Evidence map›Paper›PMID 34181170›Full record

ArticleMolecular biology reports2021

TP53 codon 72 polymorphism and type 2 diabetes: a case-control study in South Indian population.

Harshitha K Punja, Dechamma Pandyanda Nanjappa, Nishith Babu, Krithika Kalladka, B Shanti Priya Dias, Gunimala Chakraborty, Sudhindra M Rao, Anirban Chakraborty

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Article in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecular targets and mechanisms ofWorld journal of diabetes · 2023
    Article
  4. Article
  5. 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

8 authors at 2 institutions in 1 country.

Harshitha K Punja *Department of General Medicine, KS Hegde Medical Academy, Nitte (Deemed to be University), Mangaluru, 575018, India.
Dechamma Pandyanda Nanjappa *Division of Molecular Genetics and Cancer, Nitte University Centre for Science Education and Research (NUCSER), Nitte (Deemed to be University), Kotekar-Beeri Road, Deralakatte, Mangaluru, 575018, India.
Nishith BabuDivision of Molecular Genetics and Cancer, Nitte University Centre for Science Education and Research (NUCSER), Nitte (Deemed to be University), Kotekar-Beeri Road, Deralakatte, Mangaluru, 575018, India.
Krithika KalladkaDivision of Molecular Genetics and Cancer, Nitte University Centre for Science Education and Research (NUCSER), Nitte (Deemed to be University), Kotekar-Beeri Road, Deralakatte, Mangaluru, 575018, India.
B Shanti Priya DiasDivision of Molecular Genetics and Cancer, Nitte University Centre for Science Education and Research (NUCSER), Nitte (Deemed to be University), Kotekar-Beeri Road, Deralakatte, Mangaluru, 575018, India.
Gunimala ChakrabortyDivision of Molecular Genetics and Cancer, Nitte University Centre for Science Education and Research (NUCSER), Nitte (Deemed to be University), Kotekar-Beeri Road, Deralakatte, Mangaluru, 575018, India.
Sudhindra M RaoDepartment of General Medicine, KS Hegde Medical Academy, Nitte (Deemed to be University), Mangaluru, 575018, India.
Anirban ChakrabortyDivision of Molecular Genetics and Cancer, Nitte University Centre for Science Education and Research (NUCSER), Nitte (Deemed to be University), Kotekar-Beeri Road, Deralakatte, Mangaluru, 575018, India. anirban@nitte.edu.in.ORCID http://orcid.org/0000-0003-3476-6576
Nitte University · INK S Hegde Medical Academy · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TP53 functions primarily as a tumor suppressor, controlling a myriad of signalling pathways that prevent a cell from undergoing malignant transformation. This tumor suppressive function requires an activation and stabilization of TP53 in response to cell stressors. However, besides its cancer-preventive functions, TP53 is also known to be involved in diverse cellular processes including metabolism, reproduction, stem cell renewal and development. Indeed, several lines of evidence strongly suggest that TP53 plays crucial role in diabetes. A number of studies have evaluated the association of genetic alterations (single nucleotide variations) in TP53 gene with the development of diabetes. However, the results have not been consistent. The aim of this study was to evaluate whether the C/G polymorphism at codon 72 (Pro72/Arg72), located in exon 4 of TP53, is associated with type 2 diabetes in South Indian population. A total of 74 type 2 diabetic patients and 54 non-diabetic subjects were screened. None of the three genotypes, namely C/C (Pro/Pro), C/G (Pro/Arg), and G/G (Arg/Arg) was found to be significantly associated with type 2 diabetes in our study group. The findings of this study indicate that TP53 codon 72 polymorphism is not associated with increased risk of type 2 diabetes in South Indian population. Further studies with a large cohort size would be necessary to corroborate the observations of this study. Nevertheless, this study represents the first genetic analysis of TP53 variants in South Indian type 2 diabetic patients.

Indexed as

AdultAgedAllelesCase-Control StudiesCodonCohort StudiesDiabetes Mellitus, Type 2ExonsFemaleGene FrequencyGenes, p53Genes, Tumor SuppressorGenetic Predisposition to DiseaseGenotypeHumansIndiaCodonTP53 protein, humanTumor Suppressor Protein p53Genetic alterationsIndian cohortInsulin resistanceMetabolic disorderTumor protein p53

Identifiers

PMID34181170
OpenAlexW3174973449

What OpenQuestion holds

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Registered trials

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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.