ArticleMolecular cancer research : MCR2016
Cells Comprising the Prostate Cancer Microenvironment Lack Recurrent Clonal Somatic Genomic Aberrations.
Article in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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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.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Stromal-derived MAOB promotes prostate cancer growth and progression.Science advances · 2024Article
- Epigenetic regulation of cancer-associated fibroblast heterogeneity.Biochimica et biophysica acta. Reviews on cancer · 2023Review
- The Prostate Stromal Transcriptome in Aggressive and Lethal Prostate Cancer.Molecular cancer research : MCR · 2023Article
- Prostate Cancer Tumor Stroma: Responsibility in Tumor Biology, Diagnosis and Treatment.Cancers · 2022Review
- Fatty Acid Signaling Impacts Prostate Cancer Lineage Plasticity in an Autocrine and Paracrine Manner.Cancers · 2022Article
- Gene Expression Profile of Stromal Factors in Cancer-Associated Fibroblasts from Prostate Cancer.Diagnostics (Basel, Switzerland) · 2022Article
- Role of prostate and bone stromal cells on prostate cancer progression.American journal of clinical and experimental urology · 2022Review
- Dissecting esophageal squamous-cell carcinoma ecosystem by single-cell transcriptomic analysis.Nature communications · 2021Article
- Fibroblast Activation Protein (FAP)-Targeted CAR-T Cells: Launching an Attack on Tumor Stroma.ImmunoTargets and therapy · 2021Review
- Review
- Cancer-associated fibroblasts stimulate primary tumor growth and metastatic spread in an orthotopic prostate cancer xenograft model.Scientific reports · 2020Article
- Review
- Alterations in the methylome of the stromal tumour microenvironment signal the presence and severity of prostate cancer.Clinical epigenetics · 2020Article
- Fibroblast Reprogramming in Gastrointestinal Cancer.Frontiers in cell and developmental biology · 2020Review
- Determinants and Functions of CAFs Secretome During Cancer Progression and Therapy.Frontiers in cell and developmental biology · 2020Review
- Epigenetic changes in fibroblasts drive cancer metabolism and differentiation.Endocrine-related cancer · 2019Review
- Cancer-associated fibroblasts: how do they contribute to metastasis?Clinical & experimental metastasis · 2019Review
- Stromal epigenetic alterations drive metabolic and neuroendocrine prostate cancer reprogramming.The Journal of clinical investigation · 2018Article
- Integrative metabolic and transcriptomic profiling of prostate cancer tissue containing reactive stroma.Scientific reports · 2018Article
- Cellular Constituents of the Prostate Stroma: Key Contributors to Prostate Cancer Progression and Therapy Resistance.Cold Spring Harbor perspectives in medicine · 2018Review
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledProstate cancer-associated stroma (CAS) plays an active role in malignant transformation, tumor progression, and metastasis. Molecular analyses of CAS have demonstrated significant changes in gene expression; however, conflicting evidence exists on whether genomic alterations in benign cells comprising the tumor microenvironment (TME) underlie gene expression changes and oncogenic phenotypes. This study evaluates the nuclear and mitochondrial DNA integrity of prostate carcinoma cells, CAS, matched benign epithelium and benign epithelium-associated stroma by whole-genome copy-number analyses, targeted sequencing of TP53, and FISH. Array comparative genomic hybridization (aCGH) of CAS revealed a copy-neutral diploid genome with only rare and small somatic copy-number aberrations (SCNA). In contrast, several expected recurrent SCNAs were evident in the adjacent prostate carcinoma cells, including gains at 3q, 7p, and 8q, and losses at 8p and 10q. No somatic TP53 mutations were observed in CAS. Mitochondrial DNA (mtDNA) extracted from carcinoma cells and stroma identified 23 somatic mtDNA mutations in neoplastic epithelial cells, but only one mutation in stroma. Finally, genomic analyses identified no SCNAs, LOH, or copy-neutral LOH in cultured cancer-associated fibroblasts, which are known to promote prostate cancer progression in vivo IMPLICATIONS: The gene expression changes observed in prostate cancer-adjacent stroma and the attendant contribution of the stroma to the development and progression of prostate cancer are not due to frequent or recurrent genomic alterations in the TME.
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