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May 1, 2008

Scientists Uncover p53’s Role in Effectiveness of IGF-1 Inhibitors in Prostate Cancer

  • Prostate cancer developmental therapies that inhibit insulin-like growth factor’s (IGF-1) from activating its target receptor could have unexpected results especially if p53 is already compromised, according to investigators at Fred Hutchinson Cancer Research Center.

    IGF-1 is a polypeptide hormone that can influence growth, differentiation, and survival of cells expressing the type 1 receptor (IGF-1R). Past studies have strongly implicated IGF-1 as a contributing factor in prostate cancer, including linking elevated levels of IGF-1 with the risk of developing this disease.

    Through manipulation of gene expression in the epithelial compartment of the mouse prostate gland, researchers found that eliminating IGF-1R expression in an otherwise normal mouse prostate caused the cells to proliferate and become hyperplastic. Persistent loss of IGF-1R expression, however, ultimately induced cell stasis and death, both of which are regulated by the tumor suppressor gene p53.

    The team then conducted a second experiment by crossing mice carrying the prostate-specific IGF-1R knockout alleles with transgenic mice that develop spontaneous prostate cancer when p53 is compromised. The results showed that prostate epithelial-specific deletion of IGF-1R facilitated the emergence of aggressive prostate cancer in the tumor-prone mice.

    The study is published in the May 1 edition of Cancer Research.

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Scientifically Studying Ecstasy

MDMA (commonly known as the empathogen “ecstasy”) is classified as a Schedule 1 drug, which is reserved for compounds with no accepted medical use and a high abuse potential. Two researchers from Stanford, however, call for a rigorous scientific exploration of MDMA's effects to identify precisely how the drug works, the data from which could be used to develop therapeutic compounds.

Do you agree that ecstasy should be studied for its potential therapeutic benefits?

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