valproic acid has been researched along with Breast Cancer in 48 studies
Valproic Acid: A fatty acid with anticonvulsant and anti-manic properties that is used in the treatment of EPILEPSY and BIPOLAR DISORDER. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of VOLTAGE-GATED SODIUM CHANNELS.
valproic acid : A branched-chain saturated fatty acid that comprises of a propyl substituent on a pentanoic acid stem.
| Excerpt | Relevance | Reference |
|---|---|---|
| "We describe a novel ER+ breast cancer model to study de novo and acquired tamoxifen (TAM) resistance." | 7.85 | Effects of In Utero Exposure to Ethinyl Estradiol on Tamoxifen Resistance and Breast Cancer Recurrence in a Preclinical Model. ( Bouker, KB; Clarke, R; Cook, KL; Cruz, MI; de Assis, S; Hilakivi-Clarke, L; Hu, R; Jin, L; Nguyen, N; Wang, X; Wang, Y; Wärri, A; Wehrenberg, B; Xuan, J; Zhang, X; Zwart, A, 2017) |
| "Breast cancer is one of the leading causes of cancer-related death among women." | 6.58 | Valproic acid as an adjunctive therapeutic agent for the treatment of breast cancer. ( Harrelson, J; Heers, H; Lee, MW; Stanislaw, J, 2018) |
| "Valproic acid (VPA) has attracted a lot of interest in cancer research." | 5.62 | Apoptotic effects of valproic acid on miR-34a, miR-520h and HDAC1 gene in breast cancer. ( Amini-Farsani, Z; Injinari, N; Teimori, H; Yadollahi-Farsani, M, 2021) |
| "Multiple breast cancer cell models were employed to investigate whether the safe concentration of 0." | 5.46 | Valproic acid sensitizes breast cancer cells to hydroxyurea through inhibiting RPA2 hyperphosphorylation-mediated DNA repair pathway. ( Cai, Z; Feng, Z; Guo, G; Liu, G; Luo, Y; Powell, S; Tian, Y; Tian, Z; Wang, H; Wang, S; Wang, X; Zhang, F, 2017) |
| " We demonstrated that histone deacetylase inhibitors (HDACi), including low anticonvulsant dosage of VPA, induced the dose- and time-dependent up-regulation of TP transcript and protein expression in breast cancer cells, but not in the non-tumorigenic breast MCF-10A cell line." | 5.43 | Valproic acid potentiates the anticancer activity of capecitabine in vitro and in vivo in breast cancer models via induction of thymidine phosphorylase expression. ( Bruzzese, F; Budillon, A; D'Angelo, G; Di Gennaro, E; Franco, R; Leone, A; Roca, MS; Russo, D; Scogliamiglio, G; Terranova-Barberio, M; Vitagliano, C; Zotti, AI, 2016) |
| "Valproic acid (VPA) is a HDAC inhibitor that has antitumor activity at mM range." | 5.43 | N-(2-hydroxyphenyl)-2-propylpentanamide, a valproic acid aryl derivative designed in silico with improved anti-proliferative activity in HeLa, rhabdomyosarcoma and breast cancer cells. ( Bermúdez-Lugo, JA; Chávez-Blanco, A; Correa-Basurto, AM; Correa-Basurto, J; Dueñas-González, A; Fragoso-Vázquez, MJ; García-Sánchez, JR; Méndez-Luna, D; Mendieta-Wejebe, JE; Padilla-Martínez, II; Pérez-González, OA; Prestegui-Martel, B; Trujillo-Ferrara, J, 2016) |
| "It is known that chemosensitivity of breast cancer depends on its molecular subtype." | 5.42 | Valproic acid inhibits proliferation of HER2-expressing breast cancer cells by inducing cell cycle arrest and apoptosis through Hsp70 acetylation. ( Fushida, S; Harada, S; Hayashi, H; Inokuchi, M; Makino, I; Mawatari, T; Miyashita, T; Nakagawara, H; Ninomiya, I; Ohta, T; Oyama, K; Tajima, H; Takamura, H, 2015) |
| "Only in breast cancer cells, cyclin B1 expression was decreased and the cells accumulated also in G(2)." | 5.35 | Epigenetic reprogramming of breast cancer cells by valproic acid occurs regardless of estrogen receptor status. ( Billi, M; Grignani, F; Nervi, C; Travaglini, L; Vian, L, 2009) |
| "Treatment efficacy of breast cancer can be impaired by cell resistance." | 5.35 | Valproic acid is a selective antiproliferative agent in estrogen-sensitive breast cancer cells. ( Bertino, S; Boccuzzi, G; Bosco, O; Catalano, MG; Costantino, L; Fortunati, N; Vercellinatto, I, 2008) |
| "Camptothecin derivatives have been widely used for chemotherapy in patients with various cancers, but intrinsic and acquired drug resistance is major drawback to be overcome." | 5.35 | Simultaneous treatment with camptothecin and valproic acid suppresses induction of Bcl-X(L) and promotes apoptosis of MCF-7 breast cancer cells. ( Aiba, K; Arakawa, Y; Saito, S; Yamada, H, 2009) |
