Evidence map›Paper›PMID 38928318›Full record

ArticleInternational journal of molecular sciences2024

Bioinformatic Identification of TP53 Gene Mutation Hotspots in Colorectal Cancer.

Zsolt Kovács, Haruhiko Sugimura, Tamás Attila György, Eva Osvath, Felix Manirakiza, Simona Gurzu

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer.International journal of molecular sciences · 2025
    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

6 authors.

Zsolt KovácsDepartment of Pathology, "George Emil Palade" University of Medicine, Pharmacy, Science and Technology of Targu Mures, 540139 Targu Mures, Romania.
Haruhiko SugimuraSasaki Institute Sasaki Foundation, Tokyo 101-0062, Japan.ORCID 0000-0002-0779-3088
Tamás Attila GyörgyDepartment of Pathology, "George Emil Palade" University of Medicine, Pharmacy, Science and Technology of Targu Mures, 540139 Targu Mures, Romania.ORCID 0000-0001-6431-906X
Eva OsvathDepartment of Pathology, "George Emil Palade" University of Medicine, Pharmacy, Science and Technology of Targu Mures, 540139 Targu Mures, Romania.
Felix ManirakizaDepartment of Pathology, School of Medicine and Pharmacy, College of Medicine and Health Sciences, University of Rwanda, Kigali P.O. Box 3286, Rwanda.ORCID 0000-0002-9143-8758
Simona GurzuDepartment of Pathology, "George Emil Palade" University of Medicine, Pharmacy, Science and Technology of Targu Mures, 540139 Targu Mures, Romania.ORCID 0000-0003-3968-5118

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations and inactivation of the TP53 gene are frequently observed in various types of malignancies. Precise knowledge of the genetic structure and detection of mutation hotspots are crucial, as these indicate a high probability of developing cancer. The aim of our study was to perform the bioinformatic detection of mutation hotspots in the TP53 gene in patients diagnosed with malignant colon neoplasms using self-developed software (version 1). We compared TP53 gene sequences from 50 healthy individuals with those from 50 patients diagnosed with colorectal carcinoma. Of the 50 samples from cancer patients, the most frequent mutations were observed in exons 5 and 8 (12 mutations per exon) and gene sequences of 12 samples, which differed from those of the 50 samples from healthy individuals. Based on our results, the distribution of mutations in the TP53 gene structure was not even across different exons. By comparing the gene sequences of healthy individuals with those of colon cancer samples, we conclude that structural changes occurring in similar gene regions are not associated with increases in susceptibility to malignancies in every case, namely, that the pathological mechanism is multifactorial.

Indexed as

Colorectal NeoplasmsComputational BiologyExonsMutationTumor Suppressor Protein p53AgedFemaleGenetic Predisposition to DiseaseHumansMaleMiddle AgedTP53 protein, humanTumor Suppressor Protein p53bioinformaticscolorectal cancermutation hotspotsTP53 gene

Identifiers

PMID38928318
PMCPMC11203433

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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.