in severity, frequency, or duration of the condition or an association with significantly worse outcomes. Abnormal clinical laboratory findings determined by the investigator to be clinically significant were recorded as AEs. A TEAE is an AE that starts after the administration of study drug.~A SAE is any AE that is fatal, life threatening, requires in-patient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth effect or other significant medical hazard." (NCT00676663)
Timeframe: First dose to within 30 days of last dose of study drug (Up to Approximately 2 Years)
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| TEAE | SAE | |
| Exemestane 25 mg + Entinostat 5 mg | 60 | 10 |
| Exemestane 25 mg + Placebo | 56 | 8 |
5 reviews available for entinostat and Breast Neoplasms
| Article | Year |
|---|---|
Recent advances in the development of polyamine analogues as antitumor agents.
Topics: Animals; Antineoplastic Agents; Biogenic Polyamines; Breast Neoplasms; DNA; Drug Discovery; Eflornit | 2009 |
Recent advances in the development of polyamine analogues as antitumor agents.
Topics: Animals; Antineoplastic Agents; Biogenic Polyamines; Breast Neoplasms; DNA; Drug Discovery; Eflornit | 2009 |
Recent advances in the development of polyamine analogues as antitumor agents.
Topics: Animals; Antineoplastic Agents; Biogenic Polyamines; Breast Neoplasms; DNA; Drug Discovery; Eflornit | 2009 |
[Updates in hormone-receptor-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer in 2021].
Topics: Aged; Androstadienes; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Protoc | 2022 |
[Updates in hormone-receptor-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer in 2021].
Topics: Aged; Androstadienes; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Protoc | 2022 |
[Updates in hormone-receptor-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer in 2021].
Topics: Aged; Androstadienes; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Protoc | 2022 |
Endocrine therapies in postmenopausal women with hormone receptor-positive, human epidermal growth factor receptor 2-negative, pretreated, advanced breast cancer: A network meta-analysis.
Topics: Androstadienes; Antineoplastic Agents, Hormonal; Antineoplastic Combined Chemotherapy Protocols; Ben | 2020 |
Endocrine therapies in postmenopausal women with hormone receptor-positive, human epidermal growth factor receptor 2-negative, pretreated, advanced breast cancer: A network meta-analysis.
Topics: Androstadienes; Antineoplastic Agents, Hormonal; Antineoplastic Combined Chemotherapy Protocols; Ben | 2020 |
Endocrine therapies in postmenopausal women with hormone receptor-positive, human epidermal growth factor receptor 2-negative, pretreated, advanced breast cancer: A network meta-analysis.
Topics: Androstadienes; Antineoplastic Agents, Hormonal; Antineoplastic Combined Chemotherapy Protocols; Ben | 2020 |
Treatment for the endocrine resistant breast cancer: Current options and future perspectives.
Topics: Aminopyridines; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Breast Neoplasms; Drug R | 2017 |
Treatment for the endocrine resistant breast cancer: Current options and future perspectives.
Topics: Aminopyridines; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Breast Neoplasms; Drug R | 2017 |
Treatment for the endocrine resistant breast cancer: Current options and future perspectives.
Topics: Aminopyridines; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Breast Neoplasms; Drug R | 2017 |
Entinostat for the treatment of breast cancer.
Topics: Animals; Antineoplastic Agents; Apoptosis; Benzamides; Breast Neoplasms; Cell Proliferation; Epigene | 2017 |
Entinostat for the treatment of breast cancer.
Topics: Animals; Antineoplastic Agents; Apoptosis; Benzamides; Breast Neoplasms; Cell Proliferation; Epigene | 2017 |
Entinostat for the treatment of breast cancer.
Topics: Animals; Antineoplastic Agents; Apoptosis; Benzamides; Breast Neoplasms; Cell Proliferation; Epigene | 2017 |
6 trials available for entinostat and Breast Neoplasms
| Article | Year |
|---|---|
Phase 1 trial of entinostat as monotherapy and combined with exemestane in Japanese patients with hormone receptor-positive advanced breast cancer.
