Publication
CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer.
Li Qiang, Megan T Hoffman, Jung-Ho Chun, Brendan Parent, Felix Hambitzer, Frank Peprah, Courtney T S Kureshi, Birkley S Lim, Eugena Chang, Michael J Walsh, Julissa G Tello, Tavus Atajanova, Hojeong Shin, Corey Perkins, Rakeeb Kureshi, Yaniris Molina-Aponte, James M Dougan, Chong Zuo, Lauren Brais, Thomas E Clancy, James M Cleary, Jason L Hornick, Brandon M Huffman, Joseph D Mancias, George Molina, Mark Fairweather, Jonathan A Nowak, Kimberly J Perez, Douglas A Rubinson, Sarah Slater, Ritchell van Dams, Jiping Wang, Brian M Wolpin, Kwok-Kin Wong, Harshabad Singh, Andrew J Aguirre, David Baker, Michael Dougan, Stephanie K Dougan
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- PubMed
- Retrieved
- Sep 29, 2026
- Layer
- normalized (units and labels harmonized; values unchanged)
- Run
- ING-PUBMED-20260929-000001
Abstract
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Pancreatic ductal adenocarcinoma (PDAC) is refractory to most therapies, including immunotherapies, for which reinvigoration of CD8 T cells through immune checkpoint blockade is insufficient to induce long-term, durable remissions. Direct KRAS inhibitors (KRASi) have shown clinical promise,…
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Candidate 1
- cancerMalignant Pancreatic Neoplasmdictionary0.60
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