By tracking the changes in prostate cancer cells over time, researchers at the Johns Hopkins Kimmel Cancer Center have found that activation of the MYC gene -; a well-known cancer-causing gene -; sets off a cascade of events that leads to both initiation and progression of the disease.
Johns Hopkins Medicine Sep 19 2024 By tracking the changes in prostate cancer cells over time, researchers at the Johns Hopkins Kimmel Cancer Center have found that activation of the MYC gene -; a well-known cancer-causing gene -; sets off a cascade of events that leads to both initiation and progression of the disease.
Srinivasan Yegnasubramanian, M.D., Ph.D., professor of oncology, pathology, and radiation oncology and molecular radiation sciences, and director of the inHealth precision medicine initiative at Johns Hopkins The researchers found that when MYC initially becomes upregulated in precancerous cells, activity increases in pathways that alert the immune system that something is wrong. But eventually, the immune-attracting pathways are turned off. As the tumor progresses, it stops signaling to the immune system and goes undetected.
The study, which also used molecular pathology techniques, showed that increased MYC expression and activity starts in epithelial cells lining the prostate. Eventually, the epithelial cells become cancer cells, which signal to surrounding cells, dampening the immune response, causing scarring, expanding the number of tumor cells, and inducing other molecular changes.
Prostate Prostate Cancer Gene Immune Response Immune System Medicine Oncology Pathology Tumor
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