Topics: Acetylation; Aged; Androstadienes; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Proto | 2021 |
Phase 1 trial of entinostat as monotherapy and combined with exemestane in Japanese patients with hormone receptor-positive advanced breast cancer.
Topics: Acetylation; Aged; Androstadienes; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Proto | 2021 |
Phase 1 trial of entinostat as monotherapy and combined with exemestane in Japanese patients with hormone receptor-positive advanced breast cancer.
Topics: Acetylation; Aged; Androstadienes; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Proto | 2021 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Efficacy and exploratory biomarker analysis of entinostat plus exemestane in advanced or recurrent breast cancer: phase II randomized controlled trial.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Double-Blind Method; Estrogen Rece | 2023 |
Phase I Study and Pilot Efficacy Analysis of Entinostat, a Novel Histone Deacetylase Inhibitor, in Chinese Postmenopausal Women with Hormone Receptor-Positive Metastatic Breast Cancer.
Topics: Antineoplastic Combined Chemotherapy Protocols; Benzamides; Breast Neoplasms; China; Female; Histone | 2021 |
Phase I Study and Pilot Efficacy Analysis of Entinostat, a Novel Histone Deacetylase Inhibitor, in Chinese Postmenopausal Women with Hormone Receptor-Positive Metastatic Breast Cancer.
Topics: Antineoplastic Combined Chemotherapy Protocols; Benzamides; Breast Neoplasms; China; Female; Histone | 2021 |
Phase I Study and Pilot Efficacy Analysis of Entinostat, a Novel Histone Deacetylase Inhibitor, in Chinese Postmenopausal Women with Hormone Receptor-Positive Metastatic Breast Cancer.
Topics: Antineoplastic Combined Chemotherapy Protocols; Benzamides; Breast Neoplasms; China; Female; Histone | 2021 |
E2112: Randomized Phase III Trial of Endocrine Therapy Plus Entinostat or Placebo in Hormone Receptor-Positive Advanced Breast Cancer. A Trial of the ECOG-ACRIN Cancer Research Group.
Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy | 2021 |
E2112: Randomized Phase III Trial of Endocrine Therapy Plus Entinostat or Placebo in Hormone Receptor-Positive Advanced Breast Cancer. A Trial of the ECOG-ACRIN Cancer Research Group.
Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy | 2021 |
E2112: Randomized Phase III Trial of Endocrine Therapy Plus Entinostat or Placebo in Hormone Receptor-Positive Advanced Breast Cancer. A Trial of the ECOG-ACRIN Cancer Research Group.
Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy | 2021 |
A phase Ib study of entinostat plus lapatinib with or without trastuzumab in patients with HER2-positive metastatic breast cancer that progressed during trastuzumab treatment.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Breast Neoplasms; Breast Ne | 2019 |
A phase Ib study of entinostat plus lapatinib with or without trastuzumab in patients with HER2-positive metastatic breast cancer that progressed during trastuzumab treatment.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Breast Neoplasms; Breast Ne | 2019 |
A phase Ib study of entinostat plus lapatinib with or without trastuzumab in patients with HER2-positive metastatic breast cancer that progressed during trastuzumab treatment.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Breast Neoplasms; Breast Ne | 2019 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata
Topics: Adult; Aged; Aged, 80 and over; Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Arom | 2013 |
26 other studies available for entinostat and Breast Neoplasms
| Article | Year |
|---|---|
Trifluoromethyl ketones as inhibitors of histone deacetylase.
Topics: Acetylation; Blotting, Western; Breast Neoplasms; Cell Cycle; Enzyme Inhibitors; Fibrosarcoma; Histo | 2002 |
Trifluoromethyl ketones as inhibitors of histone deacetylase.
Topics: Acetylation; Blotting, Western; Breast Neoplasms; Cell Cycle; Enzyme Inhibitors; Fibrosarcoma; Histo | 2002 |
Trifluoromethyl ketones as inhibitors of histone deacetylase.
