sulforaphane has been researched along with Breast Cancer in 72 studies
sulforaphane: from Cardaria draba L.
sulforaphane : An isothiocyanate having a 4-(methylsulfinyl)butyl group attached to the nitrogen.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Breast cancer cell lines MCF-10, MCF-7 and BT-474 expressing various levels of HER2 were examined for their response to treatment with sulforaphane (SLFN), metformin (MTFN), Nano-MTFN or combinations." | 7.96 | Co-Treatment with Sulforaphane and Nano-Metformin Molecules Accelerates Apoptosis in HER2+ Breast Cancer Cells by Inhibiting Key Molecules. ( Gardaneh, M; Heidari-Keshel, S; Keshandehghan, A; Nikkhah, S; Tahermansouri, H, 2020) |
| "It is relatively unknown how dietary bioactive compound, sulforaphane, in partnership with active vitamin D3, 1,25(OH)2D3, regulates vitamin D-dependent gene expression in breast cancer (BC)." | 7.96 | Histone deacetylase activity and vitamin D-dependent gene expressions in relation to sulforaphane in human breast cancer cells. ( Hossain, S; Liu, Z; Wood, RJ, 2020) |
| "Studies have identified the potential of chemopreventive effects of sulforaphane (SFN); however, the underlying mechanisms of its effect on breast cancer require further elucidation." | 7.91 | Sulforaphane Decrease of SERTAD1 Expression Triggers G1/S Arrest in Breast Cancer Cells. ( Cheng, AC; Hsu, YC; Hung, CM; Shen, CJ, 2019) |
| " Our recent discoveries of the epigenetic effects of clofarabine (2'-deoxyadenosine analogue, antileukaemic drug) and clofarabine-based combinations with dietary bioactive compounds in breast cancer cells led us to look for more DNA methylation targets of these cancer-preventive agents." | 7.88 | Inhibition of breast cancer cell growth by the combination of clofarabine and sulforaphane involves epigenetically mediated CDKN2A upregulation. ( Fabianowska-Majewska, K; Kaufman-Szymczyk, A; Lubecka, K, 2018) |
| "To study the underlying mechanisms of sulforaphane, a natural histone deacetylase (HDAC) inhibitor, in inhibiting triple negative breast cancer cells growth and the therapeutic effects of combination of sulforaphane and doxorubicin in TNBC treatment." | 7.88 | Sulforaphane induces autophagy by inhibition of HDAC6-mediated PTEN activation in triple negative breast cancer cells. ( Cao, C; Huang, Y; Li, X; Liu, Y; Wang, F; Wang, S; Xia, Y; Yang, F, 2018) |
| "In view of the need for new, more effective therapies for the triple negative breast cancer treatment, the aim of the study was to evaluate the anticancer activity and mechanism of action of the sulforaphane and 5-fluorouracil combination in the triple negative breast cancer cell line MDA-MB-231." | 7.88 | Autophagic cell death and premature senescence: New mechanism of 5-fluorouracil and sulforaphane synergistic anticancer effect in MDA-MB-231 triple negative breast cancer cell line. ( Chilmonczyk, Z; Dąbrowska, A; Koronkiewicz, M; Lubelska, K; Matosiuk, D; Mielczarek, L; Milczarek, M; Wiktorska, K, 2018) |
| " The aim of this study was to verify whether combinations of lapatinib with one of isothiocyanates (sulforaphane, erucin or sulforaphene), targeting different levels of HER2 signaling pathway, exert stronger cytotoxic effect than therapy targeting the receptor only, using heterogeneous populations consisting of lapatinib-sensitive and lapatinib-resistant breast cancer cells." | 7.85 | Combination of lapatinib with isothiocyanates overcomes drug resistance and inhibits migration of HER2 positive breast cancer cells. ( Herman-Antosiewicz, A; Kaczyńska, A, 2017) |
| " We sought to investigate potential combinatorial effects of epigenetic bioactive botanicals including epigallocatechin-3-gallate (EGCG) in green tea polyphenols (GTPs) and sulforaphane (SFN) in broccoli sprouts (BSp) on neutralizing epigenetic aberrations in estrogen receptor-α (ERα) leading to enhanced anti-hormone therapeutic efficacy in ERα-negative breast cancer." | 7.85 | Combinatorial bioactive botanicals re-sensitize tamoxifen treatment in ER-negative breast cancer via epigenetic reactivation of ERα expression. ( Li, Y; Meeran, SM; Tollefsbol, TO, 2017) |
| "Isothiocyanates act in a synergistic way with 4-hydroxytamoxifen, and co-treatment reduces breast cancer cell viability and clonogenic potential more effectively than treatment with any single agent." | 7.83 | Sensitization of estrogen receptor-positive breast cancer cell lines to 4-hydroxytamoxifen by isothiocyanates present in cruciferous plants. ( Herman-Antosiewicz, A; Pawlik, A; Słomińska-Wojewódzka, M, 2016) |
| "The L-sulforaphane (SFN) component of broccoli sprout showed anticancer activity in several preclinical studies including breast cancer." | 7.81 | Modulating potential of L-sulforaphane in the expression of cytochrome p450 to identify potential targets for breast cancer chemoprevention and therapy using breast cell lines. ( Baer-Dubowska, W; Licznerska, B; Matuszak, I; Murias, M; Szaefer, H, 2015) |
| "The anticancer effects of sulforaphane (SFN), which is found in cruciferous vegetables, were studied on KPL-1 human breast cancer cells in vitro and in vivo." | 7.77 | Sulforaphane inhibits the growth of KPL-1 human breast cancer cells in vitro and suppresses the growth and metastasis of orthotopically transplanted KPL-1 cells in female athymic mice. ( Kanematsu, S; Kimura, A; Kuro, M; Lai, YC; Miki, H; Sasaki, T; Tsubura, A; Uehara, N; Yoshizawa, K; Yuri, T, 2011) |
| "Sulforaphane (1-5 micromol/L) decreased aldehyde dehydrogenase-positive cell population by 65% to 80% in human breast cancer cells (P < 0." | 7.76 | Sulforaphane, a dietary component of broccoli/broccoli sprouts, inhibits breast cancer stem cells. ( Clouthier, SG; Korkaya, H; Lee, HF; Li, Y; Liu, S; Newman, B; Schwartz, SJ; Sun, D; Wicha, MS; Yu, Y; Zhang, T, 2010) |
| "Sulforaphane (SFN) is an organosulfur compound obtained from cruciferous plants, such as broccoli and mustard, and it has the potential to treat breast cancer." | 6.66 | Targets and mechanisms of sulforaphane derivatives obtained from cruciferous plants with special focus on breast cancer - contradictory effects and future perspectives. ( Abiri, A; Afzalipour Khoshkbejari, M; Amanollahi, S; Cho, CH; Jabbarzadeh Kaboli, P; Li, M; Mohammadi, M; Mokhtarian, R; Shen, J; Vazifemand, R; Wu, X; Xiao, Z; Yazdi Sani, S; Zhao, Y, 2020) |
| "Breast cancer is the most prevalent type of cancer among women worldwide." | 6.66 | Breast Cancer Prevention-Is there a Future for Sulforaphane and Its Analogs? ( Kuran, D; Pogorzelska, A; Wiktorska, K, 2020) |
