ReviewCancer treatment and research2023
Ten-Eleven-Translocation Genes in Cancer.
Review in Cancer treatment and research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed, 5 citations in OpenAlex.
- Methylations in dilated cardiomyopathy and heart failure.Frontiers in cardiovascular medicine · 2025Review
- Unravelling the role of TET2 in venous thromboembolism: insights into mechanisms and therapeutic implications.Frontiers in cardiovascular medicine · 2025Review
- CanPharmaceuticals (Basel, Switzerland) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ten-Eleven-Translocation (TET) family of genes, including TET1, TET2, and TET3, play critical roles in the oxidation of 5-methylcytosine marks in both DNA and RNA, thereby regulating the epigenome and epitranscriptome in cells. These genes are frequently mutated in both hematopoietic malignancies and in solid cancers. TET2, in particular, is one of the most frequently mutated genes in clonal hematopoiesis in the general population, which impacts both the transformation of hematopoietic malignancies and the immune responses in solid tumors. While much has been learned in the 14 years since the discovery of TETs' biochemical function and mutations, many important questions remain. This review covers several aspects of TET-related biology to discuss key yet unanswered questions. What are the functions of different forms of TET mutations found in human cancers? How does TET2 mutation enable pre-malignant hematopoietic expansion? How does TET2 mutation cooperate with partner lesions to cause transformation? And how do TET mutations affect immune responses in solid cancers.
Indexed as
Identifiers
What OpenQuestion holds
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.