Evidence map›Paper›PMID 38577139›Full record

ArticleIndian journal of clinical biochemistry : IJCB2024

Identification of Genetic Variants in Exon 4 of TP53 in Lung Carcinoma and in Silico Prediction of Their Significance.

Rajendra Prasad, Kirti Sharma, Karanpreet Bhutani, Suvarna Prasad, Sunita Manhas, Jai Kishan

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Article in Indian journal of clinical biochemistry : IJCB, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Rajendra PrasadDepartment of Biochemistry, M.M. Institute of Medical Sciences and Research (MMIMSR), Maharishi Markandeshwar University (MMU), Mullana, Ambala India.ORCID 0000-0002-7104-9077
Kirti SharmaDepartment of Biochemistry, M.M. Institute of Medical Sciences and Research (MMIMSR), Maharishi Markandeshwar University (MMU), Mullana, Ambala India.
Karanpreet BhutaniDepartment of Biochemistry, M.M. Institute of Medical Sciences and Research (MMIMSR), Maharishi Markandeshwar University (MMU), Mullana, Ambala India.
Suvarna PrasadDepartment of Biochemistry, M.M. Institute of Medical Sciences and Research (MMIMSR), Maharishi Markandeshwar University (MMU), Mullana, Ambala India.
Sunita ManhasDepartment of Biochemistry, M.M. Institute of Medical Sciences and Research (MMIMSR), Maharishi Markandeshwar University (MMU), Mullana, Ambala India.
Jai KishanDepartment of Respiratory Medicine, M.M. Institute of Medical Sciences and Research (MMIMSR), Maharishi Markandeshwar University (MMU), Mullana, Ambala India.
Maharishi Markandeshwar University, Mullana · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is a severe and the leading cause of cancer related deaths in men and women all over the world. Tumor suppressor protein (TP53) encoded by the TP53 gene which plays a pivotal role in various cellular tumor suppression processes viz cell cycle arrest and apoptosis. Henceforth, the present study was aimed to TP53 exon4 variants from lung carcinoma. Histopathologic and clinically proven 20 patients of lung cancer were enrolled in this study the average age of patients was 45 ± 8 years which categorized as early onset of lung cancer. Genomic DNA was isolated from the blood specimen of patients. Extracted DNA was subjected to PCR amplification for exon 4 of TP53 using appropriate primers and subsequently amplified products were applied to nucleotide alterations via using the DNA sanger sequencing. The genetic analysis documented five variants in exon4 of TP53 which include viz. 4 substitutions [c.215 > C at codon 72, C. 358-359AA > GG at codon 120] were highly prevalent, occurring in 63% and 25% frequency in patients. Other two variants viz. C. 358 A > C at codon 120, C. 365T > G at codon 122 were present at frequency of 15% whilst one deletion variant [152 del C] was found with 5% frequency. Furthermore, alterations on codon 72, 120,122 and 51 were characterized as possibly damaging by Poly Phen-2 and decreased stability using stability bioinformatic tool. Taken together all these findings infer that TP53 gene involved in modulation and susceptibility to lung cancer.

Indexed as

Arg 72 pro variantExon 4Lung cancerMutational spectrumTP53

Identifiers

PMID38577139
PMCPMC10987423
OpenAlexW4311879179

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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.