| " This review also highlights the importance of the nanoformulation of such bioactive phytochemicals that could enhance their bioavailability by providing an efficient targeted delivery system with a reduced systemic dose while resulting in a more efficient dosing at the target site." | 6.61 | Combating breast cancer using combination therapy with 3 phytochemicals: Piperine, sulforaphane, and thymoquinone. ( Aumeeruddy, MZ; Mahomoodally, MF, 2019) |
| "Globally, breast cancer is the most common cancer and the second leading cause of cancer-related death among women." | 6.58 | Ellagic acid, sulforaphane, and ursolic acid in the prevention and therapy of breast cancer: current evidence and future perspectives. ( Jaman, MS; Sayeed, MA, 2018) |
| "Sulforaphane (SFN) is an isothiocyanate found in cruciferous vegetables and sodium butyrate (NaB) is a short-chain fatty acid produced by gut microbiota." | 5.72 | Combinatorial epigenetic mechanisms of sulforaphane, genistein and sodium butyrate in breast cancer inhibition. ( Sharma, M; Tollefsbol, TO, 2022) |
| "Results showed that Breast cancer cells treated with SFN showed reduced cell proliferation, decreased cell activity, increased apoptosis ratio, and inhibited gene expression and protein phosphorylation of MMP-9 as well as gene expression of NF-κB (P < 0." | 5.72 | Cauliflower bioactive compound sulforaphane inhibits breast cancer development by suppressing NF-κB /MMP-9 signaling pathway expression. ( Tong, C; Zhou, M; Zhou, T; Zhuo, M, 2022) |
| "Estrogen receptor (ER) positive breast cancer is frequently sensitive to endocrine therapy." | 5.56 | Targeting STAT3 signaling using stabilised sulforaphane (SFX-01) inhibits endocrine resistant stem-like cells in ER-positive breast cancer. ( Alferez, D; Andò, S; Chiodo, C; Clarke, RB; Conole, D; Eyre, R; Howell, SJ; Kohler, B; Lanzino, M; Lovell, S; Marangoni, E; Moreira, T; Morisset, L; Santiago-Gómez, A; Sarmiento-Castro, A; Simões, BM; Sims, AH; Spence, K; Tate, EW, 2020) |
| "Sulforaphane (SFN) is a compound derived from cruciferous plants shown to be effective in cancer prevention and suppression." | 5.56 | Co-administration of sulforaphane and doxorubicin attenuates breast cancer growth by preventing the accumulation of myeloid-derived suppressor cells. ( Chen, H; Huang, L; Liu, S; Rong, Y; Song, X; Wang, F; Yi, K; Yuan, C; Zhang, W, 2020) |
| "Tamoxifen has been considered as the gold line therapy for estrogen receptor positive breast cancer." | 5.51 | Tamoxifen and Sulphoraphane for the breast cancer management: A synergistic nanomedicine approach. ( Kohli, K; Mangla, B; Neupane, YR; Singh, A, 2019) |
| " Results of studies in a rat orthotopic breast cancer model indicated that SFN enhanced the efficacy of DOX in regression of tumor growth, and that the DOX dosage required to treat the tumor could be reduced when SFN was administered concomitantly." | 5.48 | Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model. ( Awasthi, S; Beneš, H; Boerma, M; Bose, C; Hauer-Jensen, M; Sharma, R; Singh, SP, 2018) |
| "We propose SFN + WA-induced breast cancer cell death is attributed, in part, to epigenetic modifications that result in the modulated expression of key genes responsible for the regulation of cancer cell senescence." | 5.48 | Withaferin A and sulforaphane regulate breast cancer cell cycle progression through epigenetic mechanisms. ( Nozell, S; Paul, B; Rajbhandari, R; Royston, KJ; Tollefsbol, TO, 2018) |
| "Sulforaphane is a small molecule isothiocyanate which exhibits anticancer potential, yet its biological targets remain poorly understood." | 5.46 | Competition-based, quantitative chemical proteomics in breast cancer cells identifies new target profiles for sulforaphane. ( Clulow, JA; Jones, LH; Kalesh, KA; Lanyon-Hogg, T; Storck, EM; Tate, EW, 2017) |
| "Nearly 25% of all breast cancer is characterized by overexpression of HER2 (human epidermal growth factor receptor 2) which leads to overactivation of prosurvival signal transduction pathways, especially through Akt-mTOR-S6K kinases, and results in enhanced proliferation, migration, induction of angiogenesis, and apoptosis inhibition." | 5.42 | Sensitization of HER2 Positive Breast Cancer Cells to Lapatinib Using Plants-Derived Isothiocyanates. ( Herman-Antosiewicz, A; Kaczyńska, A; Świerczyńska, J, 2015) |
| "Four different breast cancer cell lines were used: MDA MB 231, MCF-7, SKBR-3 and MDA MB 468." | 5.39 | Sulforaphane inhibits growth of phenotypically different breast cancer cells. ( Antosiewicz, J; Herman-Antosiewicz, A; Kaczyńska, A; Pawlik, A; Wiczk, A, 2013) |
| "Sulforaphane treatment inhibited cell growth, induced a G(2)-M cell cycle block, increased expression of cyclin B1, and induced oligonucleosomal DNA fragmentation in the four human breast cancer cell lines examined, MDA-MB-231, MDA-MB-468, MCF-7, and T47D cells." | 5.34 | Sulforaphane induces cell type-specific apoptosis in human breast cancer cell lines. ( Davidson, NE; Pledgie-Tracy, A; Sobolewski, MD, 2007) |
| "Sulforaphane is an antioxidant and a potent stimulator of natural detoxifying enzyme and associated with lowered risk of cancer that is associated with the consumption of cruciferous vegetables." | 5.34 | Efficacy of sulforaphane is mediated by p38 MAP kinase and caspase-7 activations in ER-positive and COX-2-expressed human breast cancer cells. ( Ahn, NS; Hwang, JW; Jo, EH; Kang, KS; Kim, SH; Lee, YS; Park, JS, 2007) |
| "Sulforaphane is a chemical found in cruciferous vegetables such as broccoli, sprouts and kale." | 5.32 | Sulforaphane halts breast cancer cell growth. ( Johnston, N, 2004) |
| "Breast cancer cell lines MCF-10, MCF-7 and BT-474 expressing various levels of HER2 were examined for their response to treatment with sulforaphane (SLFN), metformin (MTFN), Nano-MTFN or combinations." | 3.96 | Co-Treatment with Sulforaphane and Nano-Metformin Molecules Accelerates Apoptosis in HER2+ Breast Cancer Cells by Inhibiting Key Molecules. ( Gardaneh, M; Heidari-Keshel, S; Keshandehghan, A; Nikkhah, S; Tahermansouri, H, 2020) |
| "It is relatively unknown how dietary bioactive compound, sulforaphane, in partnership with active vitamin D3, 1,25(OH)2D3, regulates vitamin D-dependent gene expression in breast cancer (BC)." | 3.96 | Histone deacetylase activity and vitamin D-dependent gene expressions in relation to sulforaphane in human breast cancer cells. ( Hossain, S; Liu, Z; Wood, RJ, 2020) |
| "Studies have identified the potential of chemopreventive effects of sulforaphane (SFN); however, the underlying mechanisms of its effect on breast cancer require further elucidation." | 3.91 | Sulforaphane Decrease of SERTAD1 Expression Triggers G1/S Arrest in Breast Cancer Cells. ( Cheng, AC; Hsu, YC; Hung, CM; Shen, CJ, 2019) |
