D:FEND
D:FEND is a unique blend of isoflavone compounds that have a broad effect on the tumour microenvironment. D:FEND is an important part of oncology protocols, can be safely used during radiotherapy to potentiate treatment outcomes and help with recovery.*
Supplement FactsServing Size: 1 tablet Servings Per Container: 100 |
||
---|---|---|
Amount Per Serving |
% Daily Value |
|
Kudzu (root) (Pueraria lobata) (contains daidzein) | 350mg | † |
Dyer’s Broom (Genista Tinctoria) (contains genistein) | 470 mg | † |
Semen Sojae Praeparartum (contains Glycitein) | 110mg | † |
† Daily Value not established. |
Other Ingredients: Microcrystalline cellulose, stearic acid, magnesium stearate and silica.
Does Not Contain: Wheat, gluten, soy, milk, eggs, fish, crustacean shellfish, tree nuts, peanuts
D:FEND
100 x 1000mg tablets
Product Overview
D:FEND contains three potent phytoestrogens that exhibit powerful anti-oxidant actions proven by research. D:FEND may enhance antioxidant activity and help regulate normal cell life-cycle and cell function.*
Action
•Encourages healthy cell function and cell life-cycle*
•Encourages inhibition of oxidative damage*
•May enhance antioxidant actions*
Suggested Use:
3-4 tablets daily
Caution:
caution with birth control.
Warning:
Contraindicated for Pregnancy,Additive effect to insulin and metformin, may enhance blood pressure medications, enhances blood clotting medications, Methotrexate.
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
Genistein and daidzein
Genistein and daidzein inhibit the growth of cancer cells through the modulation of genes controlling cell-cycle progression. Genistein inhibits the activation of the kappa light polypeptide gene enhancer in B-cells (NF-κB), signaling pathway, which is implicated in the balance between cell survival and programmed cell death (apoptosis). Antioxidant and antiangiogenesis properties of genistein have been also described. Soy isoflavones are also implicated in reversion of epigenetic events observed in prostate cancer.*
Daidzein could be the component of soy that protects against genistein-induced metastasis. Daidzein inhibited cell growth and synergized with radiation, affecting APE1/Ref-1, NF-κB and HIF-1α, but at lower levels than genistein and soy, in AR+ and AR- PCa cells, suggesting it is an AR-independent mechanism.1*
Yu et al., (2003) determined the effect of soy isoflavones on the expression of prostate androgen-regulated transcript 1 (PART-1), a newly discovered androgen-induced gene that may represent a novel androgen-dependent prostate cancer tumour marker.2 Genistein and daidzein dose-dependently inhibited DHT-induced expression of the PART-1 transcript.*
Genistein, the major bioactive isoflavone of soybeans, acts as a radiosensitizer for prostate cancer (PCa) both in vitro and in vivo. However, pure genistein promoted increased metastasis to lymph nodes. A mixture of soy isoflavones (genistein, daidzein, glycitein) did not cause increased metastasis, but potentiated radiotherapy. Daidzein could be the component of soy that protects against genistein-induced metastasis. Daidzein inhibited cell growth and synergized with radiation, affecting APE1/Ref-1, NF-κB and HIF-1α, but at lower levels than genistein and soy, in AR+ and AR- PCa cells, suggesting it is an AR-independent mechanism.3*
Daidzein and genistein showed a synergistic effect on inhibiting cell proliferation and inducing apoptosis of both PCa cells. Twenty-five μM daidzein/50μM genistein and 50μM daidzein/50μM genistein significantly increased the apoptotic effects on C4-2B cells although they did not show any effect when used individually. Except 50μM daidzein/50μM genistein, all other combinations had no impacts on cell cycles. For treatment with soy isoflavone combination, genistein was always better taken up than daidzein by both LNCaP and C4-2B cells.4*
