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Last Updated: 3 years ago

Possible Interaction: Genistein and Docetaxel

supplement:

Genistein

Research Papers that Mention the Interaction

Genistein also shows synergistic behavior with well-known anticancer drugs, such as adriamycin, docetaxel , and tamoxifen, suggesting a potential role in combination therapy.
Advances in nutrition  •  2015  |  View Paper
It is clear from our studies that low doses of genistein can increase the sensitivity of prostate CICs to drugs such as docetaxel and cyclopamine, two drugs either used or under consideration for prostate cancer therapy.
Advances in enzyme regulation  •  2011  |  View Paper
Collectively, our results clearly suggest that genistein pretreatment inactivates NF-kappaB and may contribute to increased growth inhibition and apoptosis induced by cisplatin, docetaxel , and doxorubicin in prostate, breast, lung, and pancreatic cancer cells.
We found that 15 to 30 micromol/L genistein combined with 100 to 500 nmol/L cisplatin, 0.5 to 2 nmol/L docetaxel , or 50 ng/mL doxorubicin resulted in significantly greater inhibition of cell growth and induction of apoptosis compared with either agent alone.
Cancer research  •  2005  |  View Paper
The combination of 30 μmol/L genistein with 1 nmol/L docetaxel or 100 nmol/L cisplatin elicited significantly greater inhibition of cell growth compared with either agent alone.
These results clearly suggest that genistein pretreatment, which inactivates NF-κB activity, together with other cellular effects of genistein, may contribute to increased cell growth inhibition and apoptosis inducing effects of nontoxic doses of docetaxel and cisplatin, which could be a novel strategy for the treatment of pancreatic cancer.
Pancreas  •  2004  |  View Paper
From these results, we conclude that genistein could be a promising nontoxic agent to improve the treatment outcome of metastatic prostate cancer with docetaxel.
In this study, we found that genistein significantly potentiated the antitumor, anti-invasive, and antimetastatic activities of docetaxel both in culture and in severe combined immunodeficient (SCID)-human model of experimental prostate cancer bone metastasis.
Moreover, genistein down-regulated the expression and activity of MMP-9, which was induced by docetaxel treatment, and inhibited invasion of PC-3 cells.
These results suggest that the observed potentiation of antitumor activity of docetaxel by genistein in the SCID-human model of experimental bone metastasis could be mediated by regulation of OPG/RANK/RANKL/MMP-9 signaling, resulting in the inhibition of osteoclastic bone resorption and prostate cancer bone metastasis.
Cancer research  •  2006  |  View Paper