Cornell researchers have taken a major step toward answering a key question in cancer research: Why is testicular cancer so responsive to chemotherapy, even after it metastasizes? Professional cyclist Lance Armstrong, for example, had testicular cancer that spread to his lung and brain, yet he made a full recovery after conventional chemotherapy. The key to such success appears to lie in the cancer's stem cells, which are more sensitive to chemotherapy than stem cells found in other types of cancer. Defining why testicular cancers are so susceptible to chemotherapy could eventually provide insights for treating other, more resistant cancers. The group's study, published today (November 14, 2017) in Cell Reports, also helped confirm that risk for testicular cancer is determined in utero. The open-access article is titled “Chemotherapy-Induced Depletion of OCT4-Positive Cancer Stem Cells in a Mouse Model of Malignant Testicular Cancer.” The research offers some evidence to support a hypothesis that, in humans, testicular cancers are initiated during embryonic development and lie dormant for 18 to 35 years. "The study provides new insights into the basis for the responsiveness of testicular cancer to chemotherapy, which has always been an intriguing observation, but the basis for it was not clear," said Dr. Robert Weiss, Professor of Biomedical Sciences at Cornell's College of Veterinary Medicine and senior author of the study. Timothy Pierpont, a graduate student in Dr. Weiss' lab, is the paper's first author. Most types of tumors contain distinct populations of cells. A small fraction of these are stem cells, which have the ability to grow new tumors from a single cell and - in most cancers - are extremely resistant to therapy.
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