Evidence map›Paper›PMID 42221547›Full record

ArticleBiomedical reports2026

Determination of copy number variations and affected gene networks in breast cancer.

Violeta Larios-Serrato, Hilda-Alicia Valdez-Salazar, Javier Torres, Margarita Camorlinga-Ponce, Patricia Piña-Sánchez, Héctor Mayani, Martha-Eugenia Ruiz-Tachiquín

Abstract read
In one paragraph

Article in Biomedical reports, 2026. 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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0citing papers in PubMed
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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

7 authors.

Violeta Larios-SerratoLaboratory of Biotechnology and Genomic Bioinformatics, National School of Biological Sciences, National Polytechnic Institute, Lázaro Cárdenas Professional Unit, Mexico City 11340, Mexico.
Hilda-Alicia Valdez-SalazarInfectious and Parasitic Diseases Medical Research Unit, High Specialty Medical Unit-Pediatrics Hospital 'Dr Silvestre Frenk Freund', XXI Century National Medical Center, Mexican Social Security Institute, Mexico City 06720, Mexico.
Javier TorresInfectious and Parasitic Diseases Medical Research Unit, High Specialty Medical Unit-Pediatrics Hospital 'Dr Silvestre Frenk Freund', XXI Century National Medical Center, Mexican Social Security Institute, Mexico City 06720, Mexico.
Margarita Camorlinga-PonceInfectious and Parasitic Diseases Medical Research Unit, High Specialty Medical Unit-Pediatrics Hospital 'Dr Silvestre Frenk Freund', XXI Century National Medical Center, Mexican Social Security Institute, Mexico City 06720, Mexico.
Patricia Piña-SánchezOncological Diseases Medical Research Unit, High Specialty Medical Unit-Oncology Hospital, XXI Century National Medical Center, Mexican Social Security Institute, Mexico City 06720, Mexico.
Héctor MayaniOncological Diseases Medical Research Unit, High Specialty Medical Unit-Oncology Hospital, XXI Century National Medical Center, Mexican Social Security Institute, Mexico City 06720, Mexico.
Martha-Eugenia Ruiz-TachiquínOncological Diseases Medical Research Unit, High Specialty Medical Unit-Oncology Hospital, XXI Century National Medical Center, Mexican Social Security Institute, Mexico City 06720, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is a highly aggressive form characterized by limited therapeutic options and notable molecular diversity. The present study performed a genome-wide analysis of copy number variations (CNVs) using high-density microarrays in tumor tissue (TUM), adjacent non-tumor tissue (ADJ) and leukocytes (LEU) obtained from five patients with TNBC. The present study identified both unique and shared CNVs across tissue samples, including alterations in key chromosomal regions such as 1q23.3, 1q32.1 and 8q24.3, which harbor oncogenes such as MYC, myeloid cell leukemia 1 (MCL1) and BCL9. Losses in 6q25.2 affecting estrogen receptor 1 (ESR1) gene were also detected. CNVs were enriched in genes associated with Hallmarks of Cancer, with TUM samples showing profiles associated with 'proliferation', 'metastasis' and 'immune evasion', ADJ samples with 'growth suppression' and LEU samples with 'genomic instability'. Pathway enrichment analyses revealed disrupted functions in 'DNA repair', 'extracellular matrix organization' and 'TP53 signaling' in TUM. Notably, EGFR, excision repair cross-complementing group 4 (ERCC4) and heat shock protein 90 alpha family class B member 1 (HSP90AB1) genes emerged as potential central nodes in interaction networks and may serve as markers or therapeutic targets. To the best of our knowledge, the present study is the first CNV profiling study in TNBC in Mexican patients, highlighting the importance of including underrepresented populations in genomic research to uncover distinct molecular signatures and potential diagnostic or therapeutic avenues. Bioinformatically predicted molecular signatures of TNBC involve both common and distinct CNV-associated Hallmarks of Cancer genes, which represent candidates for screening as potential TNBC biomarkers.

Indexed as

breast cancerCNVgenehigh-density arrayinteraction network

Identifiers

PMID42221547
PMCPMC13216850

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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.