Scientists attack the root cause of pancreatic cancer

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Pancreatic cancer is a complex disease with various subtypes, yet it is often treated as a single entity with a one-size-fits-all approach.

Most cases are classified as pancreatic ductal adenocarcinoma (PDAC), but multiple other subtypes exist, each with distinct characteristics and treatment responses.

However, due to a lack of relevant models and limited understanding of these subtypes, current treatments do not consider subtype-specific information for risk assessment or therapy selection.

Unlocking the Origins of Pancreatic Cancer

Dr. Tannishtha Reya’s research at Columbia University’s Vagelos College of Physicians and Surgeons and the Herbert Irving Comprehensive Cancer Center aims to change this approach.

Her groundbreaking work focuses on unraveling the molecular underpinnings of different pancreatic cancer subtypes to develop tailored therapies.

The Role of Stem Cells in Pancreatic Cancer

Reya’s previous research had identified the MSI2 gene as a key driver of aggressive pancreatic cancers. This gene encodes a protein that maintains cells in a “stem-like” state.

The team suspected that stem cells in the pancreas, already expressing high MSI2 levels, could be the origin of these cancers.

To investigate this further, they engineered a model in which a mutated MYC gene, a known cancer inducer, was exclusively expressed in MSI2-expressing cells.

This led to the development of various pancreatic cancer subtypes, including adenosquamous carcinoma, acinar cell carcinoma, and anaplastic tumors, alongside the commonly studied PDAC.

Implications for Research and Treatment

Reya’s findings establish MSI2-expressing cells as the origin of multiple pancreatic cancer types, providing a valuable foundation for studying their progression and molecular pathways.

This discovery is particularly crucial for understanding and combating adenosquamous carcinoma, the deadliest form of the disease.

Additionally, the model offers potential for early detection strategies, helping identify when precancerous cells transition to malignancy—a critical aspect given pancreatic cancer’s late diagnosis in advanced stages.

Moreover, the research identifies potential targets for novel pancreatic cancer therapies, especially for subtypes resistant to current treatments.

Unconventional approaches, such as using late-stage cancer gene products as vaccines to trigger the immune system against early-stage tumors, are under investigation.

Conclusion

Dr. Tannishtha Reya’s groundbreaking research sheds light on the diverse subtypes of pancreatic cancer and their origins.

By understanding the molecular underpinnings of each subtype, personalized treatment approaches can be developed.

The new model not only provides insights into disease progression but also holds promise for early detection strategies and innovative therapies, offering hope to pancreatic cancer patients for more effective and tailored treatments.

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The research findings can be found in Cancer Cells.

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