{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T17:15:47Z","timestamp":1790615747563,"version":"4.1.0"},"posted":{"date-parts":[[2025,3,4]]},"group-title":"Cancer Biology","reference-count":103,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2025,3,4]],"date-time":"2025-03-04T00:00:00Z","timestamp":1741046400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2025,9,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Lack of sustained response to oncogenic Kras (Kras*) inhibition in preclinical models and patients with pancreatic ductal adenocarcinoma (PDAC) emphasizes the need to identify impactful synergistic combination therapies to achieve robust clinical benefit. Kras* targeting results in an influx of T cell infiltrates including Tregs, effector CD8\n                  <jats:sup>+<\/jats:sup>\n                  T cells and exhausted CD8\n                  <jats:sup>+<\/jats:sup>\n                  T cells expressing several immune checkpoint molecules in PDAC. Here, we probe whether the T cell influx induced by different Kras* inhibitors enable a therapeutic window to prime adaptive immune response in PDAC. Here we report a specific synergy between Kras\n                  <jats:sup>G12D<\/jats:sup>\n                  allele specific inhibitor, MRTX1133 or multi-selective pan-RAS inhibitor, RMC-6236 and anti-CTLA4 immune checkpoint blockade. In contrast, attempted therapeutic combination with multiple other immune checkpoint inhibitors, including anti-PD1, anti-Tim3, anti-Lag3, anti-Vista and anti-4-1BB agonist antibody failed due to compensatory mechanisms mediated by other checkpoints on exhausted CD8\n                  <jats:sup>+<\/jats:sup>\n                  T cells. Specifically, anti-CTLA4 therapy in Kras* targeted PDAC transcriptionally reprograms effector T regs to a na\u00efve phenotype, reverses CD8\n                  <jats:sup>+<\/jats:sup>\n                  T cell exhaustion and is associated with recruitment of tertiary lymphoid structures (TLS) containing follicular B cells, interferon (IFN)- stimulated\/ activated B cells, plasma cells and germinal center B cells to functionally enable efficacy of immunotherapy with long-term survival. In this regard, inhibition of the TLS with lymphotoxin-\u03b2 inhibitor (LTBi) or direct B cell depletion reversed the survival benefit conferred by the combination therapy and highlights the function of TLS in generating productive anti-tumor immune responses. Further, single cell ATAC sequencing analysis revealed that transcriptional reprogramming of Tregs is epigenetically regulated by downregulation of AP-1 family of transcription factors including Fos, Fos-b, Jun-b, Jun-d in the IL-35 promoter region. This study reveals an actionable vulnerability in the adaptive immune response in Kras* targeted PDAC with relevant clinical implications.\n                <\/jats:p>","DOI":"10.1101\/2025.02.28.640711","type":"posted-content","created":{"date-parts":[[2025,3,5]],"date-time":"2025-03-05T05:35:45Z","timestamp":1741152945000},"source":"Crossref","is-referenced-by-count":8,"title":["Distinct small molecule inhibitors of Kras specifically prime CTLA4 blockade therapy to transcriptionally reprogram Tregs and overcome resistance to suppress pancreas cancer"],"prefix":"10.64898","author":[{"given":"Krishnan K.","family":"Mahadevan","sequence":"first","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana S.","family":"Maldonado","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bingrui","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aaron A.","family":"Bickert","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adrian","family":"Kapercyzk-Perdyan","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shreyasee V.","family":"Kumbhar","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sujan","family":"Piya","sequence":"additional","affiliation":[{"name":"Departments of Anatomical Pathology and Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amari","family":"Sockwell","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sami J.","family":"Morse","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kent","family":"Arian","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hikaru","family":"Sugimoto","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shabnam","family":"Shalapour","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David S.","family":"Hong","sequence":"additional","affiliation":[{"name":"Department of Investigative Cancer Therapeutics, University of Texas MD Anderson Cancer Center, Houston, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Timothy P.","family":"Heffernan","sequence":"additional","affiliation":[{"name":"Insititute for Applied Science and TRACTION platform, University of Texas MD Anderson Cancer Center, Houston, TX, 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Hong 12 Preliminary Safety, Antitumor Activity, and Circulating Tumor DNA (ctDNA) Changes with Zoldonrasib (RMC-9805), an Oral, RAS(ON) G12D-Selective, Tri-Complex Inhibitor in Patients with KRAS G12D Pancreatic Ductal Adenocarcinoma (PDAC) from a Phase 1 Study in Advanced Solid Tumors."},{"key":"2026041112044457000_2025.02.28.640711v2.6","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1917239"},{"key":"2026041112044457000_2025.02.28.640711v2.7","doi-asserted-by":"publisher","DOI":"10.1021\/acs.jmedchem.9b01180"},{"key":"2026041112044457000_2025.02.28.640711v2.8","doi-asserted-by":"publisher","DOI":"10.1038\/nature12796"},{"key":"2026041112044457000_2025.02.28.640711v2.9","doi-asserted-by":"publisher","DOI":"10.1021\/acsmedchemlett.8b00382"},{"key":"2026041112044457000_2025.02.28.640711v2.10","doi-asserted-by":"publisher","DOI":"10.1158\/2159-8290.CD-19-1167"},{"key":"2026041112044457000_2025.02.28.640711v2.11","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa2204619"},{"key":"2026041112044457000_2025.02.28.640711v2.12","doi-asserted-by":"publisher","DOI":"10.1158\/2159-8290.CD-24-0027"},{"key":"2026041112044457000_2025.02.28.640711v2.13","doi-asserted-by":"publisher","DOI":"10.1038\/s41586-024-07379-z"},{"key":"2026041112044457000_2025.02.28.640711v2.14","doi-asserted-by":"publisher","DOI":"10.1038\/s41586-023-06123-3"},{"key":"2026041112044457000_2025.02.28.640711v2.15","doi-asserted-by":"publisher","DOI":"10.1038\/nature22341"},{"key":"2026041112044457000_2025.02.28.640711v2.16","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.99263"},{"key":"2026041112044457000_2025.02.28.640711v2.17","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-14-1591"},{"key":"2026041112044457000_2025.02.28.640711v2.18","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccell.2015.11.011"},{"key":"2026041112044457000_2025.02.28.640711v2.19","doi-asserted-by":"publisher","DOI":"10.1001\/jamanetworkopen.2024.9840"},{"key":"2026041112044457000_2025.02.28.640711v2.20","doi-asserted-by":"publisher","DOI":"10.1513\/pats.200809-107LC"},{"key":"2026041112044457000_2025.02.28.640711v2.21","doi-asserted-by":"publisher","DOI":"10.1054\/bjoc.2001.1964"},{"key":"2026041112044457000_2025.02.28.640711v2.22","doi-asserted-by":"publisher","DOI":"10.1158\/2159-8290.CD-20-0442"},{"key":"2026041112044457000_2025.02.28.640711v2.23","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccell.2024.08.002"},{"key":"2026041112044457000_2025.02.28.640711v2.24","unstructured":"Kathleen M. 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