Monday, February 28, 2011 9:15:11 AM
http://tinyurl.com/6hy73uk
SAN DIEGO, Feb. 28, 2011 (GLOBE NEWSWIRE) -- Harbor BioSciences, Inc. (OTCBB:HRBR), a biopharmaceutical company developing novel therapeutics for the treatment of cancer, metabolic and inflammatory diseases, today announced publication of the company's study of Apoptone (HE3235) against breast cancer in a preclinical rat model. "17a-Ethynyl-5a-androstane-3a, 17B-diol Treatment of MNU-induced Mammary Cancer in Rats," describes the activity of Apoptone in a breast cancer model that is known for its similarity to breast cancer in humans. The paper was published this month in the International Journal of Breast Cancer (Volume 2011 (2011), Article ID 618757).
As described in the publication, Apoptone dramatically decreased tumor size by inducing programmed cell death (apoptosis). A molecular analysis showed that apoptosis was triggered by decreasing the expression of genes that cancer cells use to maintain their survival, and increasing the expression of genes that promote apoptosis. Apoptone also decreased the expression of genes that are associated with treatment failure in human breast cancer. The preclinical study was conducted in collaboration with Dr. Rajkumar Laksmanaswamy, the research director at the Center of Excellence in Cancer Research at the Texas Tech University Health Sciences Center.
Apoptone aggressively shrank established tumors and prevented the appearance of new tumors in the rodent breast cancer model. The rate of tumor volume reduction and degree of tumor suppression after treatment cessation was similar for Apoptone and tamoxifen. The anti-cancer activity of Apoptone was enhanced when combined with a common chemotherapeutic drug docetaxel (Taxotere®), without evidence of increased toxicity. The combination of Apoptone and docetaxel destroyed existing tumor cells better than either anastrazole (Arimidex®) or tamoxifen, the most common therapies used to treat breast cancer. Furthermore, Apoptone in combination with docetaxel prevented the growth of new tumors for 60 days after therapy ended, whereas new tumors rapidly appeared when anastrazole, docetaxel, and tamoxifen were used as single agents.
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