ArticleCell reports2025
Conserved patterns of transcriptional dysregulation, heterogeneity, and cell states in clear cell kidney cancer.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Epithelial-Mesenchymal Transition Markers in Clear Cell Renal Cell Carcinoma: Expression Patterns and Prognostic Significance.Journal of personalized medicine · 2026Article
- ZNF395 Is a Hypoxia-Responsive Regulator of Mitochondrial Glutaminolysis in Clear Cell Renal Cell Carcinoma.Cancer research · 2026Article
- ZBED6-IGF2-PIK3C3 autophagy axis drives ccRCC progression: A multi-omics integration study.iScience · 2026Article
- Spatial atlasing of N-glycosylation in healthy control and clear cell renal cell carcinoma tissues linked with immune checkpoint inhibition response by MALDI mass spectrometry imaging.Analytica chimica acta · 2025Article
- Mapping SET1B chromatin interactions with DamID using DamMapper, a comprehensive Snakemake workflow.BMC genomics · 2025Article
- Systematically identification of survival-associated eQTLs in a Japanese kidney cancer cohort.PLoS genetics · 2025Article
- Microenvironment and Tumor Heterogeneity as Pharmacological Targets in Precision Oncology.Pharmaceuticals (Basel, Switzerland) · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
Clear cell kidney cancers are characterized both by conserved oncogenic driver events and by marked intratumor genetic and phenotypic heterogeneity, which help drive tumor progression, metastasis, and resistance to therapy. How these are reflected in transcriptional programs within the cancer and stromal cell components remains an important question with the potential to drive novel therapeutic approaches to treating cancer. To better understand these programs, we perform single-cell transcriptomics on 75 multi-regional biopsies from kidney tumors and normal kidney. We identify conserved patterns of transcriptional dysregulation and their upstream regulators within the tumor and associated vasculature. We describe recurrent subclonal transcriptional consequences of Chr14q loss linked to metastatic potential. We identify prognostically significant conserved patterns of intratumor transcriptional heterogeneity. These reflect co-existing cell states found in both cancer cells and normal kidney cells, indicating that rather than arising from genetic heterogeneity they are a consequence of lineage plasticity.
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