| " Our recent discoveries of the epigenetic effects of clofarabine (2'-deoxyadenosine analogue, antileukaemic drug) and clofarabine-based combinations with dietary bioactive compounds in breast cancer cells led us to look for more DNA methylation targets of these cancer-preventive agents." | 3.88 | Inhibition of breast cancer cell growth by the combination of clofarabine and sulforaphane involves epigenetically mediated CDKN2A upregulation. ( Fabianowska-Majewska, K; Kaufman-Szymczyk, A; Lubecka, K, 2018) |
| "To study the underlying mechanisms of sulforaphane, a natural histone deacetylase (HDAC) inhibitor, in inhibiting triple negative breast cancer cells growth and the therapeutic effects of combination of sulforaphane and doxorubicin in TNBC treatment." | 3.88 | Sulforaphane induces autophagy by inhibition of HDAC6-mediated PTEN activation in triple negative breast cancer cells. ( Cao, C; Huang, Y; Li, X; Liu, Y; Wang, F; Wang, S; Xia, Y; Yang, F, 2018) |
| "In view of the need for new, more effective therapies for the triple negative breast cancer treatment, the aim of the study was to evaluate the anticancer activity and mechanism of action of the sulforaphane and 5-fluorouracil combination in the triple negative breast cancer cell line MDA-MB-231." | 3.88 | Autophagic cell death and premature senescence: New mechanism of 5-fluorouracil and sulforaphane synergistic anticancer effect in MDA-MB-231 triple negative breast cancer cell line. ( Chilmonczyk, Z; Dąbrowska, A; Koronkiewicz, M; Lubelska, K; Matosiuk, D; Mielczarek, L; Milczarek, M; Wiktorska, K, 2018) |
| ", sulforaphane (SFN), ursolic acid (UA) and betulinic acid (BA) on nucleolar state were investigated in breast cancer cell lines of different receptor status, namely MCF-7, MDA-MB-231 and SK-BR-3 cells." | 3.85 | Phytochemical-induced nucleolar stress results in the inhibition of breast cancer cell proliferation. ( Adamczyk-Grochala, J; Bednarz, D; Lewinska, A; Wnuk, M, 2017) |
| " The aim of this study was to verify whether combinations of lapatinib with one of isothiocyanates (sulforaphane, erucin or sulforaphene), targeting different levels of HER2 signaling pathway, exert stronger cytotoxic effect than therapy targeting the receptor only, using heterogeneous populations consisting of lapatinib-sensitive and lapatinib-resistant breast cancer cells." | 3.85 | Combination of lapatinib with isothiocyanates overcomes drug resistance and inhibits migration of HER2 positive breast cancer cells. ( Herman-Antosiewicz, A; Kaczyńska, A, 2017) |
| " We sought to investigate potential combinatorial effects of epigenetic bioactive botanicals including epigallocatechin-3-gallate (EGCG) in green tea polyphenols (GTPs) and sulforaphane (SFN) in broccoli sprouts (BSp) on neutralizing epigenetic aberrations in estrogen receptor-α (ERα) leading to enhanced anti-hormone therapeutic efficacy in ERα-negative breast cancer." | 3.85 | Combinatorial bioactive botanicals re-sensitize tamoxifen treatment in ER-negative breast cancer via epigenetic reactivation of ERα expression. ( Li, Y; Meeran, SM; Tollefsbol, TO, 2017) |
| "Isothiocyanates act in a synergistic way with 4-hydroxytamoxifen, and co-treatment reduces breast cancer cell viability and clonogenic potential more effectively than treatment with any single agent." | 3.83 | Sensitization of estrogen receptor-positive breast cancer cell lines to 4-hydroxytamoxifen by isothiocyanates present in cruciferous plants. ( Herman-Antosiewicz, A; Pawlik, A; Słomińska-Wojewódzka, M, 2016) |
| "Combined treatment with epigallocatechin-3-gallate in GTPs and sulforaphane in BSp resulted in a synergistic inhibition of breast cancer cellular growth." | 3.83 | Combinatorial epigenetic mechanisms and efficacy of early breast cancer inhibition by nutritive botanicals. ( Buckhaults, P; Cui, X; Li, Y; Tollefsbol, TO, 2016) |
| "The L-sulforaphane (SFN) component of broccoli sprout showed anticancer activity in several preclinical studies including breast cancer." | 3.81 | Modulating potential of L-sulforaphane in the expression of cytochrome p450 to identify potential targets for breast cancer chemoprevention and therapy using breast cell lines. ( Baer-Dubowska, W; Licznerska, B; Matuszak, I; Murias, M; Szaefer, H, 2015) |
| " In this study we investigated the crosstalk among NRF2, AHR and ERα in MCF-7 breast cancer cells treated with the NRF2 activator sulforaphane (SFN), a dual AHR and ERα activator, 3,3'-diindolylmethane (DIM), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 17β-estradiol (E2)." | 3.79 | The aryl hydrocarbon receptor and estrogen receptor alpha differentially modulate nuclear factor erythroid-2-related factor 2 transactivation in MCF-7 breast cancer cells. ( Lo, R; Matthews, J, 2013) |
| "The anticancer effects of sulforaphane (SFN), which is found in cruciferous vegetables, were studied on KPL-1 human breast cancer cells in vitro and in vivo." | 3.77 | Sulforaphane inhibits the growth of KPL-1 human breast cancer cells in vitro and suppresses the growth and metastasis of orthotopically transplanted KPL-1 cells in female athymic mice. ( Kanematsu, S; Kimura, A; Kuro, M; Lai, YC; Miki, H; Sasaki, T; Tsubura, A; Uehara, N; Yoshizawa, K; Yuri, T, 2011) |
| "Sulforaphane (1-5 micromol/L) decreased aldehyde dehydrogenase-positive cell population by 65% to 80% in human breast cancer cells (P < 0." | 3.76 | Sulforaphane, a dietary component of broccoli/broccoli sprouts, inhibits breast cancer stem cells. ( Clouthier, SG; Korkaya, H; Lee, HF; Li, Y; Liu, S; Newman, B; Schwartz, SJ; Sun, D; Wicha, MS; Yu, Y; Zhang, T, 2010) |
| " In this paper we report our study of the ability of ITCs: sulforaphane and its analogues: isothiocyanate-2-oxohexyl and alyssin, to inhibit CYP1A1 and CYP1A2 enzyme activity induced by the PAHs, anthracene (ANT) and dibenzo[a,h]anthracene (DBA) in human breast cancer cell line Mcf7." | 3.75 | The effect of isothiocyanates on CYP1A1 and CYP1A2 activities induced by polycyclic aromatic hydrocarbons in Mcf7 cells. ( Kasprzycka-Guttman, T; Lubelska, K; Misiewicz-Krzeminska, I; Skupinska, K, 2009) |
| "Human breast cancer cells were used to detect cell viability and epigenetic-related gene expression after treatment with EGCG and/or SFN." | 3.30 | Paternal Combined Botanicals Contribute to the Prevention of Estrogen Receptor-Negative Mammary Cancer in Transgenic Mice. ( Chen, M; Li, S; Tollefsbol, TO; Wu, H, 2023) |
| " Future studies employing larger sample sizes should evaluate alternative dosing and duration regimens to inform dietary SFN strategies in breast cancer chemoprevention." | 2.80 | Sulforaphane Bioavailability and Chemopreventive Activity in Women Scheduled for Breast Biopsy. ( Atwell, LL; Farris, P; Ho, E; Mori, M; Naik, AM; Oh, KY; Shannon, J; Thuillier, P; Vetto, JT; Zhang, Z, 2015) |
