ArticleMolecular oncology2023
Integrated analysis of racial disparities in genomic architecture identifies a trans-ancestry prognostic subtype in bladder cancer.
Article in Molecular oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Genomic Characteristics of Bladder Cancer: An AACR Project GENIE Study.International journal of molecular sciences · 2025Article
- Patient-Derived Bladder Cancer Organoids as a Valuable Tool for Understanding Tumor Biology and Developing Personalized Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Deciphering gene expression patterns using large-scale transcriptomic data and its applications.Briefings in bioinformatics · 2024Article
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Authors and funding
11 authors at 5 institutions in 3 countries.
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Abstract
The incidence of bladder cancer and patient survival vary greatly among different populations, but the influence of the associated molecular features and evolutionary processes on its clinical treatment and prognostication remains unknown. Here, we analyze the genomic architectures of 505 bladder cancer patients from Asian/Black/White populations. We identify a previously unknown association between AHNAK mutations and activity of the APOBEC-a mutational signature, the activity of which varied substantially across populations. All significantly mutated genes but only half of arm-level somatic copy number alterations (SCNAs) are enriched with clonal events, indicating large-scale SCNAs as rich sources of bladder cancer clonal diversities. The prevalence of TP53 and ATM clonal mutations as well as the associated burden of SCNAs is significantly higher in Whites/Blacks than in Asians. We identify a trans-ancestry prognostic subtype of bladder cancer characterized by enrichment of non-muscle-invasive patients and muscle-invasive patients with good prognosis, increased CREBBP/FGFR3/HRAS/NFE2L2 mutations, decreased intra-tumor heterogeneity and genome instability, and an activated tumor microenvironment.
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