Isoflavones are among the major bioactive compounds found in a wide variety of plant-derived foods, especially in soybeans and soy-based foods. In this study, the effect of a soy-derived isoflavone mixture (designated as SI-I, containing 71% daidzein, 14.3% genistein and 14.7% glycitein) on HeLa cells and its mechanism were investigated. SI-I in concentration range 5-80 μg/ml significantly reduced the survival rate of HeLa cells by MTT assay, whereas showed no side effect on that of L929 cells. After HeLa cells were exposed to 10, 20 and 40 μg/ml SI-I for 4 days, typical apoptotic morphological changes, including nuclear fragmentation, cytoplasm shrinkage and decrease of cell volume, were observed by fluorescence microscope and CLSM, respectively. FCM analysis revealed that the percentages of early apoptotic cells with lost Δψm increased by 2.27, 2.74 and 4.05 folds respectively, compared with control. The results showed that SI-I inhibited HeLa cell growth through inducing apoptosis via the mitochondrial pathway and comparisons with reported data indicated that synergistic effect existed between the isoflavone species contained in SI-I. It is proposed that natural soy-derived isoflavones are potential candidates as chemotherapeutic agents against human cervical cancer.5*
Prostate Cancer
Daidzein and genistein significantly increased the apoptotic effects on androgen-dependent PCa cells (LNCaP) and bone metastatic LNCaP-derivative PCa cells (C4-2B) although they did not show any effect when used individually. Combination of low dose of genistein and daidzein has synergistic preventive effects on isogenic human prostate cancer cells when compared with individual soy isoflavone.6*
Breast Cancer
The interactions of genistein, daidzein, equol, and liquiritigenin with estrogen receptors ERα and ERβ and the regulation of gene expression and proliferation in MCF-7 breast cancer cells containing ERα and/or ERβ were examined. Unlike the endogenous estrogen, estradiol (E2), botanical estrogens (BEs) preferentially bind to ERβ. ERα drives breast cancer cell proliferation and ERβ dampens this, the relative levels of these two ERs in target cells and the BE dose greatly affect gene expression and proliferative response and will be crucial determinants of the potential benefits vs. risks of BEs.7 Given that ERβ often is coexpressed with HER2 in breast cancer, both functions of genistein might be able to enhance the antitumoral action of trastuzumab. Treatment with high-dose genistein (10 μmol/l) significantly increased the growth-inhibitory effect of trastuzumab on HER2-overexpressing, ERα/β-positive BT-474 breast cancer cells.8Genistein acts as an agonist to ERα, and in cells with ERβ alone, genistein most likely acts as an antiestrogen. These results also suggest that genistein could be useful as a chemotherapeutic agent in premenopausal women with breast cancer of the ERα-negative and ERβ-positive type.9 ERbeta has been postulated to play a role in modulating ERα-mediated cell proliferation, (ii) genistein and quercetin may be agonists for both receptor types and (iii) the ratio of ERα to ERβ is known to vary between tissues and results point at the importance of the cellular ERα/ERβ ratio for the ultimate effect of (phyto)estrogens on cell proliferation.10*
Cervical Cancer
The exposure of HeLa cells to genistein resulted in significant dose- and time-dependent growth inhibition, which was found to be mediated by apoptosis and cell cycle arrest at G(2)/M phase. In addition, it induced migration-inhibition in a time-dependent manner by modulating the expression of MMP-9 and TIMP-1.11*
References
Adjakly M, Ngollo M, Boiteux JP, et al. Genistein and daidzein: different molecular effects on prostate cancer. Anticancer Res. 2013 Jan;33(1):39-44.
Yu Ly, Blackburn GL, Zhou J-R. Genistein and Daidzein Downregulate Prostate Androgen-Regulated Transcript-1 (PART-1) Gene Expression Induced by Dihydrotestosterone in Human Prostate LNCaP Cancer Cells. J. Nutr. February 1, 2003 vol. 133 no. 2 389-392
Singh-Gupta V, Zhang H, Yunker CK, et al. Refractory Prostate Cancer In Vitro and In Vivo Compared to Genistein and Soy Extract: Potentiation of Radiotherapy. Pharmaceutical Research. June 2010, Volume 27, Issue 6, pp 1115-1127
Dong X, Xu W, Sikes RA, Wu C. (2013). Combination of low dose of genistein and daidzein has synergistic preventive effects on isogenic human prostate cancer cells when compared with individual soy isoflavone. Food Chem, 141(3):1923-33. doi: 10.1016/j.foodchem.2013.04.109.