| "Breast cancer is the most prevalent type of cancer among women worldwide." | 2.66 | Breast Cancer Prevention-Is there a Future for Sulforaphane and Its Analogs? ( Kuran, D; Pogorzelska, A; Wiktorska, K, 2020) |
| "Sulforaphane (SFN) is an organosulfur compound obtained from cruciferous plants, such as broccoli and mustard, and it has the potential to treat breast cancer." | 2.66 | Targets and mechanisms of sulforaphane derivatives obtained from cruciferous plants with special focus on breast cancer - contradictory effects and future perspectives. ( Abiri, A; Afzalipour Khoshkbejari, M; Amanollahi, S; Cho, CH; Jabbarzadeh Kaboli, P; Li, M; Mohammadi, M; Mokhtarian, R; Shen, J; Vazifemand, R; Wu, X; Xiao, Z; Yazdi Sani, S; Zhao, Y, 2020) |
| " This review also highlights the importance of the nanoformulation of such bioactive phytochemicals that could enhance their bioavailability by providing an efficient targeted delivery system with a reduced systemic dose while resulting in a more efficient dosing at the target site." | 2.61 | Combating breast cancer using combination therapy with 3 phytochemicals: Piperine, sulforaphane, and thymoquinone. ( Aumeeruddy, MZ; Mahomoodally, MF, 2019) |
| "Globally, breast cancer is the most common cancer and the second leading cause of cancer-related death among women." | 2.58 | Ellagic acid, sulforaphane, and ursolic acid in the prevention and therapy of breast cancer: current evidence and future perspectives. ( Jaman, MS; Sayeed, MA, 2018) |
| "Results showed that Breast cancer cells treated with SFN showed reduced cell proliferation, decreased cell activity, increased apoptosis ratio, and inhibited gene expression and protein phosphorylation of MMP-9 as well as gene expression of NF-κB (P < 0." | 1.72 | Cauliflower bioactive compound sulforaphane inhibits breast cancer development by suppressing NF-κB /MMP-9 signaling pathway expression. ( Tong, C; Zhou, M; Zhou, T; Zhuo, M, 2022) |
| "Sulforaphane (SFN) is an isothiocyanate found in cruciferous vegetables and sodium butyrate (NaB) is a short-chain fatty acid produced by gut microbiota." | 1.72 | Combinatorial epigenetic mechanisms of sulforaphane, genistein and sodium butyrate in breast cancer inhibition. ( Sharma, M; Tollefsbol, TO, 2022) |
| "Sulforaphane (SFN) is a compound derived from cruciferous plants shown to be effective in cancer prevention and suppression." | 1.56 | Co-administration of sulforaphane and doxorubicin attenuates breast cancer growth by preventing the accumulation of myeloid-derived suppressor cells. ( Chen, H; Huang, L; Liu, S; Rong, Y; Song, X; Wang, F; Yi, K; Yuan, C; Zhang, W, 2020) |
| "Estrogen receptor (ER) positive breast cancer is frequently sensitive to endocrine therapy." | 1.56 | Targeting STAT3 signaling using stabilised sulforaphane (SFX-01) inhibits endocrine resistant stem-like cells in ER-positive breast cancer. ( Alferez, D; Andò, S; Chiodo, C; Clarke, RB; Conole, D; Eyre, R; Howell, SJ; Kohler, B; Lanzino, M; Lovell, S; Marangoni, E; Moreira, T; Morisset, L; Santiago-Gómez, A; Sarmiento-Castro, A; Simões, BM; Sims, AH; Spence, K; Tate, EW, 2020) |
| "Tamoxifen has been considered as the gold line therapy for estrogen receptor positive breast cancer." | 1.51 | Tamoxifen and Sulphoraphane for the breast cancer management: A synergistic nanomedicine approach. ( Kohli, K; Mangla, B; Neupane, YR; Singh, A, 2019) |
| "Moreover, in an orthotopic breast cancer model, the nanoparticles achieved a significantly higher tumor accumulation and exhibited a more powerful antitumor activity." | 1.51 | Sulforaphane Mediates Glutathione Depletion via Polymeric Nanoparticles to Restore Cisplatin Chemosensitivity. ( Bao, Y; Han, X; Li, Y; Min, H; Nie, G; Qi, S; Qi, Y; Shi, J; Xu, Y; Zhang, Y; Zhao, X, 2019) |
| "We propose SFN + WA-induced breast cancer cell death is attributed, in part, to epigenetic modifications that result in the modulated expression of key genes responsible for the regulation of cancer cell senescence." | 1.48 | Withaferin A and sulforaphane regulate breast cancer cell cycle progression through epigenetic mechanisms. ( Nozell, S; Paul, B; Rajbhandari, R; Royston, KJ; Tollefsbol, TO, 2018) |
| " Results of studies in a rat orthotopic breast cancer model indicated that SFN enhanced the efficacy of DOX in regression of tumor growth, and that the DOX dosage required to treat the tumor could be reduced when SFN was administered concomitantly." | 1.48 | Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model. ( Awasthi, S; Beneš, H; Boerma, M; Bose, C; Hauer-Jensen, M; Sharma, R; Singh, SP, 2018) |
| "Sulforaphane is a small molecule isothiocyanate which exhibits anticancer potential, yet its biological targets remain poorly understood." | 1.46 | Competition-based, quantitative chemical proteomics in breast cancer cells identifies new target profiles for sulforaphane. ( Clulow, JA; Jones, LH; Kalesh, KA; Lanyon-Hogg, T; Storck, EM; Tate, EW, 2017) |
| "Sporadic breast cancer is frequently associated with aberrant DNA methylation patterns that are reversible and responsive to environmental factors, including diet." | 1.42 | Sulforaphane Alone and in Combination with Clofarabine Epigenetically Regulates the Expression of DNA Methylation-Silenced Tumour Suppressor Genes in Human Breast Cancer Cells. ( Cebula-Obrzut, B; Fabianowska-Majewska, K; Kaufman-Szymczyk, A; Lubecka-Pietruszewska, K; Smolewski, P; Stefanska, B, 2015) |
| "Nearly 25% of all breast cancer is characterized by overexpression of HER2 (human epidermal growth factor receptor 2) which leads to overactivation of prosurvival signal transduction pathways, especially through Akt-mTOR-S6K kinases, and results in enhanced proliferation, migration, induction of angiogenesis, and apoptosis inhibition." | 1.42 | Sensitization of HER2 Positive Breast Cancer Cells to Lapatinib Using Plants-Derived Isothiocyanates. ( Herman-Antosiewicz, A; Kaczyńska, A; Świerczyńska, J, 2015) |
| "Pretreatment with sulforaphane significantly attenuated nuclear localization, DNA binding and the transcriptional activity of NF-κB through inhibition of phosphorylation and subsequent degradation of IκBα in MCF-10A cells stimulated with TPA." | 1.40 | Sulforaphane inhibits phorbol ester-stimulated IKK-NF-κB signaling and COX-2 expression in human mammary epithelial cells by targeting NF-κB activating kinase and ERK. ( Cha, YN; Kim, DH; Kim, EH; Kim, HN; Kundu, JK; Lee, MH; Na, HK; Surh, YJ, 2014) |
