Health

Targeted drugs found to be effective in blocking pancreatic tumors-ScienceDaily

Pancreatic cancer is an invasive disease in which malignant cells form in the tissues of the pancreas, the long, flat glands behind the stomach that help digestion and regulate blood sugar. According to the National Cancer Institute, pancreatic cancer has a low survival rate due to the difficulty of early detection, accounting for over 3% of all new cancer cases in the United States, but 8% of all cancer deaths. Occupies nearby. ..

Performed in his previous role at the Mofit Cancer Center, Clinical cancer research, Said Sebti, Ph.D., Deputy Director of Basic Research at VCU Massey Cancer Center. Has identified a new drug that effectively blocks pancreatic tumors that are dependent on the mutant KRAS gene that causes cancer. Sebti recently met with Massey’s clinical colleagues to discuss drug evaluation in clinical trials in patients with mutant KRAS in pancreatic tumors.

“Patients who have discovered a link between CDK protein overactivation and mutant KRAS poisoning and have used this link preclinically to combat mutant KRAS-induced pancreatic cancer and suffer from this deadly disease. Guaranteed clinical research, “said Massey’s Lacy Family Chair for Cancer Research and Professor of Pharmacology and Toxicology at the VCU School of Medicine. “Our findings are very important because they have revealed a new way to fight aggressive forms of pancreatic cancer with a very poor prognosis, mainly due to resistance to conventional treatments.”

KRAS is mutated in 90% of pancreatic cancers. Previous studies from the Sebti lab and other labs have shown that some tumors, including mutant KRAS, are actually dependent on the mutant gene. Sebti sought to find out if there was a drug that could specifically kill tumors that depended on mutant KRAS.

Sebti and co-workers have used three scientific approaches to answer this question.

First, they mapped pancreatic cancer cell blueprints through global phosphorylation proteomics. This provided a snapshot of how toxic and non-toxic tumors differ at phosphoprotein levels. They discovered two proteins, CDK1 and CDK2. These show which cells are dependent on mutant KRAS.

In addition, they analyzed a comprehensive database from the MIT and Harvard Broad Institutes, including genome-wide CRISPR gRNA screening datasets. They found that CDK1 and CDK2, and CDK7 and CDK9 proteins were associated with mutant KRAS toxic tumors.

Finally, they evaluated the ability of a library of 294 FDA drugs to selectively kill mutant KRAS-dependent cancer cells over non-KRAS-dependent cancer cells in the laboratory and were most effective in preclinical trials. The drug was determined to be AT7519, an inhibitor of CDK1. CDK2, CDK7 and CDK9.

“Using three completely different approaches, the same conclusions were made. Patients with pancreatic cancer whose tumors depend on mutant KRAS could benefit significantly from treatment with the CDK inhibitor AT7519. Yes, “says Sebti.

To further validate these findings in fresh patient-derived tumors from patients with pancreatic cancer, Sebti in this study was a prominent professor of oncology by Jose Trevino, MD, Chief Surgeon and Walter Lawrence, Jr., Massey. Cooperated with. University of Florida at that time. They found that AT7519 suppressed the growth of xenograft cells from five mutant KRAS pancreatic cancer patients who relapsed with chemotherapy and / or radiation therapy.

The AT7519 has failed in many clinical trials so far, but none have been tested for pancreatic cancer.

“If our findings are correct and translated in humans, we should be able to see positive reactions in patients with pancreatic cancer whose tumors are dependent on mutant KRAS,” Sebti said.

In addition to pancreatic cancer, the authors of the study believe that these findings may also have clinical impact on patients with colorectal and non-small cell lung cancer in which KRAS mutations are widespread. I will.

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material Provided by Virginia Commonwealth University.. Original written by Blake Belden. Note: The content can be edited in style and length.

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