One of the biggest obstacles for cancer researchers today is the sheer volume of variables at play when a healthy cell turns cancerous. This often makes it difficult for researchers to determine where to focus. “We can have hundreds of candidates,” Park explained. “You want to know which one is really the driver, so we can prioritize for further study in developing therapy.”
The new approach developed by Park, of UVA’s Department of Microbiology, Immunology and Cancer Biology, and his colleagues will help with that. They have demonstrated the approach’s potential by creating a model of small-cell lung cancer (SCLC), the most aggressive and fastest growing form of lung cancer.
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The researchers were able to show that an important contributor to the development of the cancer was a common mutation in the CREBBP gene. The gene, in its non-mutated form, is thought to act as a tumor suppressor by turning on genes that attach lung neuroendocrine cells together and prevent uncontrolled growth. “Those particular cells become mutated by the carcinogens from smoke,” Park explained. “When the cells acquire that part of the mutation, CREBBP mutation, they lose their interactions with the neighboring cells. Normally, this lost cell-cell contact would prompt cells to die through a process called programmed cell death or apoptosis. However, if the same cells acquire additional mutations in other critical tumor suppressor genes such as RB and P53, as is frequently the case in SCLC, then instead of dying, they survive and continue to expand.”