| "Previously, we found that basal-like ductal carcinoma in situ (DCIS) contains cancer stem-like cells." | 1.40 | Characterization of a stem-like subpopulation in basal-like ductal carcinoma in situ (DCIS) lesions. ( Eades, G; Li, Q; Yao, Y; Zhang, Y; Zhou, Q, 2014) |
| "Four different breast cancer cell lines were used: MDA MB 231, MCF-7, SKBR-3 and MDA MB 468." | 1.39 | Sulforaphane inhibits growth of phenotypically different breast cancer cells. ( Antosiewicz, J; Herman-Antosiewicz, A; Kaczyńska, A; Pawlik, A; Wiczk, A, 2013) |
| "Breast cancer is the most common cancer and the leading cause of cancer death in women." | 1.38 | Bioactive dietary supplements reactivate ER expression in ER-negative breast cancer cells by active chromatin modifications. ( Li, Y; Meeran, SM; Patel, SN; Shukla, S; Tollefsbol, TO, 2012) |
| "These results are not limited to breast cancer cells since the Nrf2 inducer SFN stabilized Nrf2 and inhibited RON expression in carcinoma cells from various tumor types." | 1.37 | Novel function of transcription factor Nrf2 as an inhibitor of RON tyrosine kinase receptor-mediated cancer cell invasion. ( Ammanamanchi, S; Freeman, JW; Krishnegowda, NK; Rogge, J; Thangasamy, A, 2011) |
| "Sulforaphane treatment inhibited cell growth, induced a G(2)-M cell cycle block, increased expression of cyclin B1, and induced oligonucleosomal DNA fragmentation in the four human breast cancer cell lines examined, MDA-MB-231, MDA-MB-468, MCF-7, and T47D cells." | 1.34 | Sulforaphane induces cell type-specific apoptosis in human breast cancer cell lines. ( Davidson, NE; Pledgie-Tracy, A; Sobolewski, MD, 2007) |
| "Sulforaphane is an antioxidant and a potent stimulator of natural detoxifying enzyme and associated with lowered risk of cancer that is associated with the consumption of cruciferous vegetables." | 1.34 | Efficacy of sulforaphane is mediated by p38 MAP kinase and caspase-7 activations in ER-positive and COX-2-expressed human breast cancer cells. ( Ahn, NS; Hwang, JW; Jo, EH; Kang, KS; Kim, SH; Lee, YS; Park, JS, 2007) |
| "Sulforaphane is a chemical found in cruciferous vegetables such as broccoli, sprouts and kale." | 1.32 | Sulforaphane halts breast cancer cell growth. ( Johnston, N, 2004) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 14 (19.44) | 29.6817 |
| 2010's | 47 (65.28) | 24.3611 |
| 2020's | 11 (15.28) | 2.80 |
| Authors | Studies |
|---|---|
| Sharma, M | 1 |
| Tollefsbol, TO | 9 |
| Zhou, T | 1 |
| Zhou, M | 1 |
| Tong, C | 1 |
| Zhuo, M | 1 |
| Li, S | 1 |
| Wu, H | 2 |
| Chen, M | 1 |
| Mangla, B | 1 |
| Neupane, YR | 1 |
| Singh, A | 1 |
| Kohli, K | 1 |
| Keshandehghan, A | 1 |
| Nikkhah, S | 1 |
| Tahermansouri, H | 1 |
| Heidari-Keshel, S | 1 |
| Gardaneh, M | 1 |
| Xu, Y | 1 |
| Han, X | 1 |
| Li, Y | 5 |
| Min, H | 1 |
| Zhao, X | 1 |
| Zhang, Y | 2 |
| Qi, Y | 1 |
| Shi, J | 1 |
| Qi, S | 1 |
| Bao, Y | 2 |
| Nie, G | 1 |
| Jabbarzadeh Kaboli, P | 1 |
| Afzalipour Khoshkbejari, M | 1 |
| Mohammadi, M | 1 |
| Abiri, A | 1 |
| Mokhtarian, R | 1 |
| Vazifemand, R | 1 |
| Amanollahi, S | 1 |
| Yazdi Sani, S | 1 |
| Li, M | 1 |
| Zhao, Y | 1 |
| Wu, X | 1 |
| Shen, J | 1 |
| Cho, CH | 1 |
| Xiao, Z | 1 |
| Hossain, S | 1 |
| Liu, Z | 1 |
| Wood, RJ | 1 |
| Kuran, D | 1 |
| Pogorzelska, A | 1 |
| Wiktorska, K | 2 |
| Simões, BM | 1 |
| Santiago-Gómez, A | 1 |
| Chiodo, C | 1 |
| Moreira, T | 1 |
| Conole, D | 1 |
| Lovell, S | 1 |
| Alferez, D | 1 |
| Eyre, R | 1 |
| Spence, K | 1 |
| Sarmiento-Castro, A | 1 |
| Kohler, B | 1 |
| Morisset, L | 1 |
| Lanzino, M | 1 |
| Andò, S | 1 |
| Marangoni, E | 1 |
| Sims, AH | 1 |
| Tate, EW | 2 |
| Howell, SJ | 1 |
| Clarke, RB | 1 |
| Rong, Y | 1 |
| Huang, L | 1 |
| Yi, K | 1 |
| Chen, H | 1 |
| Liu, S | 2 |
| Zhang, W | 1 |
| Yuan, C | 1 |
| Song, X | 1 |
| Wang, F | 2 |
| Licznerska, B | 2 |
| Szaefer, H | 2 |
| Krajka-Kuźniak, V | 1 |
| Gu, HF | 1 |
| Ren, F | 1 |
| Mao, XY | 1 |
| Du, M | 1 |
| Lewinska, A | 1 |
| Bednarz, D | 1 |
| Adamczyk-Grochala, J | 1 |
| Wnuk, M | 1 |
| Clulow, JA | 1 |
| Storck, EM | 1 |
| Lanyon-Hogg, T | 1 |
| Kalesh, KA | 1 |
| Jones, LH | 1 |
| Royston, KJ | 2 |
| Udayakumar, N | 1 |
| Lewis, K | 1 |
| Meeran, SM | 4 |
| Gianfredi, V | 2 |
| Nucci, D | 2 |
| Vannini, S | 2 |
| Villarini, M | 2 |
| Moretti, M | 2 |
| Bragazzi, NL | 1 |
| Izzotti, A | 1 |
| Milczarek, M | 1 |
| Mielczarek, L | 1 |
| Koronkiewicz, M | 1 |
| Dąbrowska, A | 1 |
| Lubelska, K | 2 |
| Matosiuk, D | 1 |
| Chilmonczyk, Z | 1 |
| Kamal, MM | 1 |
| Nazzal, S | 1 |
| Chirumbolo, S | 1 |
| Bjørklund, G | 1 |
| Huang, J | 1 |
| Tao, C | 1 |
| Yu, Y | 2 |
| Yu, F | 1 |
| Zhang, H | 1 |
| Gao, J | 2 |
| Wang, D | 1 |
| Chen, Y | 1 |
| Zhang, G | 1 |
| Zhou, G | 1 |
| Liu, J | 1 |
| Sun, Z | 1 |
| Sun, D | 2 |
| Zou, H | 1 |
| Xu, H | 1 |
| Lu, Y | 1 |
| Zhong, Y | 1 |
| Bose, C | 1 |
| Awasthi, S | 1 |
| Sharma, R | 1 |
| Beneš, H | 1 |
| Hauer-Jensen, M | 1 |
| Boerma, M | 1 |
| Singh, SP | 1 |
| Cao, C | 2 |
| Vasilatos, SN | 1 |
| Chandran, U | 1 |
| Qin, Y | 1 |
| Wan, Y | 1 |
| Oesterreich, S | 1 |
| Davidson, NE | 2 |
| Huang, Y | 2 |
| Lubecka, K | 1 |
| Kaufman-Szymczyk, A | 2 |
| Fabianowska-Majewska, K | 2 |
| Paul, B | 1 |
| Nozell, S | 1 |
| Rajbhandari, R | 1 |
| Jaman, MS | 1 |
| Sayeed, MA | 1 |
| Yang, F | 1 |
| Liu, Y | 1 |
| Wang, S | 2 |
| Li, X | 1 |
| Xia, Y | 1 |
| Aumeeruddy, MZ | 1 |
| Mahomoodally, MF | 1 |
| Cheng, AC | 1 |
| Shen, CJ | 1 |
| Hung, CM | 1 |
| Hsu, YC | 1 |
| Lo, R | 1 |
| Matthews, J | 1 |
| Li, Q | 2 |
| Xia, J | 1 |
| Yao, Y | 2 |
| Gong, DW | 1 |
| Shi, H | 1 |
| Zhou, Q | 2 |
| Hussain, A | 1 |
| Mohsin, J | 1 |
| Prabhu, SA | 1 |
| Begum, S | 1 |
| Nusri, Qel-A | 1 |
| Harish, G | 1 |
| Javed, E | 1 |
| Khan, MA | 1 |
| Sharma, C | 1 |
| Eades, G | 1 |
| Kim, HN | 1 |
| Kim, DH | 1 |
| Kim, EH | 1 |
| Lee, MH | 1 |
| Kundu, JK | 1 |
| Na, HK | 1 |
| Cha, YN | 1 |
| Surh, YJ | 1 |
| Yager, JD | 1 |
| Matuszak, I | 1 |
| Murias, M | 1 |
| Baer-Dubowska, W | 1 |
| Sinha, S | 1 |
| Shukla, S | 2 |
| Khan, S | 1 |
| Pawlik, A | 2 |
| Słomińska-Wojewódzka, M | 1 |
| Herman-Antosiewicz, A | 4 |
| Kaczyńska, A | 3 |
| Świerczyńska, J | 1 |
| Zhang, Z | 2 |
| Atwell, LL | 2 |
| Farris, PE | 1 |
| Ho, E | 2 |
| Shannon, J | 2 |
| Lubecka-Pietruszewska, K | 1 |
| Stefanska, B | 1 |
| Cebula-Obrzut, B | 1 |
| Smolewski, P | 1 |
| Mori, M | 1 |
| Farris, P | 1 |
| Vetto, JT | 1 |
| Naik, AM | 1 |
| Oh, KY | 1 |
| Thuillier, P | 1 |
| Danafar, H | 1 |
| Sharafi, A | 1 |
| Kheiri Manjili, H | 1 |
| Andalib, S | 1 |
| Buckhaults, P | 1 |
| Cui, X | 1 |
| Ramirez, MC | 1 |
| Singletary, K | 1 |
| Azarenko, O | 1 |
| Okouneva, T | 1 |
| Singletary, KW | 2 |
| Jordan, MA | 1 |
| Wilson, L | 1 |
