Unlocking drug resistance in pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer with a median 5-year survival rate of only 8%. Surgery is not an option for most PDAC patients. This is because cancer has usually reached an advanced stage and has metastasized by the time it is diagnosed. Drug resistance develops so rapidly that even gemcitabine, the standard-of-care chemotherapy known as Gem, only adds about seven months to patients’ lives.

Qingxiang Lin is a research fellow at Massachusetts General Hospital and Harvard Medical School. “There really are few options for PDAC patients whose cancer has become drug-resistant,” he wrote in an email. It represents a very serious clinical problem.”

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When he was a graduate student in Robert M. Straubinger’s lab at the State University of New York at Buffalo, Lin and colleagues used proteomics techniques to investigate key regulators of gem resistance. “Our straightforward overall hypothesis was that a global differential proteomics analysis of highly Gem-resistant cell lines I developed would identify multiple cooperating mechanisms of drug resistance,” he said. I am writing.

Dr. Lin recent papers of Molecular and cellular proteomics About this work. Through his analysis, researchers identified drug-induced dynamic changes in protein levels associated with cancer cell metabolism, proliferation, migration, and drug response mechanisms.

Among these proteins, they wanted to analyze further the ribonucleoside-diphosphate reductase large subunit (RRM1), which plays an important role in Gem metabolism, and the possibly related S100 calcium-binding protein A4. We chose the ones that varied the most, such as (S100A4). in cellular energy production. Lin’s experiments showed that her reduction in S100A4 expression levels in Gem-resistant cells was consistent with decreased tumor cell proliferation. This may help protect these cancer cells from toxic drug action, while increased RRM1 levels enhance her Gem resistance. Moreover, clinical data from human patients showed a correlation between reduced RRM1 expression and improved clinical outcome.

“The picture painted by our data is that by altering multiple key proteins, mutant drug-resistant cells can grow more slowly to avoid toxicity, reduce the amount of activated gemstones, and reduce the amount of drug-resistant cells. suggesting that it enhances the activity of repairing DNA damage caused by “Protein-level responses of parental cells and Gem-resistant cell lines over time suggest that adaptive changes in cellular response systems related to cell proliferation, drug transport and metabolism, DNA repair and other functions contribute to Gem resistance in PDAC.” It suggests that

This information has led to multiple new hypotheses and discoveries at the protein level. Researchers have much more work to do to translate these findings into therapeutic strategies for human treatment.

“We have developed a promising drug combination strategy to reverse drug resistance in highly drug-resistant patient-derived tumors,” wrote Lin. “We hope that this drug combination will move into clinical studies and that PDAC patients will benefit from our research.”

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