MétaCan
Menu
Back to cohort
Record W4416116967 · doi:10.1158/0008-5472.can-24-3329

Response to Immune Checkpoint Blockade Is Enhanced in the Presence of Hematopoietic TET2 Inactivation

2025· article· en· W4416116967 on OpenAlexafffund
Vincent Rondeau, Suraj Bansal, Marco M. Buttigieg, Andy G.X. Zeng, Darryl Y. Chan, Michelle Chan‐Seng‐Yue, Jessica McLeod, Meghan Kates, Elisa Donato, Patrick Stelmach, Caitlyn Vlasschaert, Yitong Yang, Aarushi Gupta, Sofia Genta, Enrique Sanz‐García, Liran I. Shlush, Maurício Fernando Silva Almeida Ribeiro, Marcus O. Butler, Sagi Abelson, Mark D. Minden, Samuel D. Saibil, Steven M. Chan, Michael J. Rauh, Andreas Trumpp, John E. Dick, Robert J. Vanner

Bibliographic record

VenueCancer Research · 2025
Typearticle
Languageen
FieldMedicine
TopicCAR-T cell therapy research
Canadian institutionsOntario Institute for Cancer ResearchUniversity of TorontoPrincess Margaret Cancer CentreQueen's UniversityUniversity Health Network
FundersCanadian Cancer Society Research InstituteCanadian Institutes of Health ResearchDepartment of Medicine, University of TorontoTerry Fox Research InstituteDeutsches KrebsforschungszentrumPhysicians' Services Incorporated FoundationPrincess Margaret Cancer FoundationLeukemia and Lymphoma Society of CanadaMinistry of Health, Ontario
KeywordsBlockadeImmune checkpointHaematopoiesisImmunotherapyImmune systemCancer immunotherapy

Abstract

fetched live from OpenAlex

Somatic mutations inactivating Tet methylcytosine dioxygenase 2 (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 that it might also affect immunotherapy response. In this study, 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, ICB preferentially restricted cell states linked to tumor progression while inducing antitumor states. Tet2-mutant monocytes activated costimulatory programs, whereas Tet2-mutant T cells showed enhanced T-cell memory signatures, alongside decreased exhaustion and regulatory phenotypes. Clinically, tumors from patients with colorectal cancer and melanoma with TET2-mutant CH showed enhanced immune infiltration, inflammation, and T-cell activation. In patients with melanoma treated with ICB, TET2-mutant CH was associated with six-fold greater odds of clinical benefit. Collectively, this work demonstrates that hematopoietic TET2 inactivation primes leukocytes for antitumor states associated with immunotherapy response and provides a potential biomarker for personalized therapy. SIGNIFICANCE: TET2 mutations promote antitumor leukocyte states that can potentiate the efficacy of immunotherapy with checkpoint blockade. See related commentary by Yuan and Guryanova, p. 825.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.004

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.059
GPT teacher head0.440
Teacher spread0.381 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations2
Published2025
Admission routes2
Has abstractyes

Explore more

Same venueCancer ResearchSame topicCAR-T cell therapy researchFrench-language works237,207