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Pancreatic cancer is characterized by oncogenic activation of K‐Ras and inactivation of the cell cycle inhibitor p16INK4a. We previously demonstrated that reintroduction of p16INK4a reversed anoikis resistance and clonogenicity of human pancreatic cancer cells, properties commonly attributed to the transforming potential of oncogenic K‐Ras. Therefore, we aimed to determine the role of Ras after p16...
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