| Telang, U | 1 |
| Brazeau, DA | 1 |
| Morris, ME | 1 |
| Shabbeer, S | 1 |
| Sobolewski, M | 1 |
| Anchoori, RK | 1 |
| Kachhap, S | 1 |
| Hidalgo, M | 1 |
| Jimeno, A | 1 |
| Davidson, N | 1 |
| Carducci, MA | 1 |
| Khan, SR | 1 |
| Skupinska, K | 1 |
| Misiewicz-Krzeminska, I | 1 |
| Kasprzycka-Guttman, T | 1 |
| Hunakova, L | 1 |
| Sedlakova, O | 1 |
| Cholujova, D | 1 |
| Gronesova, P | 1 |
| Duraj, J | 1 |
| Sedlak, J | 1 |
| Zhang, T | 1 |
| Korkaya, H | 1 |
| Lee, HF | 1 |
| Newman, B | 1 |
| Clouthier, SG | 1 |
| Schwartz, SJ | 1 |
| Wicha, MS | 1 |
| Patel, SN | 2 |
| Jeong, HS | 1 |
| Choi, HY | 1 |
| Lee, ER | 1 |
| Kim, JH | 1 |
| Jeon, K | 1 |
| Lee, HJ | 1 |
| Cho, SG | 1 |
| Kanematsu, S | 2 |
| Uehara, N | 2 |
| Miki, H | 2 |
| Yoshizawa, K | 2 |
| Kawanaka, A | 1 |
| Yuri, T | 2 |
| Tsubura, A | 2 |
| Sasaki, T | 1 |
| Kuro, M | 1 |
| Lai, YC | 1 |
| Kimura, A | 1 |
| Thangasamy, A | 1 |
| Rogge, J | 1 |
| Krishnegowda, NK | 1 |
| Freeman, JW | 1 |
| Ammanamanchi, S | 1 |
| Sakao, K | 1 |
| Singh, SV | 1 |
| Kang, HJ | 1 |
| Hong, YB | 1 |
| Kim, HJ | 1 |
| Wang, A | 1 |
| Bae, I | 1 |
| Sarkar, R | 1 |
| Mukherjee, S | 1 |
| Biswas, J | 1 |
| Roy, M | 1 |
| Wiczk, A | 1 |
| Antosiewicz, J | 1 |
| Jackson, SJ | 1 |
| Johnston, N | 1 |
| Zhang, DD | 1 |
| Lo, SC | 1 |
| Cross, JV | 1 |
| Templeton, DJ | 1 |
| Hannink, M | 1 |
| Wang, W | 1 |
| Howie, AF | 1 |
| Beckett, GJ | 1 |
| Mithen, R | 1 |
| Rose, P | 1 |
| Huang, Q | 1 |
| Ong, CN | 1 |
| Whiteman, M | 1 |
| Pledgie-Tracy, A | 1 |
| Sobolewski, MD | 1 |
| Jo, EH | 1 |
| Kim, SH | 1 |
| Ahn, NS | 1 |
| Park, JS | 1 |
| Hwang, JW | 1 |
| Lee, YS | 1 |
| Kang, KS | 1 |
| Sibhatu, MB | 1 |
| Smitherman, PK | 1 |
| Townsend, AJ | 1 |
| Morrow, CS | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Sulforaphane: A Dietary Histone Deacetylase (HDAC) Inhibitor in Ductal Carcinoma in Situ (DCIS)[NCT00843167] | Phase 2 | 54 participants (Actual) | Interventional | 2009-08-31 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
PBMC HDAC activity was evaluated using the positive control, sodium butyrate.HDAC activity is expressed relative to PBMC protein content and negative control. (NCT00843167)
Timeframe: Baseline and End of Study (up to 8 weeks)
| Intervention | pmol/min/mg protein (Mean) |
|---|---|
| Sulforaphane Supplement | -80.39 |
| Placebo | 27.52 |
Isothiocyante including sulforaphane in micromolar (µM) concentration was measured following standard chemical measurement procedures and divided by the creatinine values in millimolar (mM) concentration. (NCT00843167)
Timeframe: Baseline and end of study (up to 8 weeks)
| Intervention | µM/mM creatinine (Mean) |
|---|---|
| Sulforaphane Supplement | 1.00 |
| Placebo | -0.05 |
For treatment compliance, participants who take >=80% of the prescribed pills will be considered to be treatment-compliant. (NCT00843167)
Timeframe: Baseline and end of study (up to 8 weeks)
| Intervention | participants (Number) |
|---|---|
| Sulforaphane Supplement | 19 |
| Treatment | 16 |
Ki-67 was measured through immunohistochemistry method. A modified H-score was recorded, which involved semi-quantitative assessment of both staining intensity (graded as 1-3 with 1 representing weak staining, 2 moderate staining, and 3 strong staining) and percentage of positive cells. The range of the H-score was 0-300. The maximum score indicates the strongest expression, the minimum score indicates no expression of positive tumor area. (NCT00843167)
Timeframe: Baseline and end of study (up to 8 weeks)
| Intervention | Log 2 (H-score) (Least Squares Mean) | |
|---|---|---|
| Sulforaphane Supplement | Placebo | |
| Benign Tissue; Ki-67 | -1.39 | 0.23 |
| DCIS Tissue; Ki-67 | 0.42 | -0.48 |
| Invasive Ductal Carcinoma Tissue; Ki-67 | 0.98 | 0.28 |
7 reviews available for sulforaphane and Breast Cancer
| Article | Year |
|---|---|
Targets and mechanisms of sulforaphane derivatives obtained from cruciferous plants with special focus on breast cancer - contradictory effects and future perspectives.
Topics: Animals; Brassicaceae; Breast Neoplasms; Female; Humans; Isothiocyanates; Plant Preparations; Sulfox | 2020 |
Breast Cancer Prevention-Is there a Future for Sulforaphane and Its Analogs?
Topics: Animals; Antineoplastic Agents; Brassicaceae; Breast Neoplasms; Chemoprevention; Female; Humans; Iso | 2020 |
In vitro Biological Effects of Sulforaphane (SFN), Epigallocatechin-3-gallate (EGCG), and Curcumin on Breast Cancer Cells: A Systematic Review of the Literature.
Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Breast Neoplasms; Catechin; Cell Cycle; Cell Line, Tum | 2017 |
Sulforaphane and Epigallocatechin Gallate Restore Estrogen Receptor Expression by Modulating Epigenetic Events in the Breast Cancer Cell Line MDA-MB-231: A Systematic Review and Meta-Analysis.
Topics: Anticarcinogenic Agents; Apoptosis; Breast Neoplasms; Catechin; Cell Line, Tumor; Epigenesis, Geneti | 2017 |
Ellagic acid, sulforaphane, and ursolic acid in the prevention and therapy of breast cancer: current evidence and future perspectives.
Topics: Animals; Anticarcinogenic Agents; Antineoplastic Agents, Phytogenic; Antineoplastic Combined Chemoth | 2018 |
Combating breast cancer using combination therapy with 3 phytochemicals: Piperine, sulforaphane, and thymoquinone.
Topics: Alkaloids; Antineoplastic Agents; Benzodioxoles; Benzoquinones; Breast Neoplasms; Cell Line, Tumor; | 2019 |
Mechanisms of estrogen carcinogenesis: The role of E2/E1-quinone metabolites suggests new approaches to preventive intervention--A review.
Topics: Animals; Anticarcinogenic Agents; Breast Neoplasms; Carcinogens; Disease Models, Animal; Estradiol; | 2015 |
3 trials available for sulforaphane and Breast Cancer
| Article | Year |
|---|---|
Paternal Combined Botanicals Contribute to the Prevention of Estrogen Receptor-Negative Mammary Cancer in Transgenic Mice.
Topics: Animals; Antioxidants; Breast Neoplasms; Epigenesis, Genetic; Female; Humans; Male; Mammary Neoplasm | 2023 |
Associations between cruciferous vegetable intake and selected biomarkers among women scheduled for breast biopsies.
Topics: Adult; Aged; Biomarkers; Biopsy; Body Mass Index; Breast Neoplasms; Carcinoma, Intraductal, Noninfil | 2016 |
Sulforaphane Bioavailability and Chemopreventive Activity in Women Scheduled for Breast Biopsy.
Topics: Anticarcinogenic Agents; Biological Availability; Biomarkers, Tumor; Breast Neoplasms; Carcinoma, In | 2015 |
62 other studies available for sulforaphane and Breast Cancer
| Article | Year |
|---|---|
Combinatorial epigenetic mechanisms of sulforaphane, genistein and sodium butyrate in breast cancer inhibition.
