<?xml version="1.0" encoding="UTF-8" standalone="no"?>
<ArticleSet>
<Article>
<Journal>
<PublisherName>International Academy of Ecology and Environmental Sciences</PublisherName>
<JournalTitle>Network Biology</JournalTitle>
<eissn>2220-8879</eissn>
<Volume>16</Volume>
<Issue>2</Issue>
<PubDate PubStatus="ppublish">
<Year>2026</Year>
<Month>6</Month>
<Day>1</Day>
</PubDate>
</Journal>
<ArticleTitle>Convergent transcriptomic signatures reveal cell cycle and DNA repair dependencies in triple-negative breast cancer: A network-based multi-dataset analysis</ArticleTitle>
<Pages>82-102</Pages>
<Language>EN</Language>
<AuthorList>
<Author>Chaitanya Kumar</Author>
<Author>Ravi Verma</Author>
<Author>Ashok Sharma</Author>
<Author>Vishnupriya Veeraraghavan</Author>
</AuthorList>
<ArticleList>
<ArticleId IdType="url">http://www.iaees.org/publications/journals/nb/articles/2026-16(2)/convergent-transcriptomic-signatures.pdf</ArticleId>>
</ArticleList>
<Abstract>
Triple-negative breast cancer (TNBC) remains one of the most aggressive and therapeutically challenging breast cancer subtypes due to the absence of hormone receptors and HER2 expression. To uncover reproducible molecular signatures and potential therapeutic targets, we performed an integrative transcriptomic analysis using three independent GEO datasets (GSE38959, GSE65216, and GSE65194). Differentially expressed genes were examined through protein-protein interaction network construction, enrichment analysis, and survival validation. A highly connected gene cluster comprising CHEK1, PLK1, AURKA, CCNA2, CCNB1, RAD51, TOP2A, KIF11, and KIF23 was consistently upregulated across datasets. These genes were predominantly involved in cell-cycle regulation and DNA-repair pathways and showed significant association with poor overall survival in TNBC cohorts. The findings suggest that dysregulation of the mitotic checkpoint and homologous recombination processes defines a conserved oncogenic program in TNBC. This study highlights druggable molecular targets that could guide the development of pathway-directed therapies in TNBC.
</Abstract>
</Article>
</ArticleSet>