Topics: Acetylation; Blotting, Western; Breast Neoplasms; Cell Cycle; Enzyme Inhibitors; Fibrosarcoma; Histo | 2002 |
Design, synthesis and evaluation of antiestrogen and histone deacetylase inhibitor molecular hybrids.
Topics: Antineoplastic Agents; Benzamides; Breast; Breast Neoplasms; Cell Line, Tumor; Estradiol; Estrogen R | 2015 |
Design, synthesis and evaluation of antiestrogen and histone deacetylase inhibitor molecular hybrids.
Topics: Antineoplastic Agents; Benzamides; Breast; Breast Neoplasms; Cell Line, Tumor; Estradiol; Estrogen R | 2015 |
Design, synthesis and evaluation of antiestrogen and histone deacetylase inhibitor molecular hybrids.
Topics: Antineoplastic Agents; Benzamides; Breast; Breast Neoplasms; Cell Line, Tumor; Estradiol; Estrogen R | 2015 |
Entinostat Decreases Immune Suppression to Promote Antitumor Responses in a HER2+ Breast Tumor Microenvironment.
Topics: Animals; Benzamides; Breast Neoplasms; Female; Humans; Immunosuppression Therapy; Mice; Myeloid-Deri | 2022 |
Entinostat Decreases Immune Suppression to Promote Antitumor Responses in a HER2+ Breast Tumor Microenvironment.
Topics: Animals; Benzamides; Breast Neoplasms; Female; Humans; Immunosuppression Therapy; Mice; Myeloid-Deri | 2022 |
Entinostat Decreases Immune Suppression to Promote Antitumor Responses in a HER2+ Breast Tumor Microenvironment.
Topics: Animals; Benzamides; Breast Neoplasms; Female; Humans; Immunosuppression Therapy; Mice; Myeloid-Deri | 2022 |
Histone deacetylase inhibition promotes intratumoral CD8
Topics: Animals; Antibodies, Monoclonal; Benzamides; Breast Neoplasms; CD8-Positive T-Lymphocytes; Cell Line | 2019 |
Histone deacetylase inhibition promotes intratumoral CD8
Topics: Animals; Antibodies, Monoclonal; Benzamides; Breast Neoplasms; CD8-Positive T-Lymphocytes; Cell Line | 2019 |
Histone deacetylase inhibition promotes intratumoral CD8
Topics: Animals; Antibodies, Monoclonal; Benzamides; Breast Neoplasms; CD8-Positive T-Lymphocytes; Cell Line | 2019 |
Tumour-targeted interleukin-12 and entinostat combination therapy improves cancer survival by reprogramming the tumour immune cell landscape.
Topics: Adaptive Immunity; Animals; Benzamides; Breast Neoplasms; CD8-Positive T-Lymphocytes; Cell Line, Tum | 2021 |
Tumour-targeted interleukin-12 and entinostat combination therapy improves cancer survival by reprogramming the tumour immune cell landscape.
Topics: Adaptive Immunity; Animals; Benzamides; Breast Neoplasms; CD8-Positive T-Lymphocytes; Cell Line, Tum | 2021 |
Tumour-targeted interleukin-12 and entinostat combination therapy improves cancer survival by reprogramming the tumour immune cell landscape.
Topics: Adaptive Immunity; Animals; Benzamides; Breast Neoplasms; CD8-Positive T-Lymphocytes; Cell Line, Tum | 2021 |
Entinostat: a promising treatment option for patients with advanced breast cancer.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzamides; Breast Neoplasms; Cell Line, | 2017 |
Entinostat: a promising treatment option for patients with advanced breast cancer.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzamides; Breast Neoplasms; Cell Line, | 2017 |
Entinostat: a promising treatment option for patients with advanced breast cancer.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzamides; Breast Neoplasms; Cell Line, | 2017 |
Identification of Jun loss promotes resistance to histone deacetylase inhibitor entinostat through Myc signaling in luminal breast cancer.