| "0 or 5 mM), but melatonin (1 or 10 nM) was ineffective alone or in combination with valproic acid, in the first (MCF-7A) subline examined." | 5.34 | Human melatonin MT1 receptor induction by valproic acid and its effects in combination with melatonin on MCF-7 breast cancer cell proliferation. ( Brown, GM; Jawed, S; Kim, B; Niles, LP; Ottenhof, T; Werstiuk, ES, 2007) |
| "Valproic acid (VPA), which has long been used in the treatment of epilepsy, was shown recently to be an effective histone deacetylase inhibitor that can induce differentiation of neoplastically transformed cells." | 5.33 | Valproic acid, in combination with all-trans retinoic acid and 5-aza-2'-deoxycytidine, restores expression of silenced RARbeta2 in breast cancer cells. ( Gudas, LJ; Mongan, NP, 2005) |
| " As epigenetic alterations are common to breast cancer, in this proof-of-concept study demethylating hydralazine, plus the HDAC inhibitor magnesium valproate, were added to neoadjuvant doxorubicin and cyclophosphamide in locally advanced breast cancer to assess their safety and biological efficacy." | 5.12 | A proof-of-principle study of epigenetic therapy added to neoadjuvant doxorubicin cyclophosphamide for locally advanced breast cancer. ( Arce, C; Bargallo, E; Camargo, MF; Candelaria, M; Chávez-Blanco, A; de la Cruz-Hernández, E; Dueñas-González, A; González-Fierro, A; Pérez-Cárdenas, E; Pérez-Plasencia, C; Ramírez, T; Revilla-Vázquez, A; Robles, E; Taja-Chayeb, L; Trejo-Becerril, C; Vela, T; Villarreal, P, 2006) |
| "We describe a novel ER+ breast cancer model to study de novo and acquired tamoxifen (TAM) resistance." | 3.85 | Effects of In Utero Exposure to Ethinyl Estradiol on Tamoxifen Resistance and Breast Cancer Recurrence in a Preclinical Model. ( Bouker, KB; Clarke, R; Cook, KL; Cruz, MI; de Assis, S; Hilakivi-Clarke, L; Hu, R; Jin, L; Nguyen, N; Wang, X; Wang, Y; Wärri, A; Wehrenberg, B; Xuan, J; Zhang, X; Zwart, A, 2017) |
| "We report the cases of 2 breast cancer patients who received capecitabine(CAP)and concomitant anticonvulsant therapy with either phenytoin(PHT)or valproate(VPA)for brain metastasis." | 3.80 | [Effect of capecitabine therapy on the blood levels of antiepileptic drugs - report of two cases]. ( Ibayashi, Y; Jotoku, H; Takahashi, M; Takasaki, M; Tanaka, H; Watanabe, K, 2014) |
| " Valproic acid (VA) is a histone deacetylase (HDAC) inhibitor that promotes self-renewal and expansion of hematopoietic stem cells and facilitates the generation of induced pluripotent stem cells from somatic cells and is currently being investigated in breast cancer clinical trials." | 3.78 | Histone deacetylase inhibitors stimulate dedifferentiation of human breast cancer cells through WNT/β-catenin signaling. ( Atkinson, R; Buchholz, TA; Debeb, BG; Krishnamurthy, S; Lacerda, L; Larson, R; Reuben, JM; Solley, T; Sulman, EP; Ueno, NT; Woodward, WA; Xu, W, 2012) |
| " The aim of the study was to investigate the influence of the antiepileptic drugs PHT, PB, VPA and lamotrigine (LTG) on estrogen-stimulated cell growth of human breast cancer cells (MCF-7), and to evaluate whether this effect could be related to a direct estrogen receptor (ER) binding." | 3.72 | Antiepileptic drugs inhibit cell growth in the human breast cancer cell line MCF7. ( Meussen-Elholm, ET; Olsen, CM; Røste, LS; Taubøll, E, 2004) |
| "Breast cancer is one of the leading causes of cancer-related death among women." | 2.58 | Valproic acid as an adjunctive therapeutic agent for the treatment of breast cancer. ( Harrelson, J; Heers, H; Lee, MW; Stanislaw, J, 2018) |
| "From these analyses, breast tumors are predicted to be sensitive to VPA." | 2.47 | A pharmacogenomic method for individualized prediction of drug sensitivity. ( Bild, AH; Chang, JT; Cohen, AL; Gustafson, AM; Jeffrey, SS; Johnson, E; Soldi, R; Spira, A; Welm, BE; Wilcox, R; Zhang, H, 2011) |
| "To target breast cancer (BC), epigenetic modulation could be a promising therapy strategy due to its role in the genesis, growth, and metastases of BC." | 1.72 | Untargeted LC-MS/MS Metabolomics Study on the MCF-7 Cell Line in the Presence of Valproic Acid. ( Bakalara, N; Correa-Basurto, J; Estrada-Pérez, AR; Fromager, B; García-Vázquez, JB; Rosales-Hernández, MC, 2022) |
| " The aim of this study was to compare the differential effects of standard chemotherapy regimens (FEC: 5-fluorouracil plus epirubicine plus cyclophosphamide) in combination with epigenetic modulators (decitabine, valproic acid): (a) on gene methylation levels of selected tumour biomarkers (LINE-1, uPA, PAI-1, DAPK); (b) their expression status (uPA and PAI-1); (c) differentiation status (5meC and H3K27me3)." | 1.62 | Epigenetic modulators combination with chemotherapy in breast cancer cells. ( Akgun, O; Ari, F; Magdolen, V; Napieralski, R; Ulukaya, E, 2021) |
