ArticleMolecular cancer therapeutics2015
Identifying actionable targets through integrative analyses of GEM model and human prostate cancer genomic profiling.
Article in Molecular cancer therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed.
- Cellular senescence in metastatic prostate cancer: A therapeutic opportunity or challenge (Review).Molecular medicine reports · 2024Review
- Identification of cancer-associated fibroblasts subtypes in prostate cancer.Frontiers in immunology · 2023Article
- Elevated serum CEA is associated with liver metastasis and distinctive circulating tumor DNA alterations in patients with castration-resistant prostate cancer.The Prostate · 2022Article
- The Hippo Pathway in Prostate Cancer.Cells · 2019Review
- Nuclear MET requires ARF and is inhibited by carbon nanodots through binding to phospho-tyrosine in prostate cancer.Oncogene · 2019Article
- Genetically Engineered Mouse Models of Prostate Cancer in the Postgenomic Era.Cold Spring Harbor perspectives in medicine · 2019Review
- Systematic analysis of NLMP suggests nuclear localization of RTK/MET kinases resemble cancer cell clearance.Journal of experimental & clinical cancer research : CR · 2019Article
- Minimal residual disease in prostate cancer patients after primary treatment: theoretical considerations, evidence and possible use in clinical management.Biological research · 2018Review
- Identification of potential therapeutic targets in prostate cancer through a cross-species approach.EMBO molecular medicine · 2018Article
- p53 shades of Hippo.Cell death and differentiation · 2018Review
- Dysregulation of YAP by ARF Stimulated with Tea-derived Carbon Nanodots.Scientific reports · 2017Article
- An approach to suppress the evolution of resistance in BRAFNature medicine · 2017Article
- Cabozantinib Eradicates Advanced Murine Prostate Cancer by Activating Antitumor Innate Immunity.Cancer discovery · 2017Article
- Recurrent patterns of DNA copy number alterations in tumors reflect metabolic selection pressures.Molecular systems biology · 2017Article
- Review
- Role of Yes-associated protein in cancer: An update.Oncology letters · 2016Article
- Multidisciplinary intervention of early, lethal metastatic prostate cancer: Report from the 2015 Coffey-Holden Prostate Cancer Academy Meeting.The Prostate · 2016Review
- Integrating Murine and Clinical Trials with Cabozantinib to Understand Roles of MET and VEGFR2 as Targets for Growth Inhibition of Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Mechanistic Support for Combined MET and AR Blockade in Castration-Resistant Prostate Cancer.Neoplasia (New York, N.Y.) · 2016Article
- Stem cells in genetically-engineered mouse models of prostate cancer.Endocrine-related cancer · 2015Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Copy-number alterations (CNA) are among the most common molecular events in human prostate cancer genomes and are associated with worse prognosis. Identification of the oncogenic drivers within these CNAs is challenging due to the broad nature of these genomic gains or losses which can include large numbers of genes within a given region. Here, we profiled the genomes of four genetically engineered mouse prostate cancer models that reflect oncogenic events common in human prostate tumors, with the goal of integrating these data with human prostate cancer datasets to identify shared molecular events. Met was amplified in 67% of prostate tumors from Pten p53 prostate conditional null mice and in approximately 30% of metastatic human prostate cancer specimens, often in association with loss of PTEN and TP53. In murine tumors with Met amplification, Met copy-number gain and expression was present in some cells but not others, revealing intratumoral heterogeneity. Forced MET overexpression in non-MET-amplified prostate tumor cells activated PI3K and MAPK signaling and promoted cell proliferation and tumor growth, whereas MET kinase inhibition selectively impaired the growth of tumors with Met amplification. However, the impact of MET inhibitor therapy was compromised by the persistent growth of non-Met-amplified cells within Met-amplified tumors. These findings establish the importance of MET in prostate cancer progression but reveal potential limitations in the clinical use of MET inhibitors in late-stage prostate cancer.
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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.