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@ARTICLE{Rondeau:305751,
      author       = {V. Rondeau and S. Bansal and M. M. Buttigieg and A. G. X.
                      Zeng and D. Y. Chan and M. Chan-Seng-Yue and L. Jin and J.
                      McLeod and M. Kates and E. Donato$^*$ and P. Stelmach$^*$
                      and C. Vlasschaert and Y. Yang and A. Gupta and S. Genta and
                      E. Sanz-Garcia and L. Shlush and M. Ribeiro and M. O. Butler
                      and S. Abelson and M. D. Minden and S. D. Saibil and S. M.
                      Chan and M. J. Rauh and A. Trumpp$^*$ and J. E. Dick and R.
                      Vanner$^*$},
      title        = {{R}esponse to {I}mmune {C}heckpoint {B}lockade is
                      {E}nhanced in the {P}resence of {H}ematopoietic {TET}2
                      {I}nactivation.},
      journal      = {Cancer research},
      volume       = {86},
      number       = {4},
      issn         = {0099-7013},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2025-02371},
      pages        = {845-857},
      year         = {2026},
      note         = {2026 Feb 16;86(4):845-857 / DKFZ-ZMBH Alliance / #LA:A010#},
      abstract     = {Somatic mutations inactivating TET2 are among the most
                      common drivers of clonal hematopoiesis (CH). TET2
                      inactivation is associated with monocyte-derived
                      inflammation and improved chimeric antigen receptor T cell
                      function, suggesting it might also impact immunotherapy
                      response. Here, we found that hematopoietic Tet2 mutation in
                      mouse models enhanced the immune checkpoint blockade (ICB)
                      response, which required the combined presence of
                      phagocytes, CD4+, and CD8+ T cells. The effect was lost with
                      myeloid- or T-cell restricted Tet2 inactivation or in mice
                      with $20\%$ Tet2-mutant hematopoiesis. Mechanistically, in
                      Tet2-mutant tumor-infiltrating leukocytes (TILs), ICB
                      preferentially restricted cell states linked to tumor
                      progression while inducing anti-tumor states. Tet2-mutant
                      monocytes activated costimulatory programs, while
                      Tet2-mutant T cells showed enhanced T cell memory
                      signatures, alongside decreased exhaustion and regulatory
                      phenotypes. Clinically, tumors from colorectal cancer and
                      melanoma patients with TET2 driver mutation-CH (TET2-CH)
                      showed enhanced immune infiltration, inflammation, and T
                      cell activation. In melanoma patients treated with ICB,
                      TET2-CH was associated with 6-fold greater odds of clinical
                      benefit. Collectively, this work demonstrates that
                      hematopoietic TET2 inactivation primes leukocytes for
                      anti-tumor states associated with immunotherapy response and
                      provides a potential biomarker for personalized therapy.},
      cin          = {A010 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)A010-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41218172},
      doi          = {10.1158/0008-5472.CAN-24-3329},
      url          = {https://inrepo02.dkfz.de/record/305751},
}