A large international collaboration led by researchers from the Johns Hopkins Kimmel Cancer Center has identified promising new targets for pancreatic cancer treatment and early diagnosis after examining various aspects of these tumors’ genes and proteins. Their findings were published in Cell.
Searching for new ways to fight pancreatic cancer, the team compared 140 tumor samples with 67 samples of normal adjacent pancreatic tissue from the same patients and nine samples of pancreatic tissue from patients who did not have cancer. Then, they took an accounting of proteins produced in pancreatic cancer cells, including various modifications to these proteins, such as adding phosphate groups or sugar molecules that can change their function.
The team confirmed that pancreatic tumors are more likely to have mutations in several genes identified in previous studies, including KRAS, TP53, CDKN2A, and SMAD4. In addition, they identified 222 proteins with at least a twofold increase in abundance between pancreatic cancerous cells and normal cells; nearly 5,000 sites in these proteins with increased phosphorylation abundance patterns; and more than 1,700 sites with an increase in attached carbohydrates, or glycosylation.
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Several of these glycosylated proteins are secreted from pancreatic cancer cells, the team says suggesting they could potentially be captured in the blood for early diagnosis. In addition, PAK1 and PAK2—two specialized proteins, called kinases, that place phosphate groups onto other proteins— that are dysregulated in pancreatic cancer could offer previously unrecognized targets to treat this disease. There are several small-molecule inhibitors targeting PAK1, offering a potential path toward treating pancreatic tumors, which are still under investigation. Other protein differences between the cancer cells and normal tissue appear to be roadblocks that stymie immune system attack, adds lead researcher Hui Zhang, suggesting new ways to improve immune response to these tumors.