Pancreatic cancer: The RAS paradigm shift
Related Experiment Video
Updated: Oct 31, 2026

07:08
Reprogramming Pancreatic Ductal Adenocarcinoma to Pluripotency
Published on: February 2, 2024
Samuel P Soff1,2, Eileen M O'Reilly1,2
1Department of Medicine, Weill Cornell Medicine, New York, New York, United States of America.
Plos Medicine
|October 29, 2026
Abstract:
Treatment approaches for pancreatic adenocarcinoma, an aggressive disease with poor prognosis, are evolving beyond cytotoxic chemotherapy. Recent advances in RAS targeting with small molecules are redefining therapeutic paradigms.
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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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