Loss of Commonly Mutated Gene in Prostate Tumors May Be Potential Biomarker for Targeted Treatment

Loss of Commonly Mutated Gene in Prostate Tumors May Be Potential Biomarker for Targeted Treatment
A new research study found that the loss of CHD1, one of the most commonly mutated genes in prostate tumors, may be a potential biomarker for targeted prostate cancer therapy. In the study, "Loss of CHD1 causes DNA repair defects and enhances prostate cancer therapeutic responsiveness," published in EMBO Reports, researchers showed that CDH1 is involved in DNA damage repair mechanisms, and its loss sensitizes human prostate cancer cells to different drugs, including PARP inhibitors like Lynparza (olaparib). The CHD1 gene is mutated in 15 to 27 percent of all prostate tumors, with mutations in this gene correlating with chromosomal instability and poor prognosis for prostate cancer patients. However, the importance of CHD1 deletion for prostate cancer cells was not known. In this study, a team of researchers in Germany and Denmark sought to examine the role of CHD1 to understand how its loss was beneficial for prostate cancer cells. By studying human prostate cancer cell lines lacking the CHD1 gene, investigators found that CHD1 was involved in DNA damage repair mechanisms. It functions by loosening the DNA around break sites to facilitate access of DNA repair proteins. Similar to descriptions of cancer cells with mutations in other proteins involved in DNA repair mechanisms, such as BRCA1 and BRCA2, researchers found that prostate cancer cells lacking CHD1 were particularly more sensitive to chemotherapy drugs that caused DNA damage, such as Mitomycin C, Camptosar (ironotecan), and PARP inhibitors such as Lynparza. The PARP protein also helps the cells
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