| "Valproic acid (VPA) has attracted a lot of interest in cancer research." | 1.62 | Apoptotic effects of valproic acid on miR-34a, miR-520h and HDAC1 gene in breast cancer. ( Amini-Farsani, Z; Injinari, N; Teimori, H; Yadollahi-Farsani, M, 2021) |
| "1." | 1.56 | Metabolomics reveals the effect of valproic acid on MCF-7 and MDA-MB-231 cells. ( Jiang, G; Li, Z; Liu, S; Shan, C; Wang, X; Zhou, X, 2020) |
| "Multiple breast cancer cell models were employed to investigate whether the safe concentration of 0." | 1.46 | Valproic acid sensitizes breast cancer cells to hydroxyurea through inhibiting RPA2 hyperphosphorylation-mediated DNA repair pathway. ( Cai, Z; Feng, Z; Guo, G; Liu, G; Luo, Y; Powell, S; Tian, Y; Tian, Z; Wang, H; Wang, S; Wang, X; Zhang, F, 2017) |
| "Valproic acid (VPA) is a HDAC inhibitor that has antitumor activity at mM range." | 1.43 | N-(2-hydroxyphenyl)-2-propylpentanamide, a valproic acid aryl derivative designed in silico with improved anti-proliferative activity in HeLa, rhabdomyosarcoma and breast cancer cells. ( Bermúdez-Lugo, JA; Chávez-Blanco, A; Correa-Basurto, AM; Correa-Basurto, J; Dueñas-González, A; Fragoso-Vázquez, MJ; García-Sánchez, JR; Méndez-Luna, D; Mendieta-Wejebe, JE; Padilla-Martínez, II; Pérez-González, OA; Prestegui-Martel, B; Trujillo-Ferrara, J, 2016) |
| " We demonstrated that histone deacetylase inhibitors (HDACi), including low anticonvulsant dosage of VPA, induced the dose- and time-dependent up-regulation of TP transcript and protein expression in breast cancer cells, but not in the non-tumorigenic breast MCF-10A cell line." | 1.43 | Valproic acid potentiates the anticancer activity of capecitabine in vitro and in vivo in breast cancer models via induction of thymidine phosphorylase expression. ( Bruzzese, F; Budillon, A; D'Angelo, G; Di Gennaro, E; Franco, R; Leone, A; Roca, MS; Russo, D; Scogliamiglio, G; Terranova-Barberio, M; Vitagliano, C; Zotti, AI, 2016) |
| "It is known that chemosensitivity of breast cancer depends on its molecular subtype." | 1.42 | Valproic acid inhibits proliferation of HER2-expressing breast cancer cells by inducing cell cycle arrest and apoptosis through Hsp70 acetylation. ( Fushida, S; Harada, S; Hayashi, H; Inokuchi, M; Makino, I; Mawatari, T; Miyashita, T; Nakagawara, H; Ninomiya, I; Ohta, T; Oyama, K; Tajima, H; Takamura, H, 2015) |
| "Treatment of breast cancer cells with a demethylating agent and histone deacetylase inhibitors reduced methylation of the CR-1 promoter and reactivated CR-1 mRNA and protein expression in these cells, promoting migration and invasion of breast cancer cells." | 1.39 | Regulation of human Cripto-1 expression by nuclear receptors and DNA promoter methylation in human embryonal and breast cancer cells. ( Baraty, C; Bianco, C; Castro, NP; Gonzales, M; Held, N; Karasawa, H; Rangel, MC; Rollman, K; Salomon, DS; Strizzi, L, 2013) |
| "In vivo, pre-treatment of AR breast tumors in the brain with valproate restored the chemo-sensitivity of the tumors and prolonged animal survival." | 1.39 | Histone deacetylase inhibitors restore toxic BH3 domain protein expression in anoikis-resistant mammary and brain cancer stem cells, thereby enhancing the response to anti-ERBB1/ERBB2 therapy. ( Booth, L; Cruickshanks, N; Dent, P; Grant, S; Hamed, HA; Poklepovic, A; Sajithlal, GB; Syed, J; Tavallai, S, 2013) |
| "Valproic acid (VPA) is a broad-spectrum inhibitor of class I and II histone deacetylases and shows great anticancer activity in a variety of human cancers including breast cancer." | 1.38 | VPA inhibits breast cancer cell migration by specifically targeting HDAC2 and down-regulating Survivin. ( Kang, J; Leng, Y; Song, C; Wang, G; Wang, L; Wang, X; Zhang, L, 2012) |
| "The role of estrogen receptor-α (ER) in breast cancer development, and as a primary clinical marker for breast cancer prognosis, has been well documented." | 1.38 | Twist contributes to hormone resistance in breast cancer by downregulating estrogen receptor-α. ( Artemov, D; Carraway, H; Domek, J; Kato, Y; Kimble, B; Kowalski, J; Lisok, A; Raman, V; van der Groep, P; van Diest, P; Vesuna, F, 2012) |
