Evidence map›Paper›PMID 33913031›Full record

ReviewJournal of cancer research and clinical oncology2021

Ten-eleven translocase: key regulator of the methylation landscape in cancer.

Jyoti Shekhawat, Kavya Gauba, Shruti Gupta, Bikram Choudhury, Purvi Purohit, Praveen Sharma, Mithu Banerjee

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cancer research and clinical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. CanPharmaceuticals (Basel, Switzerland) · 2024
    Review
  3. Review
  4. Article
  5. Aging Hallmarks and the Role of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023
    Review
  6. Article
  7. Article
  8. Mechanisms that regulate the activities of TET proteins.Cellular and molecular life sciences : CMLS · 2022
    Review
  9. Article
  10. Article
  11. Review
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

7 authors at 1 institution in 1 country.

Jyoti ShekhawatDepartment of Biochemistry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India.ORCID http://orcid.org/0000-0002-6787-3450
Kavya GaubaDepartment of Biochemistry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India.ORCID http://orcid.org/0000-0001-8625-6055
Shruti GuptaDepartment of Biochemistry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India.ORCID http://orcid.org/0000-0002-7435-3496
Bikram ChoudhuryDepartment of E.N.T.-Otorhinolaryngology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India.
Purvi PurohitDepartment of Biochemistry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India.
Praveen SharmaDepartment of Biochemistry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India.
Mithu BanerjeeDepartment of Biochemistry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India. mithu.banerjee.3@gmail.com.ORCID http://orcid.org/0000-0002-4107-3076
All India Institute of Medical Sciences Jodhpur · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMethylation of 5th residue of cytosine in CpG island forms 5-methylcytosine which is stable, heritable epigenetic mark. Methylation levels are broadly governed by methyltransferases and demethylases. An aberration in the demethylation process contributes to the silencing of gene expression. Ten eleven translocation (TET) dioxygenase (1-3) the de novo demethylase is responsible for conversion of 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC), 5-formylcytosisne (5-fC) and 5-carboxycytosine (5-caC) during demethylation process. Mutations and abnormal expression of TET proteins contribute to carcinogenesis. Discovery of TET proteins has offered various pathways for the reversal of methylation levels thus, enhancing our knowledge as to how methylation effects cancer progression.

methodsWe searched "PubMed" and "Google scholar" databases and selected studies with the following keywords "TET enzyme", "cancer", "5-hmC", and "DNA demethylation". In this review, we have discussed combinatorial use of vitamin C in inhibiting tumour growth by enhancing the catalytic activity of TET enzymes and consequently, increasing the 5-hmC levels. 5-Hydroxymethylcytosine holds promise as a prognostic biomarker in solid cancers. The contribution of induction and suppression of TET enzymes and 5-hmC carcinogenesis are discussed in haematological and solid cancers.

resultsWe found that TET enzymes play central role in maintaining the methylation balance. Any anomaly in their expression may dip the balance towards cancer progression. Low levels of TET enzymes and 5-hmC correlate with tumour invasion, progression and metastasis. Also, use of vitamin C enhances TET activity.

conclusionTET enzymes play vital role in shaping the methylation landscape in body. 5-hmC can be used as prognostic marker in solid cancers.

Indexed as

DNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansMixed Function OxygenasesNeoplasmsProto-Oncogene ProteinsMixed Function OxygenasesProto-Oncogene ProteinsTET1 protein, human5-Hydroxymethylcytosine5-MethylcytosineCancerDNA demethylationEpigeneticsTET enzymes

Identifiers

PMID33913031
PMCPMC11802082
OpenAlexW3158350975

What OpenQuestion holds

Textmetadata
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.