In a new study, researchers found that a DNA mutation that occurs frequently in the development of many pancreatic tumors appears to make these cancers vulnerable to an existing type of drug known as PARP inhibitors.
The research was conducted by a team at the University of Pennsylvania.
The discovery centers on a gene called MYBBP1A.
Studies suggest that as many as two-thirds of patient cases of the most common type of pancreatic tumor have the deletion of one copy of this gene in the tumor cells.
The scientists found that while this deletion appears to contribute to tumor growth, the loss of the remaining copy of MYBBP1A in the tumor cells has the opposite effect, drastically reducing cell growth.
The team found, with experiments in pancreatic cancer cells and in mouse models, that they could exploit this vulnerability with an existing class of drug called PARP1 inhibitors, which have the effect of inactivating the MYBBP1A protein when its levels are already low in cells.
PARP1 inhibitors are mostly used to treat ovarian and breast cancers.
This is an exciting finding because there are no highly effective treatments for pancreatic cancer at present.
Moreover, this approach in principle could be used to find new treatments for other cancers that feature DNA deletions.
The American Cancer Society estimates that nearly 60,000 people in the United States are diagnosed with pancreatic cancers each year, and nearly 50,000 people die of these cancers.
The cure rate for pancreatic cancers is very low, largely because these cancers tend to be detected only in late stages when they have begun to spread in the body and are relatively resistant to chemotherapies and other treatments.
Better therapeutic approaches to pancreatic cancers are desperately needed.
One author of the study is Kenneth Zaret, Ph.D., a professor of Cell and Developmental Biology.
The study is published in Science Advances.
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