Topics: Animals; Antineoplastic Agents; Benzamides; Breast Neoplasms; Cell Line, Tumor; DNA Copy Number Vari | 2018 |
Identification of Jun loss promotes resistance to histone deacetylase inhibitor entinostat through Myc signaling in luminal breast cancer.
Topics: Animals; Antineoplastic Agents; Benzamides; Breast Neoplasms; Cell Line, Tumor; DNA Copy Number Vari | 2018 |
Identification of Jun loss promotes resistance to histone deacetylase inhibitor entinostat through Myc signaling in luminal breast cancer.
Topics: Animals; Antineoplastic Agents; Benzamides; Breast Neoplasms; Cell Line, Tumor; DNA Copy Number Vari | 2018 |
HDAC7 regulates histone 3 lysine 27 acetylation and transcriptional activity at super-enhancer-associated genes in breast cancer stem cells.
Topics: Acetylation; Benzamides; Breast Neoplasms; Down-Regulation; Enhancer Elements, Genetic; Female; Gene | 2019 |
HDAC7 regulates histone 3 lysine 27 acetylation and transcriptional activity at super-enhancer-associated genes in breast cancer stem cells.
Topics: Acetylation; Benzamides; Breast Neoplasms; Down-Regulation; Enhancer Elements, Genetic; Female; Gene | 2019 |
HDAC7 regulates histone 3 lysine 27 acetylation and transcriptional activity at super-enhancer-associated genes in breast cancer stem cells.
Topics: Acetylation; Benzamides; Breast Neoplasms; Down-Regulation; Enhancer Elements, Genetic; Female; Gene | 2019 |
Functional cooperation of miR-125a, miR-125b, and miR-205 in entinostat-induced downregulation of erbB2/erbB3 and apoptosis in breast cancer cells.
Topics: Antineoplastic Agents; Apoptosis; Benzamides; Breast Neoplasms; Cell Line, Tumor; Epigenesis, Geneti | 2013 |
Functional cooperation of miR-125a, miR-125b, and miR-205 in entinostat-induced downregulation of erbB2/erbB3 and apoptosis in breast cancer cells.
Topics: Antineoplastic Agents; Apoptosis; Benzamides; Breast Neoplasms; Cell Line, Tumor; Epigenesis, Geneti | 2013 |
Functional cooperation of miR-125a, miR-125b, and miR-205 in entinostat-induced downregulation of erbB2/erbB3 and apoptosis in breast cancer cells.
Topics: Antineoplastic Agents; Apoptosis; Benzamides; Breast Neoplasms; Cell Line, Tumor; Epigenesis, Geneti | 2013 |
Entinostat plus exemestane has activity in ER+ advanced breast cancer.
Topics: Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Aromatase Inhibitors; Benzamides; Br | 2013 |
Entinostat plus exemestane has activity in ER+ advanced breast cancer.
Topics: Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Aromatase Inhibitors; Benzamides; Br | 2013 |
Entinostat plus exemestane has activity in ER+ advanced breast cancer.
Topics: Androstadienes; Antineoplastic Combined Chemotherapy Protocols; Aromatase Inhibitors; Benzamides; Br | 2013 |
Histone deacetylase inhibitor entinostat reverses epithelial to mesenchymal transition of breast cancer cells by reversing the repression of E-cadherin.
Topics: Benzamides; Breast Neoplasms; Cadherins; Cell Line, Tumor; Cell Movement; DNA Helicases; DNA-Binding | 2014 |
Histone deacetylase inhibitor entinostat reverses epithelial to mesenchymal transition of breast cancer cells by reversing the repression of E-cadherin.
Topics: Benzamides; Breast Neoplasms; Cadherins; Cell Line, Tumor; Cell Movement; DNA Helicases; DNA-Binding | 2014 |
Histone deacetylase inhibitor entinostat reverses epithelial to mesenchymal transition of breast cancer cells by reversing the repression of E-cadherin.