| "Basal-like breast cancers are triple-negative (estrogen receptor negative, progesterone receptor negative, erythroblastic leukemia viral oncogene homolog 2 (ERBB2) negative) tumors with an aggressive clinical behavior that lacks effective molecular targets for therapy." | 1.36 | Epigenetic alteration of the NF-κB-inducing kinase (NIK) gene is involved in enhanced NIK expression in basal-like breast cancer. ( Inoue, J; Ishida, T; Ito, T; Semba, K; Shimizu, T; Watanabe, S; Yamaguchi, N; Yamamoto, M, 2010) |
| "Only in breast cancer cells, cyclin B1 expression was decreased and the cells accumulated also in G(2)." | 1.35 | Epigenetic reprogramming of breast cancer cells by valproic acid occurs regardless of estrogen receptor status. ( Billi, M; Grignani, F; Nervi, C; Travaglini, L; Vian, L, 2009) |
| "Camptothecin derivatives have been widely used for chemotherapy in patients with various cancers, but intrinsic and acquired drug resistance is major drawback to be overcome." | 1.35 | Simultaneous treatment with camptothecin and valproic acid suppresses induction of Bcl-X(L) and promotes apoptosis of MCF-7 breast cancer cells. ( Aiba, K; Arakawa, Y; Saito, S; Yamada, H, 2009) |
| "Treatment efficacy of breast cancer can be impaired by cell resistance." | 1.35 | Valproic acid is a selective antiproliferative agent in estrogen-sensitive breast cancer cells. ( Bertino, S; Boccuzzi, G; Bosco, O; Catalano, MG; Costantino, L; Fortunati, N; Vercellinatto, I, 2008) |
| "0 or 5 mM), but melatonin (1 or 10 nM) was ineffective alone or in combination with valproic acid, in the first (MCF-7A) subline examined." | 1.34 | Human melatonin MT1 receptor induction by valproic acid and its effects in combination with melatonin on MCF-7 breast cancer cell proliferation. ( Brown, GM; Jawed, S; Kim, B; Niles, LP; Ottenhof, T; Werstiuk, ES, 2007) |
| "Valproic acid (VPA), which has long been used in the treatment of epilepsy, was shown recently to be an effective histone deacetylase inhibitor that can induce differentiation of neoplastically transformed cells." | 1.33 | Valproic acid, in combination with all-trans retinoic acid and 5-aza-2'-deoxycytidine, restores expression of silenced RARbeta2 in breast cancer cells. ( Gudas, LJ; Mongan, NP, 2005) |
| "Exposure of breast cancer cells to VPA resulted in rapid dose-dependent hyperacetylation of the histones H3 and H4." | 1.33 | Valproic acid alters chromatin structure by regulation of chromatin modulation proteins. ( Bicaku, E; Daud, AI; Marchion, DC; Munster, PN; Sullivan, DM, 2005) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 1 (2.08) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 11 (22.92) | 29.6817 |
| 2010's | 26 (54.17) | 24.3611 |
| 2020's | 10 (20.83) | 2.80 |
| Authors | Studies |
|---|---|
| Conde Giner, S | 1 |
| Belles Medall, MD | 1 |
| Ferrando Piqueres, R | 1 |
| Estrada-Pérez, AR | 2 |
| Rosales-Hernández, MC | 2 |
| García-Vázquez, JB | 2 |
| Bakalara, N | 1 |
| Fromager, B | 1 |
| Correa-Basurto, J | 3 |
| Kukal, S | 3 |
| Bora, S | 3 |
| Kanojia, N | 3 |
| Singh, P | 3 |
| Paul, PR | 3 |
| Rawat, C | 3 |
| Sagar, S | 3 |
| Bhatraju, NK | 3 |
| Grewal, GK | 3 |
| Singh, A | 3 |
| Kukreti, S | 3 |
| Satyamoorthy, K | 3 |
| Kukreti, R | 3 |
| Meschi, M | 1 |
| Khorsandi, K | 1 |
| Kianmehr, Z | 1 |
| Awchi, M | 1 |
| Singh, KD | 1 |
| Dill, PE | 1 |
| Frey, U | 1 |
| Datta, AN | 1 |
| Sinues, P | 1 |
| Mendoza-Figueroa, HL | 1 |
| Fernández-Pomares, C | 1 |
| Zhang, S | 1 |
| Tang, Z | 1 |
| Qing, B | 1 |
| Tang, R | 1 |
| Duan, Q | 1 |
| Ding, S | 1 |
| Deng, D | 1 |
| Laengle, J | 1 |
| Kabiljo, J | 1 |
| Hunter, L | 1 |
| Homola, J | 1 |
| Prodinger, S | 1 |
| Egger, G | 1 |
| Bergmann, M | 1 |
| Injinari, N | 1 |
| Amini-Farsani, Z | 1 |
| Yadollahi-Farsani, M | 1 |
| Teimori, H | 1 |
| Ari, F | 2 |
| Napieralski, R | 1 |
| Akgun, O | 1 |
| Magdolen, V | 1 |
| Ulukaya, E | 2 |
| Tian, Y | 1 |
| Liu, G | 1 |
| Wang, H | 1 |
| Tian, Z | 1 |
| Cai, Z | 1 |
| Zhang, F | 1 |
| Luo, Y | 1 |
| Wang, S | 1 |
| Guo, G | 1 |
| Wang, X | 4 |
| Powell, S | 1 |
| Feng, Z | 1 |
| Tarasenko, N | 1 |
| Chekroun-Setti, H | 1 |
| Nudelman, A | 1 |
| Rephaeli, A | 1 |
| Aztopal, N | 1 |
| Erkisa, M | 1 |
| Erturk, E | 1 |
| Tokullugil, AH | 1 |
| Barneh, F | 1 |
| Salimi, M | 1 |
| Goshadrou, F | 1 |
| Ashtiani, M | 1 |
| Mirzaie, M | 1 |
| Zali, H | 1 |
| Jafari, M | 1 |
| Heers, H | 1 |
| Stanislaw, J | 1 |
| Harrelson, J | 1 |
| Lee, MW | 1 |
| Zhou, X | 1 |
| Li, Z | 1 |
| Jiang, G | 2 |
