ReviewCell biochemistry and function2026
TET2 as a Context-Dependent Epigenetic Integrator in Clonal Hematopoiesis, Inflammation, Cancer, and Immunotherapy.
Review in Cell biochemistry and function, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- TET2 as a Context-Dependent Epigenetic Integrator in Clonal Hematopoiesis, Inflammation, Cancer, and Immunotherapy.Cell biochemistry and function · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Ten-Eleven Translocation 2 (TET2) is an Fe(II)- and α-ketoglutarate-dependent dioxygenase that initiates active DNA demethylation by oxidizing 5-methylcytosine (5mC). Beyond this enzymatic role, TET2 links DNA methylation dynamics with chromatin regulation, cellular metabolism, immune-cell identity, and treatment response in a context-dependent manner. Loss-of-function mutations in TET2 are among the most frequent genetic events in age-related clonal hematopoiesis of indeterminate potential (CHIP), where they are associated with higher risks of hematological malignancies and cardiovascular disease. Human genetic and clinical studies support these associations, while experimental models suggest that mutant hematopoietic clones can promote myeloid inflammatory programs through enhancer remodeling, NLRP3 inflammasome activation, IL-1β/IL-6 signaling, and altered inflammatory resolution. In solid tumors and cancer therapy, TET2 has more variable effects: tumor-cell-intrinsic TET2 loss can contribute to immune escape or therapeutic resistance in selected settings, whereas TET2 disruption in engineered T cells can enhance memory-like persistence and anti-tumor activity, with possible long-term oncogenic risk. This narrative, mechanism-oriented review integrates current evidence on TET2 biology across clonal hematopoiesis, inflammation, cancer, and immunotherapy. We focus on evidence level, cell type, direction of TET2 alteration, and metabolic or therapeutic context as determinants of divergent TET2 functions. TET2 has traditionally been described as a DNA demethylation enzyme, but recent studies increasingly place it among context-dependent regulators of immune and disease phenotypes. The unresolved issue is why TET2 loss, inhibition, activation, or engineered deletion can produce distinct, and sometimes opposing, effects in hematopoietic stem/progenitor cells, macrophages, tumor cells, neurons, microglia, and CAR-T cells. This review uses four variables-cell type, direction of alteration, functional layer, and microenvironmental or therapeutic context-to interpret evidence from CHIP, hematologic malignancies, cardiovascular inflammation, solid tumors, and immunotherapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.