Topics: Benzamides; Breast Neoplasms; Cadherins; Cell Line, Tumor; Cell Movement; DNA Helicases; DNA-Binding | 2014 |
A class I histone deacetylase inhibitor, entinostat, enhances lapatinib efficacy in HER2-overexpressing breast cancer cells through FOXO3-mediated Bim1 expression.
Topics: Animals; Antineoplastic Agents; Apoptosis Regulatory Proteins; Benzamides; Breast Neoplasms; Cell Li | 2014 |
A class I histone deacetylase inhibitor, entinostat, enhances lapatinib efficacy in HER2-overexpressing breast cancer cells through FOXO3-mediated Bim1 expression.
Topics: Animals; Antineoplastic Agents; Apoptosis Regulatory Proteins; Benzamides; Breast Neoplasms; Cell Li | 2014 |
A class I histone deacetylase inhibitor, entinostat, enhances lapatinib efficacy in HER2-overexpressing breast cancer cells through FOXO3-mediated Bim1 expression.
Topics: Animals; Antineoplastic Agents; Apoptosis Regulatory Proteins; Benzamides; Breast Neoplasms; Cell Li | 2014 |
Integrating genomics and proteomics data to predict drug effects using binary linear programming.
Topics: Antineoplastic Agents; Benzamides; Breast Neoplasms; Cell Cycle; Cell Line, Tumor; Cyclin-Dependent | 2014 |
Integrating genomics and proteomics data to predict drug effects using binary linear programming.
Topics: Antineoplastic Agents; Benzamides; Breast Neoplasms; Cell Cycle; Cell Line, Tumor; Cyclin-Dependent | 2014 |
Integrating genomics and proteomics data to predict drug effects using binary linear programming.
Topics: Antineoplastic Agents; Benzamides; Breast Neoplasms; Cell Cycle; Cell Line, Tumor; Cyclin-Dependent | 2014 |
Loss-of-function RNAi screens in breast cancer cells identify AURKB, PLK1, PIK3R1, MAPK12, PRKD2, and PTK6 as sensitizing targets of rapamycin activity.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Aurora Kinase B; Benzamides; Breast Neoplas | 2014 |
Loss-of-function RNAi screens in breast cancer cells identify AURKB, PLK1, PIK3R1, MAPK12, PRKD2, and PTK6 as sensitizing targets of rapamycin activity.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Aurora Kinase B; Benzamides; Breast Neoplas | 2014 |
Loss-of-function RNAi screens in breast cancer cells identify AURKB, PLK1, PIK3R1, MAPK12, PRKD2, and PTK6 as sensitizing targets of rapamycin activity.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Aurora Kinase B; Benzamides; Breast Neoplas | 2014 |
Histone deacetylase inhibitor entinostat in combination with a retinoid downregulates HER2 and reduces the tumor initiating cell population in aromatase inhibitor-resistant breast cancer.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Aromatase Inhibitors; Benzamides; Breast Ne | 2015 |
Histone deacetylase inhibitor entinostat in combination with a retinoid downregulates HER2 and reduces the tumor initiating cell population in aromatase inhibitor-resistant breast cancer.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Aromatase Inhibitors; Benzamides; Breast Ne | 2015 |
Histone deacetylase inhibitor entinostat in combination with a retinoid downregulates HER2 and reduces the tumor initiating cell population in aromatase inhibitor-resistant breast cancer.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Aromatase Inhibitors; Benzamides; Breast Ne | 2015 |
Phosphodiesterase inhibitor, pentoxifylline enhances anticancer activity of histone deacetylase inhibitor, MS-275 in human breast cancer in vitro and in vivo.
Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzami | 2015 |
Phosphodiesterase inhibitor, pentoxifylline enhances anticancer activity of histone deacetylase inhibitor, MS-275 in human breast cancer in vitro and in vivo.
Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzami | 2015 |
Phosphodiesterase inhibitor, pentoxifylline enhances anticancer activity of histone deacetylase inhibitor, MS-275 in human breast cancer in vitro and in vivo.
Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzami | 2015 |
Inhibitors of histone deacetylase 1 reverse the immune evasion phenotype to enhance T-cell mediated lysis of prostate and breast carcinoma cells.
Topics: Apoptosis; Benzamides; Blotting, Western; Breast Neoplasms; Cell Proliferation; Female; Flow Cytomet | 2016 |
Inhibitors of histone deacetylase 1 reverse the immune evasion phenotype to enhance T-cell mediated lysis of prostate and breast carcinoma cells.
Topics: Apoptosis; Benzamides; Blotting, Western; Breast Neoplasms; Cell Proliferation; Female; Flow Cytomet | 2016 |
Inhibitors of histone deacetylase 1 reverse the immune evasion phenotype to enhance T-cell mediated lysis of prostate and breast carcinoma cells.
Topics: Apoptosis; Benzamides; Blotting, Western; Breast Neoplasms; Cell Proliferation; Female; Flow Cytomet | 2016 |
Pattern of RECK CpG methylation as a potential marker for predicting breast cancer prognosis and drug-sensitivity.
Topics: Antineoplastic Agents; Azacitidine; Benzamides; Breast Neoplasms; CpG Islands; Decitabine; DNA Methy | 2016 |
Pattern of RECK CpG methylation as a potential marker for predicting breast cancer prognosis and drug-sensitivity.
Topics: Antineoplastic Agents; Azacitidine; Benzamides; Breast Neoplasms; CpG Islands; Decitabine; DNA Methy | 2016 |
Pattern of RECK CpG methylation as a potential marker for predicting breast cancer prognosis and drug-sensitivity.
Topics: Antineoplastic Agents; Azacitidine; Benzamides; Breast Neoplasms; CpG Islands; Decitabine; DNA Methy | 2016 |
Sp1-mediated TRAIL induction in chemosensitization.
Topics: Animals; Antibiotics, Antineoplastic; Apoptosis; Benzamides; Blotting, Northern; Breast Neoplasms; C | 2008 |
Sp1-mediated TRAIL induction in chemosensitization.
Topics: Animals; Antibiotics, Antineoplastic; Apoptosis; Benzamides; Blotting, Northern; Breast Neoplasms; C | 2008 |
Sp1-mediated TRAIL induction in chemosensitization.
Topics: Animals; Antibiotics, Antineoplastic; Apoptosis; Benzamides; Blotting, Northern; Breast Neoplasms; C | 2008 |
HDAC inhibitor SNDX-275 induces apoptosis in erbB2-overexpressing breast cancer cells via down-regulation of erbB3 expression.
Topics: Apoptosis; Benzamides; Blotting, Western; Breast Neoplasms; Cell Cycle; Cell Proliferation; Female; | 2009 |
HDAC inhibitor SNDX-275 induces apoptosis in erbB2-overexpressing breast cancer cells via down-regulation of erbB3 expression.
Topics: Apoptosis; Benzamides; Blotting, Western; Breast Neoplasms; Cell Cycle; Cell Proliferation; Female; | 2009 |
HDAC inhibitor SNDX-275 induces apoptosis in erbB2-overexpressing breast cancer cells via down-regulation of erbB3 expression.
Topics: Apoptosis; Benzamides; Blotting, Western; Breast Neoplasms; Cell Cycle; Cell Proliferation; Female; | 2009 |
MS-275 sensitizes TRAIL-resistant breast cancer cells, inhibits angiogenesis and metastasis, and reverses epithelial-mesenchymal transition in vivo.
Topics: Animals; Apoptosis; Benzamides; Breast Neoplasms; Caspase 3; Cell Line, Tumor; Cell Proliferation; D | 2010 |
MS-275 sensitizes TRAIL-resistant breast cancer cells, inhibits angiogenesis and metastasis, and reverses epithelial-mesenchymal transition in vivo.
Topics: Animals; Apoptosis; Benzamides; Breast Neoplasms; Caspase 3; Cell Line, Tumor; Cell Proliferation; D | 2010 |
MS-275 sensitizes TRAIL-resistant breast cancer cells, inhibits angiogenesis and metastasis, and reverses epithelial-mesenchymal transition in vivo.