| Shan, C | 1 |
| Liu, S | 1 |
| Cruickshanks, N | 2 |
| Hamed, HA | 1 |
| Booth, L | 2 |
| Tavallai, S | 1 |
| Syed, J | 1 |
| Sajithlal, GB | 1 |
| Grant, S | 2 |
| Poklepovic, A | 2 |
| Dent, P | 2 |
| Jafary, H | 1 |
| Ahmadian, S | 1 |
| Soleimani, M | 1 |
| Roberts, JL | 1 |
| Conley, A | 1 |
| Ridder, T | 1 |
| Tanaka, H | 1 |
| Jotoku, H | 1 |
| Takasaki, M | 1 |
| Ibayashi, Y | 1 |
| Watanabe, K | 1 |
| Takahashi, M | 1 |
| Tong, XH | 1 |
| Zheng, C | 2 |
| Jiang, GJ | 1 |
| Dong, SY | 1 |
| Mawatari, T | 1 |
| Ninomiya, I | 1 |
| Inokuchi, M | 1 |
| Harada, S | 1 |
| Hayashi, H | 1 |
| Oyama, K | 1 |
| Makino, I | 1 |
| Nakagawara, H | 1 |
| Miyashita, T | 1 |
| Tajima, H | 1 |
| Takamura, H | 1 |
| Fushida, S | 1 |
| Ohta, T | 1 |
| Terranova-Barberio, M | 1 |
| Roca, MS | 1 |
| Zotti, AI | 1 |
| Leone, A | 1 |
| Bruzzese, F | 1 |
| Vitagliano, C | 1 |
| Scogliamiglio, G | 1 |
| Russo, D | 1 |
| D'Angelo, G | 1 |
| Franco, R | 1 |
| Budillon, A | 1 |
| Di Gennaro, E | 1 |
| Prestegui-Martel, B | 1 |
| Bermúdez-Lugo, JA | 1 |
| Chávez-Blanco, A | 2 |
| Dueñas-González, A | 2 |
| García-Sánchez, JR | 1 |
| Pérez-González, OA | 1 |
| Padilla-Martínez, II | 1 |
| Fragoso-Vázquez, MJ | 1 |
| Mendieta-Wejebe, JE | 1 |
| Correa-Basurto, AM | 1 |
| Méndez-Luna, D | 1 |
| Trujillo-Ferrara, J | 1 |
| Hilakivi-Clarke, L | 1 |
| Wärri, A | 1 |
| Bouker, KB | 1 |
| Zhang, X | 1 |
| Cook, KL | 1 |
| Jin, L | 1 |
| Zwart, A | 1 |
| Nguyen, N | 1 |
| Hu, R | 1 |
| Cruz, MI | 1 |
| de Assis, S | 1 |
| Xuan, J | 1 |
| Wang, Y | 1 |
| Wehrenberg, B | 1 |
| Clarke, R | 1 |
| Travaglini, L | 1 |
| Vian, L | 1 |
| Billi, M | 1 |
| Grignani, F | 1 |
| Nervi, C | 1 |
| Arakawa, Y | 1 |
| Saito, S | 1 |
| Yamada, H | 1 |
| Aiba, K | 1 |
| Fortunati, N | 2 |
| Bertino, S | 2 |
| Costantino, L | 2 |
| De Bortoli, M | 1 |
| Compagnone, A | 1 |
| Bandino, A | 1 |
| Catalano, MG | 2 |
| Boccuzzi, G | 2 |
| Yamamoto, M | 1 |
| Ito, T | 1 |
| Shimizu, T | 1 |
| Ishida, T | 1 |
| Semba, K | 1 |
| Watanabe, S | 1 |
| Yamaguchi, N | 1 |
| Inoue, J | 1 |
| Thomas, S | 1 |
| Thurn, KT | 1 |
| Biçaku, E | 3 |
| Marchion, DC | 3 |
| Münster, PN | 3 |
| Cohen, AL | 2 |
| Soldi, R | 2 |
| Zhang, H | 1 |
| Gustafson, AM | 1 |
| Wilcox, R | 1 |
| Welm, BE | 1 |
| Chang, JT | 1 |
| Johnson, E | 1 |
| Spira, A | 1 |
| Jeffrey, SS | 1 |
| Bild, AH | 2 |
| Zhang, L | 1 |
| Wang, G | 1 |
| Wang, L | 1 |
| Song, C | 1 |
| Leng, Y | 1 |
| Kang, J | 1 |
| Vesuna, F | 1 |
| Lisok, A | 1 |
| Kimble, B | 1 |
| Domek, J | 1 |
| Kato, Y | 1 |
| van der Groep, P | 1 |
| Artemov, D | 1 |
| Kowalski, J | 1 |
| Carraway, H | 1 |
| van Diest, P | 1 |
| Raman, V | 1 |
| Cheng, L | 1 |
| Sun, Y | 1 |
| Moos, PJ | 1 |
| Li, GF | 1 |
| Qian, TL | 1 |
| Li, GS | 1 |
| Yang, CX | 1 |
| Qin, M | 1 |
| Huang, J | 1 |
| Sun, M | 1 |
| Han, YQ | 1 |
| Debeb, BG | 1 |
| Lacerda, L | 1 |
| Xu, W | 1 |
| Larson, R | 1 |
| Solley, T | 1 |
| Atkinson, R | 1 |
| Sulman, EP | 1 |
| Ueno, NT | 1 |
| Krishnamurthy, S | 1 |
| Reuben, JM | 1 |
| Buchholz, TA | 1 |
| Woodward, WA | 1 |
| Bianco, C | 1 |
| Castro, NP | 1 |
| Baraty, C | 1 |
| Rollman, K | 1 |
| Held, N | 1 |
| Rangel, MC | 1 |
| Karasawa, H | 1 |
| Gonzales, M | 1 |
| Strizzi, L | 1 |
| Salomon, DS | 1 |
| Dong, S | 1 |
| Tong, X | 1 |
| Han, X | 1 |
| Olsen, CM | 1 |
| Meussen-Elholm, ET | 1 |
| Røste, LS | 1 |
| Taubøll, E | 1 |
| Mongan, NP | 1 |
| Gudas, LJ | 1 |
| Daud, AI | 2 |
| Sullivan, DM | 2 |
| Reid, G | 1 |
| Métivier, R | 1 |
| Lin, CY | 1 |
| Denger, S | 1 |
| Ibberson, D | 1 |
| Ivacevic, T | 1 |
| Brand, H | 1 |
| Benes, V | 1 |
| Liu, ET | 1 |
| Gannon, F | 1 |
| Arce, C | 1 |
| Pérez-Plasencia, C | 1 |
| González-Fierro, A | 1 |
| de la Cruz-Hernández, E | 1 |
| Revilla-Vázquez, A | 1 |
| Trejo-Becerril, C | 1 |
| Pérez-Cárdenas, E | 1 |
| Taja-Chayeb, L | 1 |
| Bargallo, E | 1 |
| Villarreal, P | 1 |
| Ramírez, T | 1 |
| Vela, T | 1 |
| Candelaria, M | 1 |
| Camargo, MF | 1 |
| Robles, E | 1 |
| Hodges-Gallagher, L | 1 |
| Valentine, CD | 1 |
| Bader, SE | 1 |
| Kushner, PJ | 1 |
| Jawed, S | 1 |
| Kim, B | 1 |
| Ottenhof, T | 1 |
| Brown, GM | 1 |
| Werstiuk, ES | 1 |
| Niles, LP | 1 |
| Bosco, O | 1 |
| Vercellinatto, I | 1 |
| Stalldecker, GB | 1 |
| Pigni, J | 1 |
| Fuentes, AM | 1 |
| Vegh, I | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Phase I Study of Cytolytic Viral Activation Therapy (CVAT) for Recurrent/Metastatic Nasopharyngeal Carcinoma[NCT02761291] | Phase 1 | 18 participants (Anticipated) | Interventional | 2016-05-31 | Recruiting | ||
