KRASG12D inhibition reprograms the microenvironment of early and advanced pancreatic cancer to promote FAS-mediated killing by CD8+ T cells
Open accessAbstract
The KRAS G12D mutation is present in nearly half of pancreatic adenocarcinomas (PDAC). We investigated the effects of inhibiting the KRAS G12D mutant protein with MRTX1133, a non-covalent small molecule inhibitor of KRAS G12D, on early and advanced PDAC and its influence on the tumor microenvironment. Employing 16 different models of KRAS G12D-driven PDAC, we demonstrate that MRTX1133 reverses early PDAC growth, increases intratumoral CD8+ effector T cells, decreases myeloid infiltration, and reprograms cancer-associated fibroblasts. MRTX1133 leads to regression of both established PanINs and advanced PDAC. Regression of advanced PDAC requires CD8+ T cells and immune checkpoint blockade (ICB) synergizes with MRTX1133 to eradicate PDAC and prolong overall survival. Mechanistically, inhibition of KRAS G12D in advanced PDAC and human patient derived organoids induces FAS expression in cancer cells and facilitates CD8+ T cell-mediated death. Collectively, this study provides a rationale for a synergistic combination of MRTX1133 with ICB in clinical trials.
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Short-term treatment with MRTX1133 resulted in increases in CD4+ and CD8+ T cells in the orthotopic model.
“Consistent with prior reports (32, 33), short-term treatment with MRTX1133 resulted in increases in CD4+ and CD8+ T cells in this orthotopic model (Supplementary Fig. S9A–S9C).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [32]
The passage accompanying Figure 5 reports increased proportions of naïve CD4+ cells, CD8+ cells, and CD8+ effector cells after MRTX1133 treatment in the orthotopic KPC689 model. It does not specify that these T-cell increases followed short-term treatment, so the timing qualifier is not established by the cited passage (page unavailable). (LLM, conf=0.82)
Experimental — accuracy not yet measuredMRTX1133 has been shown to confer robust short-term responses in genetically engineered mouse models of PDAC and displayed increased efficacy when combined with immune checkpoint blockade.
“Moreover, MRTX1133 has been shown to confer robust short-term responses in genetically engineered mouse models (GEMM) of PDAC (33) and displayed increased efficacy when combined with immune checkpoint blockade (32).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [32]
Recent preclinical work with MRTX1133 has demonstrated excellent responses in cell line and xenograft models of PDAC.
“Recent preclinical work with MRTX1133 has demonstrated excellent responses in cell line and xenograft models of PDAC (30, 32).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [32]
Combining MRTX1133 with one or more immune checkpoint blockades was more effective than MRTX1133 as a single agent in a murine model of PDAC.
“Combining the KRAS G12D inhibitor MRTX1133 with one or more immune checkpoint blockades was more effective than MRTX1133 as a single agent in a murine model of PDAC [132].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [132]
Addition of αCTLA-4 or αCTLA-4 with αPD-1 to MRTX1133 sustained tumor inhibition and facilitated immune-mediated cancer clearance in a murine PDAC model.
“Unlike MRTX1133 monotherapy, which eventually allowed tumor escape leading to PDAC progression, the addition of either αCTLA-4 or αCTLA-4 with αPD-1 sustained tumor inhibition and facilitated immune-mediated cancer clearance [132].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [132]
Recent work has shown that KRASG12D inhibition leads to an immunogenic response.
“Recent work has also shown that KRASG12D inhibition leads to an immunogenic response (32, 33); thus, therapies that activate the immune response should be further investigated in combination with KRAS inhibitors in preclinical models and ultimately clinical trials (32, 70).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [32]
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Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer
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“…G12C inhibitors against sensitive mouse tumors, possibly because they prevent feedback reactivation driven by the loss of ERK-mediated EGFR repression when KRAS activity is abrogated and/or because SHP2 inhibitors drive KRAS to be in the G12C inhibitor-sensitive GDP-bound state of KRAS [50,133].”
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- Authors
- Mahadevan, K. K., McAndrews, K. M., LeBleu, V. S., Yang, S., Lyu, H., Li, B., Sockwell, A. M., Kirtley, M. L., Morse, S. J., Moreno Diaz, B. A., Kim, M. P., Feng, N., Lopez, A. M., Guerrero, P. A., Paradiso, F., Sugimoto, H., Arian, K. A., Ying, H., Barekatain, Y., Sthanam, L. K., Kelly, P. J., Maitra, A., Heffernan, T. P., & Kalluri, R.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Northwestern University (US)
- Corresponding author
- Maitra, Anirban
- Heffernan, Timothy P.
- Kalluri, Raghu
- ORCID
- Mahadevan, Krishnan K.
- McAndrews, Kathleen M.
- LeBleu, Valerie S.
- Yang, Sujuan
- Li, Bingrui
- Sockwell, Amari M.
- Kirtley, Michelle L.
- Morse, Sami J.
- Kim, Michael P.
- Feng, Ningping
- Lopez, Anastasia M.
- Guerrero, Paola A.
- Paradiso, Francesca
- Sugimoto, Hikaru
- Ying, Haoqiang
- Barekatain, Yasaman
- Sthanam, Lakshmi Kavitha
- Maitra, Anirban
- Heffernan, Timothy P.
- Kalluri, Raghu
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2023-09
- Volume
- 41
- Issue
- 9
- Pages
- 1606-1620.e8
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC10785700
- OpenAlex
- W4386150010
- Cited by
- 258
- References
- 43
- Citations by year
- 2026: 88 · 2025: 93 · 2024: 72 · 2023: 5
- FWCI
- 31.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 376 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Commons-TMC (Texas Medical Center) (submittedVersion)
- Funders
- Break Through Cancer
- National Cancer Institute (P01 CA117969, P30CA16672, R35CA263815, U54CA274371)
- Sid W. Richardson Foundation
- Lustgarten Foundation
- Johns Hopkins University
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- KRAS G12D, pancreatic ductal adenocarcinoma, MRTX1133, KRAS inhibitors, tumor microenvironment, CD8+ T cells, cancer-associated fibroblasts, myeloid cell infiltration, pancreatic intraepithelial neoplasia, immune checkpoint blockade, combination therapy, patient-derived organoids
- MeSH terms
- Heterocyclic Compounds, 2-Ring, Humans, Naphthalenes, Pancreatic Neoplasms, Proto-Oncogene Proteins p21(ras), CD8-Positive T-Lymphocytes, Tumor Microenvironment
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