Topics: Animals; Apoptosis; Benzamides; Breast Neoplasms; Caspase 3; Cell Line, Tumor; Cell Proliferation; D | 2010 |
Aromatase inhibitors and xenograft studies.
Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemothe | 2011 |
Aromatase inhibitors and xenograft studies.
Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemothe | 2011 |
Aromatase inhibitors and xenograft studies.
Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemothe | 2011 |
HDAC inhibitor SNDX-275 enhances efficacy of trastuzumab in erbB2-overexpressing breast cancer cells and exhibits potential to overcome trastuzumab resistance.
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Prot | 2011 |
HDAC inhibitor SNDX-275 enhances efficacy of trastuzumab in erbB2-overexpressing breast cancer cells and exhibits potential to overcome trastuzumab resistance.
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Prot | 2011 |
HDAC inhibitor SNDX-275 enhances efficacy of trastuzumab in erbB2-overexpressing breast cancer cells and exhibits potential to overcome trastuzumab resistance.
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Prot | 2011 |
Gene expression profiling of multiple histone deacetylase (HDAC) inhibitors: defining a common gene set produced by HDAC inhibition in T24 and MDA carcinoma cell lines.
Topics: Benzamides; Breast Neoplasms; Chromatin; DNA Primers; DNA, Neoplasm; Enzyme Inhibitors; Gene Express | 2003 |
Gene expression profiling of multiple histone deacetylase (HDAC) inhibitors: defining a common gene set produced by HDAC inhibition in T24 and MDA carcinoma cell lines.
Topics: Benzamides; Breast Neoplasms; Chromatin; DNA Primers; DNA, Neoplasm; Enzyme Inhibitors; Gene Express | 2003 |
Gene expression profiling of multiple histone deacetylase (HDAC) inhibitors: defining a common gene set produced by HDAC inhibition in T24 and MDA carcinoma cell lines.
Topics: Benzamides; Breast Neoplasms; Chromatin; DNA Primers; DNA, Neoplasm; Enzyme Inhibitors; Gene Express | 2003 |
MS-275, a histone deacetylase inhibitor, selectively induces transforming growth factor beta type II receptor expression in human breast cancer cells.
Topics: Acetylation; Antineoplastic Agents; Benzamides; Breast Neoplasms; Cell Division; Chromatin; Enzyme I | 2001 |
MS-275, a histone deacetylase inhibitor, selectively induces transforming growth factor beta type II receptor expression in human breast cancer cells.
Topics: Acetylation; Antineoplastic Agents; Benzamides; Breast Neoplasms; Cell Division; Chromatin; Enzyme I | 2001 |
MS-275, a histone deacetylase inhibitor, selectively induces transforming growth factor beta type II receptor expression in human breast cancer cells.
Topics: Acetylation; Antineoplastic Agents; Benzamides; Breast Neoplasms; Cell Division; Chromatin; Enzyme I | 2001 |
Transcriptional regulation of the transforming growth factor beta type II receptor gene by histone acetyltransferase and deacetylase is mediated by NF-Y in human breast cancer cells.
Topics: Acetyltransferases; Base Sequence; Benzamides; Breast Neoplasms; CCAAT-Binding Factor; Cell Nucleus; | 2002 |
Transcriptional regulation of the transforming growth factor beta type II receptor gene by histone acetyltransferase and deacetylase is mediated by NF-Y in human breast cancer cells.
Topics: Acetyltransferases; Base Sequence; Benzamides; Breast Neoplasms; CCAAT-Binding Factor; Cell Nucleus; | 2002 |
Transcriptional regulation of the transforming growth factor beta type II receptor gene by histone acetyltransferase and deacetylase is mediated by NF-Y in human breast cancer cells.
Topics: Acetyltransferases; Base Sequence; Benzamides; Breast Neoplasms; CCAAT-Binding Factor; Cell Nucleus; | 2002 |