| A Phase II Clinical Study of Hydralazine and Valproic Acid in Combination With Neoadjuvant Cytotoxic Chemotherapy in Stage IIB and IIIA Breast Carcinoma[NCT00395655] | Phase 2 | 43 participants | Interventional | 2005-06-30 | Terminated | ||
| "Phase III Clinical Trial: Evaluation of the Combination of TRANSKRIP ® Plus Carboplatin and Paclitaxel as First Line Chemotherapy on Survival of Patients With Recurrent - Persistent Cervical Cancer"[NCT02446652] | Phase 3 | 230 participants (Anticipated) | Interventional | 2015-07-31 | Not yet recruiting | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
2 reviews available for valproic acid and Breast Cancer
| Article | Year |
|---|---|
Valproic acid as an adjunctive therapeutic agent for the treatment of breast cancer.
Topics: Animals; Breast Neoplasms; Drug Synergism; Histone Deacetylase Inhibitors; Humans; Valproic Acid | 2018 |
A pharmacogenomic method for individualized prediction of drug sensitivity.
Topics: Animals; Biomarkers, Tumor; Breast Neoplasms; Cell Line, Tumor; Drug Resistance, Neoplasm; Female; G | 2011 |
2 trials available for valproic acid and Breast Cancer
| Article | Year |
|---|---|
Design and validation of a predictive equation to estimate unbound valproic acid concentration.
Topics: Adult; Anticonvulsants; Breast Neoplasms; Drug Monitoring; Female; Humans; Retrospective Studies; Va | 2023 |
A proof-of-principle study of epigenetic therapy added to neoadjuvant doxorubicin cyclophosphamide for locally advanced breast cancer.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Cyclophosphamide; DNA | 2006 |
A proof-of-principle study of epigenetic therapy added to neoadjuvant doxorubicin cyclophosphamide for locally advanced breast cancer.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Cyclophosphamide; DNA | 2006 |
A proof-of-principle study of epigenetic therapy added to neoadjuvant doxorubicin cyclophosphamide for locally advanced breast cancer.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Cyclophosphamide; DNA | 2006 |
A proof-of-principle study of epigenetic therapy added to neoadjuvant doxorubicin cyclophosphamide for locally advanced breast cancer.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Cyclophosphamide; DNA | 2006 |
44 other studies available for valproic acid and Breast Cancer
| Article | Year |
|---|---|
Untargeted LC-MS/MS Metabolomics Study on the MCF-7 Cell Line in the Presence of Valproic Acid.
Topics: Apoptosis; Breast Neoplasms; Chromatography, Liquid; Female; Histone Deacetylase Inhibitors; Humans; | 2022 |
Valproic Acid-Induced Upregulation of Multidrug Efflux Transporter ABCG2/BCRP via PPAR
Topics: Anticonvulsants; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Trans | 2023 |
Valproic Acid-Induced Upregulation of Multidrug Efflux Transporter ABCG2/BCRP via PPAR
Topics: Anticonvulsants; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Trans | 2023 |
Valproic Acid-Induced Upregulation of Multidrug Efflux Transporter ABCG2/BCRP via PPAR
Topics: Anticonvulsants; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Trans | 2023 |
Valproic Acid-Induced Upregulation of Multidrug Efflux Transporter ABCG2/BCRP via PPAR
Topics: Anticonvulsants; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Trans | 2023 |
Valproic Acid-Induced Upregulation of Multidrug Efflux Transporter ABCG2/BCRP via PPAR
Topics: Anticonvulsants; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Trans | 2023 |
Valproic Acid-Induced Upregulation of Multidrug Efflux Transporter ABCG2/BCRP via PPAR
Topics: Anticonvulsants; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Trans | 2023 |
Valproic Acid-Induced Upregulation of Multidrug Efflux Transporter ABCG2/BCRP via PPAR
Topics: Anticonvulsants; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Trans | 2023 |
Valproic Acid-Induced Upregulation of Multidrug Efflux Transporter ABCG2/BCRP via PPAR
Topics: Anticonvulsants; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Trans | 2023 |
Valproic Acid-Induced Upregulation of Multidrug Efflux Transporter ABCG2/BCRP via PPAR
Topics: Anticonvulsants; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding Cassette Trans | 2023 |
The Effect of Berberine Follow by Blue Light Irradiation and Valproic Acid on the Growth Inhibition of MDA-MB-231 Breast Cancer Cells.