Xiao JX, Huang GQ, Geng X, Qiu HW. (2011). Soy-derived isoflavones inhibit HeLa cell growth by inducing apoptosis. Plant Foods Hum Nutr, 66(2):122-8. doi: 10.1007/s11130-011-0224-6.
Dong X, Xu W, Sikes RA, Wu C. (2013). Combination of low dose of genistein and daidzein has synergistic preventive effects on isogenic human prostate cancer cells when compared with individual soy isoflavone. Food Chem, 141(3):1923-33. doi: 10.1016/j.foodchem.2013.04.109.
Jiang Y, Gong P, Madak-Erdogan Z, Martin T, Jeyakumar M, et al. (2013). Mechanisms enforcing the estrogen receptor β selectivity of botanical estrogens. FASEB J, 27(11):4406-18. doi: 10.1096/fj.13-234617.
Lattrich C, Lubig J, Springwald A, Goerse R, Ortmann O, Treeck O. (2011). Additive effects of trastuzumab and genistein on human breast cancer cells. Anticancer Drugs. 22(3):253-61. doi: 10.1097/CAD.0b013e3283427bb5.
Rajah TT, Du N, Drews N, Cohn R. (2009). Genistein in the presence of 17beta-estradiol inhibits proliferation of ERbeta breast cancer cells. Pharmacology, 84(2):68-73. doi: 10.1159/000226123.
Sotoca AM, Ratman D, van der Saag P, et al. (2008). Phytoestrogen-mediated inhibition of proliferation of the human T47D breast cancer cells depends on the ERalpha/ERbeta ratio. J Steroid Biochem Mol Biol, 112(4-5):171-8. doi: 10.1016/j.jsbmb.2008.10.002.
Hussain A, Harish G, Prabhu SA, et al. (2012). Inhibitory effect of genistein on the invasive potential of human cervical cancer cells via modulation of matrix metalloproteinase-9 and tissue inhibitors of matrix metalloproteinase-1 expression. Cancer Epidemiol, 36(6):e387-93. doi: 10.1016/j.canep.2012.07.005.
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
Supplement FactsServing Size: 1 tablet Servings Per Container: 100 |
||
---|---|---|
Amount Per Serving |
% Daily Value |
|
Kudzu (root) (Pueraria lobata) (contains daidzein) | 350mg | † |
Dyer’s Broom (Genista Tinctoria) (contains genistein) | 470 mg | † |
Semen Sojae Praeparartum (contains Glycitein) | 110mg | † |
† Daily Value not established. |
Other Ingredients: Microcrystalline cellulose, stearic acid, magnesium stearate and silica.
Does Not Contain: Wheat, gluten, soy, milk, eggs, fish, crustacean shellfish, tree nuts, peanuts
D:FEND
100 x 1000mg tablets
Product Overview
D:FEND contains three potent phytoestrogens that exhibit powerful anti-oxidant actions proven by research. D:FEND may enhance antioxidant activity and help regulate normal cell life-cycle and cell function.*
Action
•Encourages healthy cell function and cell life-cycle*
•Encourages inhibition of oxidative damage*
•May enhance antioxidant actions*
Suggested Use:
3-4 tablets daily
Caution:
caution with birth control.
Warning:
Contraindicated for Pregnancy,Additive effect to insulin and metformin, may enhance blood pressure medications, enhances blood clotting medications, Methotrexate.
