PQ - 6 What are the molecular and cellular mechanisms by which patients with certain chronic diseases have increased or decreased risks for developing cancer, and can these connections be exploited to develop novel preventive or therapeutic strategies? Background: People with Alzheimer’s, Parkinson’s and Huntington’s diseases, as well as Fragile X Syndrome patients, have a significantly lower risk of most cancers. An exception is melanoma, for which there is an increased risk for Parkinson’s patients. The reverse correlations also hold true. Cancer survivors have a significantly lower risk of developing many of these neurological diseases. It seems likely that if we understood in molecular terms why patients with these diseases or other chronic diseases have altered risk for cancer development, we might find leads for cancer prevention or treatment. Feasibility: Exploiting this dichotomy may be difficult. Comprehensive databases needed to identify clinical correlations between chronic disease and cancer risk are not commonly annotated for these anti-correlations. However, the technology exists to find these disease/risk relationships. The molecular causes of these diseases or understanding the mechanisms of action for common therapies might be useful places to search for plausible links to cancer development. In some cases, there may be candidate genes or pathways for study. For example, some evidence suggests that suspected anti-cancer targets such as Pin1 are essential for the development of Alzheimer’s disease. Overall, finding the molecular linkage to explain these correlations would be a powerful base for future work. Implications of success: Understanding the biochemical and genetic bases for these striking disease correlations may reveal novel insights into the mechanisms of cancer development as well as insights into the corresponding diseases. These molecular mechanisms would potentially provide new targets for therapies or prevention. |
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