Topics: Apoptosis; Berberine; Breast Neoplasms; Cell Line, Tumor; Female; Humans; Photochemotherapy; Photose | 2023 |
Prediction of systemic free and total valproic acid by off-line analysis of exhaled breath in epileptic children and adolescents.
Topics: Adolescent; Algorithms; Body Fluids; Breast Neoplasms; Breath Tests; Child; Female; Humans; Valproic | 2023 |
Untargeted LC-MS/MS Metabolomics Study of HO-AAVPA and VPA on Breast Cancer Cell Lines.
Topics: Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Chromatography, Liquid; Female; Humans; MCF- | 2023 |
Valproic acid promotes the epithelial-to-mesenchymal transition of breast cancer cells through stabilization of Snail and transcriptional upregulation of Zeb1.
Topics: Breast Neoplasms; Epithelial-Mesenchymal Transition; Humans; MCF-7 Cells; Phosphorylation; Protein S | 2019 |
Histone deacetylase inhibitors valproic acid and vorinostat enhance trastuzumab-mediated antibody-dependent cell-mediated phagocytosis.
Topics: Antibody-Dependent Cell Cytotoxicity; Antineoplastic Agents, Immunological; Antineoplastic Combined | 2020 |
Apoptotic effects of valproic acid on miR-34a, miR-520h and HDAC1 gene in breast cancer.
Topics: Adult; Aged; Aged, 80 and over; Apoptosis; Breast Neoplasms; Cell Line, Tumor; Cell Survival; Female | 2021 |
Epigenetic modulators combination with chemotherapy in breast cancer cells.
Topics: Antimetabolites, Antineoplastic; Breast Neoplasms; Cell Proliferation; Cell Survival; Decitabine; Dr | 2021 |
Valproic acid sensitizes breast cancer cells to hydroxyurea through inhibiting RPA2 hyperphosphorylation-mediated DNA repair pathway.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; DNA; DNA Breaks, Double-S | 2017 |
Comparison of the anticancer properties of a novel valproic acid prodrug to leading histone deacetylase inhibitors.
Topics: Antineoplastic Agents; Brain Neoplasms; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell | 2018 |
Valproic acid, a histone deacetylase inhibitor, induces apoptosis in breast cancer stem cells.
Topics: Acetylation; Apoptosis; Breast Neoplasms; Caspase 3; Caspase 7; Cell Line, Tumor; Cell Proliferation | 2018 |
Valproic acid inhibits the protective effects of stromal cells against chemotherapy in breast cancer: Insights from proteomics and systems biology.
Topics: Breast Neoplasms; Cell Line, Tumor; Doxorubicin; Female; Humans; Mesenchymal Stem Cells; NF-kappa B; | 2018 |
Metabolomics reveals the effect of valproic acid on MCF-7 and MDA-MB-231 cells.
Topics: Breast Neoplasms; Cell Line, Tumor; Chromatography, Liquid; Histone Deacetylase Inhibitors; Humans; | 2020 |
Histone deacetylase inhibitors restore toxic BH3 domain protein expression in anoikis-resistant mammary and brain cancer stem cells, thereby enhancing the response to anti-ERBB1/ERBB2 therapy.
Topics: Animals; Anoikis; Antineoplastic Agents, Hormonal; Apoptosis Regulatory Proteins; bcl-2 Homologous A | 2013 |
The enhanced apoptosis and antiproliferative response to combined treatment with valproate and nicotinamide in MCF-7 breast cancer cells.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Blotting, Western; Breast Neoplasms; Cell | 2014 |
HDAC inhibitors enhance the lethality of low dose salinomycin in parental and stem-like GBM cells.
Topics: Antineoplastic Agents; Apoptosis; Autophagy; Breast Neoplasms; Cell Line, Tumor; Drug Synergism; Fem | 2014 |
[Effect of capecitabine therapy on the blood levels of antiepileptic drugs - report of two cases].
Topics: Anticonvulsants; Antimetabolites, Antineoplastic; Brain Neoplasms; Breast Neoplasms; Capecitabine; D | 2014 |
[Sodium valproate enhances doxorubicin cytotoxicity in breast cancer cells in vitro].
Topics: Apoptosis; Breast Neoplasms; Cell Line, Tumor; Cell Survival; Connexin 43; Doxorubicin; Drug Synergi | 2015 |
Valproic acid inhibits proliferation of HER2-expressing breast cancer cells by inducing cell cycle arrest and apoptosis through Hsp70 acetylation.
Topics: Acetylation; Apoptosis; Blotting, Western; Breast Neoplasms; Cell Cycle Checkpoints; Cell Line, Tumo | 2015 |
Valproic acid potentiates the anticancer activity of capecitabine in vitro and in vivo in breast cancer models via induction of thymidine phosphorylase expression.
Topics: Animals; Anticonvulsants; Antimetabolites, Antineoplastic; Apoptosis; Blotting, Western; Breast Neop | 2016 |
N-(2-hydroxyphenyl)-2-propylpentanamide, a valproic acid aryl derivative designed in silico with improved anti-proliferative activity in HeLa, rhabdomyosarcoma and breast cancer cells.
Topics: Amides; Antineoplastic Agents; Breast Neoplasms; Cell Proliferation; Computer Simulation; Dose-Respo | 2016 |
Effects of In Utero Exposure to Ethinyl Estradiol on Tamoxifen Resistance and Breast Cancer Recurrence in a Preclinical Model.