Topics: Apoptosis; Breast Neoplasms; Butyric Acid; Cell Line, Tumor; Epigenesis, Genetic; Female; Genistein; | 2022 |
Cauliflower bioactive compound sulforaphane inhibits breast cancer development by suppressing NF-κB /MMP-9 signaling pathway expression.
Topics: Animals; Apoptosis; Brassica; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Female; Humans | 2022 |
Tamoxifen and Sulphoraphane for the breast cancer management: A synergistic nanomedicine approach.
Topics: Animals; Antineoplastic Agents, Hormonal; Antineoplastic Combined Chemotherapy Protocols; Breast Neo | 2019 |
Co-Treatment with Sulforaphane and Nano-Metformin Molecules Accelerates Apoptosis in HER2+ Breast Cancer Cells by Inhibiting Key Molecules.
Topics: Anticarcinogenic Agents; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; beta Catenin; Br | 2020 |
Sulforaphane Mediates Glutathione Depletion via Polymeric Nanoparticles to Restore Cisplatin Chemosensitivity.
Topics: Animals; Antineoplastic Agents; Apoptosis; Breast Neoplasms; Cell Proliferation; Cell Survival; Cisp | 2019 |
Histone deacetylase activity and vitamin D-dependent gene expressions in relation to sulforaphane in human breast cancer cells.
Topics: Breast Neoplasms; Female; Gene Expression; Histone Deacetylases; Humans; Isothiocyanates; Sulfoxides | 2020 |
Targeting STAT3 signaling using stabilised sulforaphane (SFX-01) inhibits endocrine resistant stem-like cells in ER-positive breast cancer.
Topics: Animals; Anticarcinogenic Agents; Breast Neoplasms; Cell Line, Tumor; Drug Resistance, Neoplasm; Fem | 2020 |
Co-administration of sulforaphane and doxorubicin attenuates breast cancer growth by preventing the accumulation of myeloid-derived suppressor cells.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; CD8-Positive T-Lymphocyte | 2020 |
R-sulforaphane modulates the expression profile of AhR, ERα, Nrf2, NQO1, and GSTP in human breast cell lines.
Topics: Anticarcinogenic Agents; Basic Helix-Loop-Helix Transcription Factors; Breast Neoplasms; Cell Line, | 2021 |
Mineralized and GSH-responsive hyaluronic acid based nano-carriers for potentiating repressive effects of sulforaphane on breast cancer stem cells-like properties.
Topics: Animals; Breast Neoplasms; Disulfides; Drug Carriers; Drug Liberation; Female; Glutathione; Humans; | 2021 |
Phytochemical-induced nucleolar stress results in the inhibition of breast cancer cell proliferation.
Topics: Antineoplastic Agents, Phytogenic; Betulinic Acid; Breast Neoplasms; Cell Line, Tumor; Cell Nucleolu | 2017 |
Competition-based, quantitative chemical proteomics in breast cancer cells identifies new target profiles for sulforaphane.
Topics: Anticarcinogenic Agents; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Dose-Response Relat | 2017 |
A Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells.
Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Breast Neoplasms; | 2017 |
Combinatorial bioactive botanicals re-sensitize tamoxifen treatment in ER-negative breast cancer via epigenetic reactivation of ERα expression.
Topics: Animals; Antineoplastic Agents, Hormonal; Breast Neoplasms; Catechin; Cell Line, Tumor; Disease Mode | 2017 |
Autophagic cell death and premature senescence: New mechanism of 5-fluorouracil and sulforaphane synergistic anticancer effect in MDA-MB-231 triple negative breast cancer cell line.
Topics: Antineoplastic Agents; Autophagy; Breast Neoplasms; Cell Line, Tumor; Cell Survival; Drug Synergism; | 2018 |
Novel sulforaphane-enabled self-microemulsifying delivery systems (SFN-SMEDDS) of taxanes: Formulation development and in vitro cytotoxicity against breast cancer cells.
Topics: Antineoplastic Agents; Breast Neoplasms; Cell Line, Tumor; Chemistry, Pharmaceutical; Docetaxel; Dru | 2018 |
Sulforaphane and 5-fluorouracil synergistically inducing autophagy in breast cancer: A possible role for the Nrf2-Keap1-ARE signaling?
Topics: Autophagy; Breast Neoplasms; Fluorouracil; Humans; Isothiocyanates; Kelch-Like ECH-Associated Protei | 2018 |
Simultaneous Targeting of Differentiated Breast Cancer Cells and Breast Cancer Stem Cells by Combination of Docetaxel- and Sulforaphane-Loaded Self-Assembled Poly(D, L-lactide-co-glycolide)/Hyaluronic Acid Block Copolymer-Based Nanoparticles.
Topics: Animals; Antineoplastic Agents; Breast Neoplasms; Cell Line, Tumor; Cell Survival; Docetaxel; Drug C | 2016 |
Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model.
Topics: Animals; Anticarcinogenic Agents; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; | 2018 |
HDAC5-LSD1 axis regulates antineoplastic effect of natural HDAC inhibitor sulforaphane in human breast cancer cells.
Topics: Animals; Apoptosis; Biomarkers, Tumor; Breast Neoplasms; Cell Proliferation; Epigenesis, Genetic; Fe | 2018 |
Inhibition of breast cancer cell growth by the combination of clofarabine and sulforaphane involves epigenetically mediated CDKN2A upregulation.
Topics: Adenine Nucleotides; Antineoplastic Agents; Arabinonucleosides; Breast Neoplasms; Cell Line, Tumor; | 2018 |
Withaferin A and sulforaphane regulate breast cancer cell cycle progression through epigenetic mechanisms.
Topics: Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Cell Cycle; Cell Division; Cell Li | 2018 |
Sulforaphane induces autophagy by inhibition of HDAC6-mediated PTEN activation in triple negative breast cancer cells.
Topics: Animals; Antineoplastic Agents; Apoptosis; Autophagy; Breast Neoplasms; Cell Line, Tumor; Cell Proli | 2018 |
Sulforaphane Decrease of SERTAD1 Expression Triggers G1/S Arrest in Breast Cancer Cells.
Topics: Antineoplastic Agents, Phytogenic; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Cyclin D2 | 2019 |
The aryl hydrocarbon receptor and estrogen receptor alpha differentially modulate nuclear factor erythroid-2-related factor 2 transactivation in MCF-7 breast cancer cells.
Topics: Breast Neoplasms; Estradiol; Estrogen Receptor alpha; Female; Heme Oxygenase-1; Humans; Indoles; Iso | 2013 |
Sulforaphane inhibits mammary adipogenesis by targeting adipose mesenchymal stem cells.
Topics: Adipocytes; Adipogenesis; Animals; Breast Neoplasms; Cell Communication; Cell Differentiation; Cell | 2013 |
Sulforaphane inhibits growth of human breast cancer cells and augments the therapeutic index of the chemotherapeutic drug, gemcitabine.
Topics: Anti-Inflammatory Agents; Antineoplastic Agents; Apoptosis; Breast Neoplasms; Cell Death; Cell Line, | 2013 |
Characterization of a stem-like subpopulation in basal-like ductal carcinoma in situ (DCIS) lesions.
Topics: Aldehyde Dehydrogenase 1 Family; Animals; Anticarcinogenic Agents; Breast Neoplasms; Carcinoma, Intr | 2014 |
Sulforaphane inhibits phorbol ester-stimulated IKK-NF-κB signaling and COX-2 expression in human mammary epithelial cells by targeting NF-κB activating kinase and ERK.
Topics: Anticarcinogenic Agents; Breast Neoplasms; Cell Line; Cyclooxygenase 2; Drug Screening Assays, Antit | 2014 |
Modulating potential of L-sulforaphane in the expression of cytochrome p450 to identify potential targets for breast cancer chemoprevention and therapy using breast cell lines.
Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Aromatase; Breast Neoplasms; Cell Line, Tumor; Cell Su | 2015 |
Epigenetic reactivation of p21CIP1/WAF1 and KLOTHO by a combination of bioactive dietary supplements is partially ERα-dependent in ERα-negative human breast cancer cells.
