Evidence map›Paper›PMID 33509440›Full record

ReviewSeminars in hematology2021

TET-dioxygenase deficiency in oncogenesis and its targeting for tumor-selective therapeutics.

Yihong Guan, Metis Hasipek, Anand D Tiwari, Jaroslaw P Maciejewski, Babal K Jha

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in hematology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 21% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. The role of TET2 in solid tumors and its therapeutic potential: a comprehensive review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review
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  5. Article
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  7. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yihong GuanDepartment of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.
Metis HasipekDepartment of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.
Anand D TiwariDepartment of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.
Jaroslaw P MaciejewskiDepartment of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.
Babal K JhaDepartment of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH. Electronic address: jhab@ccf.org.
Cleveland Clinic · US

Funding

Therapeutic Implications of Molecular Defects in Bone Marrow FailureR35HL135795 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI MACIEJEWSKI, JAROSLAW P. · 2017 to 2023
$5.7M
Targeting TET DNA Dioxygenases as Therapeutic Principle in Myeloid NeoplasmsR01CA257544 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI JHA, BABAL K, MACIEJEWSKI, JAROSLAW P. · 2021 to 2025
$3.0M
Translational Hematology and Oncology Research Laboratory Expansion ProjectC06RR028655 · NCRR · CLEVELAND CLINIC LERNER COM-CWRU · PI MACIEJEWSKI, JAROSLAW P. · 2010 to 2010
$2.0M
NCI NIH HHS R01 CA257544NCRR NIH HHS C06 RR028655NHLBI NIH HHS R35 HL135795
6 · The paper itself

Abstract

TET2 is one of the most frequently mutated genes in myeloid neoplasms. TET2 loss-of-function perturbs myeloid differentiation and causes clonal expansion. Despite extensive knowledge regarding biochemical mechanisms underlying distorted myeloid differentiation, targeted therapies are lagging. Here we review known biochemical mechanisms and candidate therapies that emerge from this. Specifically, we discuss the potential utility of vitamin C to compensate for TET-dioxygenase deficiency, to thereby restore the biochemical function. An alternative approach exploits the TET-deficient state for synthetic lethality, exploiting the fact that a minimum level of TET-dioxygenase activity is required for cell survival, rendering TET2-mutant malignant cells selectively vulnerable to inhibitors of TET-function.

Indexed as

CarcinogenesisDioxygenasesAscorbic AcidDNA-Binding ProteinsDNA MethylationHematopoiesisHumansProto-Oncogene ProteinsAscorbic AcidDioxygenasesDNA-Binding ProteinsProto-Oncogene ProteinsTET2 protein, humanAscorbic AcidIDH1/2MDSTET-dioxygenasesTherapeutic targeting

Identifiers

PMID33509440
PMCPMC7938524
OpenAlexW3116759727

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.