Topics: 9,10-Dimethyl-1,2-benzanthracene; Adenovirus E1A Proteins; Animals; Antineoplastic Combined Chemothe | 2017 |
Epigenetic reprogramming of breast cancer cells by valproic acid occurs regardless of estrogen receptor status.
Topics: Acetylation; Apoptosis; Breast Neoplasms; Cell Cycle Proteins; Cell Line, Tumor; Cell Proliferation; | 2009 |
Simultaneous treatment with camptothecin and valproic acid suppresses induction of Bcl-X(L) and promotes apoptosis of MCF-7 breast cancer cells.
Topics: Apoptosis; bcl-X Protein; Breast Neoplasms; Camptothecin; Caspase 3; Cell Cycle; Cell Line, Tumor; D | 2009 |
Valproic acid restores ER alpha and antiestrogen sensitivity to ER alpha-negative breast cancer cells.
Topics: Animals; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Enzyme Inhibitors; Estradiol; Estro | 2010 |
Epigenetic alteration of the NF-κB-inducing kinase (NIK) gene is involved in enhanced NIK expression in basal-like breast cancer.
Topics: Acetylation; Azacitidine; Blotting, Western; Breast Neoplasms; Cell Line; Cell Line, Tumor; CpG Isla | 2010 |
Addition of a histone deacetylase inhibitor redirects tamoxifen-treated breast cancer cells into apoptosis, which is opposed by the induction of autophagy.
Topics: Apoptosis; Apoptosis Regulatory Proteins; Autophagy; Beclin-1; Breast Neoplasms; Cell Line, Tumor; D | 2011 |
VPA inhibits breast cancer cell migration by specifically targeting HDAC2 and down-regulating Survivin.
Topics: Antineoplastic Agents; Breast Neoplasms; Cell Line, Tumor; Cell Movement; Cell Survival; Down-Regula | 2012 |
Twist contributes to hormone resistance in breast cancer by downregulating estrogen receptor-α.
Topics: Acetylation; Animals; Antineoplastic Agents; Azacitidine; Breast Neoplasms; Capillary Permeability; | 2012 |
A genomic approach to predict synergistic combinations for breast cancer treatment.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Cell Cycle; Cell Line, Tumor; Cycl | 2013 |
Sodium valproate inhibits MDA-MB-231 breast cancer cell migration by upregulating NM23H1 expression.
Topics: Breast Neoplasms; Cell Line, Tumor; Cell Movement; Enzyme Inhibitors; Female; Gene Expression Regula | 2012 |
Histone deacetylase inhibitors stimulate dedifferentiation of human breast cancer cells through WNT/β-catenin signaling.
Topics: Aldehyde Dehydrogenase; Animals; Antineoplastic Agents; Breast Neoplasms; Cell Dedifferentiation; Ce | 2012 |
Regulation of human Cripto-1 expression by nuclear receptors and DNA promoter methylation in human embryonal and breast cancer cells.
Topics: Azacitidine; Binding Sites; Breast Neoplasms; Carcinoma, Ductal, Breast; Carcinoma, Embryonal; Cell | 2013 |
[Functional enhancement of gap junction by valproate acid sodium in breast cancer cells and the mechanism].
Topics: Breast Neoplasms; Cell Communication; Cell Line, Tumor; Connexin 43; Female; Gap Junctions; Humans; | 2013 |
Antiepileptic drugs inhibit cell growth in the human breast cancer cell line MCF7.
Topics: Anticonvulsants; Breast Neoplasms; Cell Division; Cell Line, Tumor; Drug Screening Assays, Antitumor | 2004 |
Valproic acid, in combination with all-trans retinoic acid and 5-aza-2'-deoxycytidine, restores expression of silenced RARbeta2 in breast cancer cells.
Topics: Azacitidine; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Chromatin Immunoprecipitation; | 2005 |
Valproic acid alters chromatin structure by regulation of chromatin modulation proteins.
Topics: Acetylation; Animals; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Cell Growth | 2005 |
Multiple mechanisms induce transcriptional silencing of a subset of genes, including oestrogen receptor alpha, in response to deacetylase inhibition by valproic acid and trichostatin A.
Topics: Base Sequence; Breast Neoplasms; Cell Line, Tumor; DNA Primers; Enzyme Inhibitors; Estrogen Receptor | 2005 |
In vivo synergy between topoisomerase II and histone deacetylase inhibitors: predictive correlates.
Topics: Acetylation; Animals; Breast Neoplasms; Cell Line, Tumor; Chromatin; Comet Assay; Enzyme Inhibitors; | 2005 |
Inhibition of histone deacetylase enhances the anti-proliferative action of antiestrogens on breast cancer cells and blocks tamoxifen-induced proliferation of uterine cells.
Topics: Aromatase; Breast Neoplasms; Cell Line; Cell Proliferation; Enzyme Inhibitors; Estrogen Antagonists; | 2007 |
Human melatonin MT1 receptor induction by valproic acid and its effects in combination with melatonin on MCF-7 breast cancer cell proliferation.
Topics: Animals; Anticonvulsants; Apoptosis; Blotting, Western; Breast Neoplasms; Cell Line, Tumor; Cell Pro | 2007 |
Valproic acid is a selective antiproliferative agent in estrogen-sensitive breast cancer cells.
Topics: Antineoplastic Agents; Apoptosis; bcl-2 Homologous Antagonist-Killer Protein; Breast Neoplasms; Casp | 2008 |
Prolactin response to dopamine and valproate administration in breast cancer patients.
Topics: Adult; Breast Neoplasms; Dopamine; Female; Humans; Prolactin; Time Factors; Valproic Acid | 1989 |