Topics: Breast Neoplasms; Cell Cycle Checkpoints; Cell Line, Tumor; Chromatin; Cyclin-Dependent Kinase Inhib | 2015 |
Sensitization of estrogen receptor-positive breast cancer cell lines to 4-hydroxytamoxifen by isothiocyanates present in cruciferous plants.
Topics: Antineoplastic Agents, Phytogenic; Apoptosis; bcl-2-Associated X Protein; Brassicaceae; Breast Neopl | 2016 |
Sensitization of HER2 Positive Breast Cancer Cells to Lapatinib Using Plants-Derived Isothiocyanates.
Topics: Antineoplastic Agents, Phytogenic; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Breast | 2015 |
Sulforaphane Alone and in Combination with Clofarabine Epigenetically Regulates the Expression of DNA Methylation-Silenced Tumour Suppressor Genes in Human Breast Cancer Cells.
Topics: Adenine Nucleotides; Arabinonucleosides; Breast Neoplasms; Cell Line, Tumor; Clofarabine; DNA Methyl | 2015 |
Sulforaphane delivery using mPEG-PCL co-polymer nanoparticles to breast cancer cells.
Topics: Breast Neoplasms; Drug Carriers; Female; Humans; Isothiocyanates; Nanoparticles; Polyesters; Polyeth | 2017 |
Combination of lapatinib with isothiocyanates overcomes drug resistance and inhibits migration of HER2 positive breast cancer cells.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Breast Neoplasms; Cell Line, Tumor; Cell | 2017 |
Combinatorial epigenetic mechanisms and efficacy of early breast cancer inhibition by nutritive botanicals.
Topics: Animals; Antineoplastic Agents, Phytogenic; Brassica; Breast Neoplasms; Carcinogenesis; Catechin; Ce | 2016 |
Regulation of estrogen receptor alpha expression in human breast cancer cells by sulforaphane.
Topics: Breast; Breast Neoplasms; Cell Line; Cell Proliferation; Down-Regulation; Estrogen Receptor alpha; H | 2009 |
Suppression of microtubule dynamic instability and turnover in MCF7 breast cancer cells by sulforaphane.
Topics: Acetylation; Anticarcinogenic Agents; Apoptosis; Breast Neoplasms; Cell Line, Tumor; Cell Proliferat | 2008 |
Comparison of the effects of phenethyl isothiocyanate and sulforaphane on gene expression in breast cancer and normal mammary epithelial cells.
Topics: Breast Neoplasms; Cell Line; Epithelial Cells; Gene Expression Regulation, Neoplastic; Humans; Isoth | 2009 |
Fenugreek: a naturally occurring edible spice as an anticancer agent.
Topics: Anticarcinogenic Agents; Breast Neoplasms; Cell Death; Cell Line, Tumor; Diosgenin; Dose-Response Re | 2009 |
The effect of isothiocyanates on CYP1A1 and CYP1A2 activities induced by polycyclic aromatic hydrocarbons in Mcf7 cells.
Topics: Anthracenes; Anticarcinogenic Agents; Benz(a)Anthracenes; Brassica; Breast Neoplasms; Carcinogens; C | 2009 |
Modulation of markers associated with aggressive phenotype in MDA-MB-231 breast carcinoma cells by sulforaphane.
Topics: Anticarcinogenic Agents; Biomarkers, Tumor; Blotting, Western; Breast Neoplasms; Cytokines; Female; | 2009 |
Sulforaphane, a dietary component of broccoli/broccoli sprouts, inhibits breast cancer stem cells.
Topics: Aldehyde Dehydrogenase; Aldehyde Dehydrogenase 1 Family; Animals; Anticarcinogenic Agents; Apoptosis | 2010 |
Sulforaphane causes epigenetic repression of hTERT expression in human breast cancer cell lines.
Topics: Acetylation; Apoptosis; Blotting, Western; Breast Neoplasms; CCCTC-Binding Factor; Cell Line, Tumor; | 2010 |
Involvement of caspase-9 in autophagy-mediated cell survival pathway.
Topics: Antibiotics, Antineoplastic; Anticarcinogenic Agents; Antineoplastic Agents, Phytogenic; Apoptosis; | 2011 |
Autophagy inhibition enhances sulforaphane-induced apoptosis in human breast cancer cells.
Topics: Anticarcinogenic Agents; Apoptosis; Autophagy; Blotting, Western; Breast Neoplasms; Cell Line, Tumor | 2010 |
Sulforaphane inhibits the growth of KPL-1 human breast cancer cells in vitro and suppresses the growth and metastasis of orthotopically transplanted KPL-1 cells in female athymic mice.
Topics: Animals; Antineoplastic Agents; Apoptosis; Body Weight; Breast Neoplasms; Cell Line, Tumor; Cell Pro | 2011 |
Novel function of transcription factor Nrf2 as an inhibitor of RON tyrosine kinase receptor-mediated cancer cell invasion.
Topics: Anticarcinogenic Agents; Breast Neoplasms; Cell Line, Tumor; Female; Gene Expression Regulation, Enz | 2011 |
D,L-sulforaphane-induced apoptosis in human breast cancer cells is regulated by the adapter protein p66Shc.
Topics: Animals; Anticarcinogenic Agents; Apoptosis; Breast Neoplasms; Cell Line, Tumor; Cell Survival; Fema | 2012 |
Bioactive food components prevent carcinogenic stress via Nrf2 activation in BRCA1 deficient breast epithelial cells.
Topics: Anticarcinogenic Agents; Benzo(a)pyrene; Blotting, Western; BRCA1 Protein; Breast Neoplasms; Cell Li | 2012 |
Bioactive dietary supplements reactivate ER expression in ER-negative breast cancer cells by active chromatin modifications.
Topics: Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Chromatin; Dietary Supplements; DNA Methylat | 2012 |
Sulphoraphane, a naturally occurring isothiocyanate induces apoptosis in breast cancer cells by targeting heat shock proteins.
Topics: Apoptosis; Breast Neoplasms; Cell Line, Tumor; DNA-Binding Proteins; Female; Heat Shock Transcriptio | 2012 |
Sulforaphane inhibits growth of phenotypically different breast cancer cells.
Topics: Autophagy; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell Survival; Female; Humans; Is | 2013 |
Sulforaphane inhibits human MCF-7 mammary cancer cell mitotic progression and tubulin polymerization.
Topics: Adenocarcinoma; Animals; Anticarcinogenic Agents; Breast Neoplasms; Cattle; Cell Cycle; Cell Divisio | 2004 |
Sulforaphane halts breast cancer cell growth.
Topics: Animals; Breast Neoplasms; Growth Inhibitors; Humans; Isothiocyanates; Phytotherapy; Sulfoxides; Thi | 2004 |
Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex.
Topics: Adaptor Proteins, Signal Transducing; Amino Acid Sequence; Amino Acid Substitution; Animals; Anticar | 2004 |
Sulforaphane, erucin, and iberin up-regulate thioredoxin reductase 1 expression in human MCF-7 cells.
Topics: Breast Neoplasms; Gene Expression Regulation, Enzymologic; Humans; Isothiocyanates; RNA, Messenger; | 2005 |
Broccoli and watercress suppress matrix metalloproteinase-9 activity and invasiveness of human MDA-MB-231 breast cancer cells.
Topics: Anticarcinogenic Agents; Brassica; Breast Neoplasms; Carcinogens; Cell Line, Tumor; Cell Survival; C | 2005 |
Sulforaphane induces cell type-specific apoptosis in human breast cancer cell lines.
Topics: Anticarcinogenic Agents; Antineoplastic Agents; Apoptosis; Breast Neoplasms; Caspases; Cell Cycle; C | 2007 |
Efficacy of sulforaphane is mediated by p38 MAP kinase and caspase-7 activations in ER-positive and COX-2-expressed human breast cancer cells.
Topics: Antineoplastic Agents; Apoptosis; Breast Neoplasms; Caspase 7; Cell Line, Transformed; Cell Nucleus | 2007 |
Expression of MRP1 and GSTP1-1 modulate the acute cellular response to treatment with the chemopreventive isothiocyanate, sulforaphane.
Topics: Anticarcinogenic Agents; Biological Transport; Breast Neoplasms; Cell Line, Tumor; Female; Gene Expr | 2008 |