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
Genistein and daidzein
Genistein and daidzein inhibit the growth of cancer cells through the modulation of genes controlling cell-cycle progression. Genistein inhibits the activation of the kappa light polypeptide gene enhancer in B-cells (NF-κB), signaling pathway, which is implicated in the balance between cell survival and programmed cell death (apoptosis). Antioxidant and antiangiogenesis properties of genistein have been also described. Soy isoflavones are also implicated in reversion of epigenetic events observed in prostate cancer.*
Daidzein could be the component of soy that protects against genistein-induced metastasis. Daidzein inhibited cell growth and synergized with radiation, affecting APE1/Ref-1, NF-κB and HIF-1α, but at lower levels than genistein and soy, in AR+ and AR- PCa cells, suggesting it is an AR-independent mechanism.1*
Yu et al., (2003) determined the effect of soy isoflavones on the expression of prostate androgen-regulated transcript 1 (PART-1), a newly discovered androgen-induced gene that may represent a novel androgen-dependent prostate cancer tumour marker.2 Genistein and daidzein dose-dependently inhibited DHT-induced expression of the PART-1 transcript.*
Genistein, the major bioactive isoflavone of soybeans, acts as a radiosensitizer for prostate cancer (PCa) both in vitro and in vivo. However, pure genistein promoted increased metastasis to lymph nodes. A mixture of soy isoflavones (genistein, daidzein, glycitein) did not cause increased metastasis, but potentiated radiotherapy. Daidzein could be the component of soy that protects against genistein-induced metastasis. Daidzein inhibited cell growth and synergized with radiation, affecting APE1/Ref-1, NF-κB and HIF-1α, but at lower levels than genistein and soy, in AR+ and AR- PCa cells, suggesting it is an AR-independent mechanism.3*
Daidzein and genistein showed a synergistic effect on inhibiting cell proliferation and inducing apoptosis of both PCa cells. Twenty-five μM daidzein/50μM genistein and 50μM daidzein/50μM genistein significantly increased the apoptotic effects on C4-2B cells although they did not show any effect when used individually. Except 50μM daidzein/50μM genistein, all other combinations had no impacts on cell cycles. For treatment with soy isoflavone combination, genistein was always better taken up than daidzein by both LNCaP and C4-2B cells.4*
Isoflavones are among the major bioactive compounds found in a wide variety of plant-derived foods, especially in soybeans and soy-based foods. In this study, the effect of a soy-derived isoflavone mixture (designated as SI-I, containing 71% daidzein, 14.3% genistein and 14.7% glycitein) on HeLa cells and its mechanism were investigated. SI-I in concentration range 5-80 μg/ml significantly reduced the survival rate of HeLa cells by MTT assay, whereas showed no side effect on that of L929 cells. After HeLa cells were exposed to 10, 20 and 40 μg/ml SI-I for 4 days, typical apoptotic morphological changes, including nuclear fragmentation, cytoplasm shrinkage and decrease of cell volume, were observed by fluorescence microscope and CLSM, respectively. FCM analysis revealed that the percentages of early apoptotic cells with lost Δψm increased by 2.27, 2.74 and 4.05 folds respectively, compared with control. The results showed that SI-I inhibited HeLa cell growth through inducing apoptosis via the mitochondrial pathway and comparisons with reported data indicated that synergistic effect existed between the isoflavone species contained in SI-I. It is proposed that natural soy-derived isoflavones are potential candidates as chemotherapeutic agents against human cervical cancer.5*
Prostate Cancer
Daidzein and genistein significantly increased the apoptotic effects on androgen-dependent PCa cells (LNCaP) and bone metastatic LNCaP-derivative PCa cells (C4-2B) although they did not show any effect when used individually. Combination of low dose of genistein and daidzein has synergistic preventive effects on isogenic human prostate cancer cells when compared with individual soy isoflavone.6*
Breast Cancer
The interactions of genistein, daidzein, equol, and liquiritigenin with estrogen receptors ERα and ERβ and the regulation of gene expression and proliferation in MCF-7 breast cancer cells containing ERα and/or ERβ were examined. Unlike the endogenous estrogen, estradiol (E2), botanical estrogens (BEs) preferentially bind to ERβ. ERα drives breast cancer cell proliferation and ERβ dampens this, the relative levels of these two ERs in target cells and the BE dose greatly affect gene expression and proliferative response and will be crucial determinants of the potential benefits vs. risks of BEs.7 Given that ERβ often is coexpressed with HER2 in breast cancer, both functions of genistein might be able to enhance the antitumoral action of trastuzumab. Treatment with high-dose genistein (10 μmol/l) significantly increased the growth-inhibitory effect of trastuzumab on HER2-overexpressing, ERα/β-positive BT-474 breast cancer cells.8Genistein acts as an agonist to ERα, and in cells with ERβ alone, genistein most likely acts as an antiestrogen. These results also suggest that genistein could be useful as a chemotherapeutic agent in premenopausal women with breast cancer of the ERα-negative and ERβ-positive type.9 ERbeta has been postulated to play a role in modulating ERα-mediated cell proliferation, (ii) genistein and quercetin may be agonists for both receptor types and (iii) the ratio of ERα to ERβ is known to vary between tissues and results point at the importance of the cellular ERα/ERβ ratio for the ultimate effect of (phyto)estrogens on cell proliferation.10*
Cervical Cancer
The exposure of HeLa cells to genistein resulted in significant dose- and time-dependent growth inhibition, which was found to be mediated by apoptosis and cell cycle arrest at G(2)/M phase. In addition, it induced migration-inhibition in a time-dependent manner by modulating the expression of MMP-9 and TIMP-1.11*
References
Adjakly M, Ngollo M, Boiteux JP, et al. Genistein and daidzein: different molecular effects on prostate cancer. Anticancer Res. 2013 Jan;33(1):39-44.
