Evidence map›Paper›PMID 39681652›Full record

ArticleJournal of molecular evolution2025

Positive Selection Shapes Breast Cancer Tumor Suppressor Genes: Unveiling Insights into BRCA1, BRCA2, and MDC1 Stability.

Youssef M Fadel, Marwan Khaled, Mohamed Emam, Nour H Marzouk, Sief El-Din Sobih, Habiba Abd-Elaty, Wafaa M Elrashedy, Gehad Mostafa, Salma Alm Eldeen, Mohaned Bador and 2 more

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Article in Journal of molecular evolution, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Youssef M Fadel *Bioinformatics Group, Center for Informatics Sciences (CIS), Nile University, Giza, Egypt.
Marwan Khaled *Bioinformatics Group, Center for Informatics Sciences (CIS), Nile University, Giza, Egypt.
Mohamed Emam *CIIMAR/CIMAR, Interdisciplinary Centre of Marine and Environmental Research, University of Porto, Terminal de Cruzeiros Do Porto de Leixões, Av. General Norton de Matos, S/N, 4450-208, Porto, Portugal.
Nour H MarzoukBioinformatics Group, Center for Informatics Sciences (CIS), Nile University, Giza, Egypt.
Sief El-Din SobihDepartment of Biology, Faculty of Sciences, Utah State University, Logan, UT, 84321, USA.
Habiba Abd-ElatyBioinformatics Group, Center for Informatics Sciences (CIS), Nile University, Giza, Egypt.
Wafaa M ElrashedyBioinformatics Group, Center for Informatics Sciences (CIS), Nile University, Giza, Egypt.
Gehad MostafaBioinformatics Group, Center for Informatics Sciences (CIS), Nile University, Giza, Egypt.
Salma Alm EldeenBioinformatics Group, Center for Informatics Sciences (CIS), Nile University, Giza, Egypt.
Mohaned BadorBioinformatics Group, Center for Informatics Sciences (CIS), Nile University, Giza, Egypt.
Agostinho AntunesCIIMAR/CIMAR, Interdisciplinary Centre of Marine and Environmental Research, University of Porto, Terminal de Cruzeiros Do Porto de Leixões, Av. General Norton de Matos, S/N, 4450-208, Porto, Portugal. aantunes@ciimar.up.pt.ORCID http://orcid.org/0000-0002-1328-1732
Mohamed El HadidiBioinformatics Group, Center for Informatics Sciences (CIS), Nile University, Giza, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Worldwide, breast cancer is the leading cause of death in women with cancers. Given this situation, new approaches to treatment are urgently needed. Tumor Suppressor Genes (TSGs) defects play a crucial role in tumor development, and recent studies propose their reactivation as a promising way for clinical intervention in breast cancer. Here, we performed detailed evolutionary analyses of 241 breast cancer TSGs across 25 mammalian genomes, revealing 28 genes under strong positive selection. These genes exhibit elevated molecular pressure in codons corresponding to amino acids located in crucial protein domains and motifs. Notably, one positively selected site in the BRCA1 C-terminal domain is known for its role in DNA damage response, suggesting potential interference with DNA repair mechanisms. Moreover, the substitution of some other sites found in important key motifs, namely two codons in BRCA2 (752 and 939) localized within the phosphoinositide-3-OH-kinase-related and playing a crucial role in the DNA repair and the DNA damage checkpoints. Our findings could be inspirational to foster future recommendations for drug-targeting sites and further illuminate the function of these proteins. Finally, the code developed in our study is delivered in the Automated tool for positive selection (ATPs) ( https://github.com/APS-P/Automated-Tool-for-Positive-Selection-ATPS-/wiki ) to assist the easy reproducibility and support future evolutionary genomics analyses.

Indexed as

BRCA1 ProteinBRCA2 ProteinBreast NeoplasmsCell Cycle ProteinsGenes, Tumor SuppressorNuclear ProteinsSelection, GeneticAnimalsDNA RepairEvolution, MolecularFemaleHumansBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanCell Cycle ProteinsNuclear ProteinsBreast cancerDrug targetingEvolutionary analysisPositive selectionTumor suppressor genes

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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.