Yu Ly, Blackburn GL, Zhou J-R. Genistein and Daidzein Downregulate Prostate Androgen-Regulated Transcript-1 (PART-1) Gene Expression Induced by Dihydrotestosterone in Human Prostate LNCaP Cancer Cells. J. Nutr. February 1, 2003 vol. 133 no. 2 389-392
Singh-Gupta V, Zhang H, Yunker CK, et al. Refractory Prostate Cancer In Vitro and In Vivo Compared to Genistein and Soy Extract: Potentiation of Radiotherapy. Pharmaceutical Research. June 2010, Volume 27, Issue 6, pp 1115-1127
Dong X, Xu W, Sikes RA, Wu C. (2013). Combination of low dose of genistein and daidzein has synergistic preventive effects on isogenic human prostate cancer cells when compared with individual soy isoflavone. Food Chem, 141(3):1923-33. doi: 10.1016/j.foodchem.2013.04.109.
Xiao JX, Huang GQ, Geng X, Qiu HW. (2011). Soy-derived isoflavones inhibit HeLa cell growth by inducing apoptosis. Plant Foods Hum Nutr, 66(2):122-8. doi: 10.1007/s11130-011-0224-6.
Dong X, Xu W, Sikes RA, Wu C. (2013). Combination of low dose of genistein and daidzein has synergistic preventive effects on isogenic human prostate cancer cells when compared with individual soy isoflavone. Food Chem, 141(3):1923-33. doi: 10.1016/j.foodchem.2013.04.109.
Jiang Y, Gong P, Madak-Erdogan Z, Martin T, Jeyakumar M, et al. (2013). Mechanisms enforcing the estrogen receptor β selectivity of botanical estrogens. FASEB J, 27(11):4406-18. doi: 10.1096/fj.13-234617.
Lattrich C, Lubig J, Springwald A, Goerse R, Ortmann O, Treeck O. (2011). Additive effects of trastuzumab and genistein on human breast cancer cells. Anticancer Drugs. 22(3):253-61. doi: 10.1097/CAD.0b013e3283427bb5.
Rajah TT, Du N, Drews N, Cohn R. (2009). Genistein in the presence of 17beta-estradiol inhibits proliferation of ERbeta breast cancer cells. Pharmacology, 84(2):68-73. doi: 10.1159/000226123.
Sotoca AM, Ratman D, van der Saag P, et al. (2008). Phytoestrogen-mediated inhibition of proliferation of the human T47D breast cancer cells depends on the ERalpha/ERbeta ratio. J Steroid Biochem Mol Biol, 112(4-5):171-8. doi: 10.1016/j.jsbmb.2008.10.002.
Hussain A, Harish G, Prabhu SA, et al. (2012). Inhibitory effect of genistein on the invasive potential of human cervical cancer cells via modulation of matrix metalloproteinase-9 and tissue inhibitors of matrix metalloproteinase-1 expression. Cancer Epidemiol, 36(6):e387-93. doi: 10.1016/j.canep.2012.07.005.
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.