ArticleGenes & cancer2010
MYC and Prostate Cancer.
Article in Genes & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
186 citing papers in PubMed, 300 citations in OpenAlex.
- MYC Overexpression at the Protein and mRNA Level and Cancer Outcomes among Men Treated with Radical Prostatectomy for Prostate Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018Trial
- Senolytic Interventions Enhance the Anti-metastatic Activity of Chemotherapy in Prostate Cancer.Cancer research · 2026Article
- A MYC family switch: L-MYC drives and maintains neuroendocrine lineage programs in prostate cancer.Neoplasia (New York, N.Y.) · 2026Article
- Dynamic Profiling of Circulating Tumor Cells and MYC/PTEN Alterations in Prostate Cancer Patients Undergoing Radical Prostatectomy in Amazon Population.Molecular carcinogenesis · 2026Article
- ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth.Cell communication and signaling : CCS · 2026Article
- MIAAIM: Multi-omics image integration with dimensional reduction for tissue state mapping.PLoS computational biology · 2026Article
- Article
- Transcriptional and epigenetic reprogramming, lineage plasticity and therapy resistance in prostate cancer.Journal of the National Cancer Center · 2026Review
- Bibliometric Insights into Aging and Immune Function in Prostate Cancer: Focus on Chronic Inflammation.Journal of inflammation research · 2026Review
- Prostate Cancer: Etiology, Diagnosis, and Treatment.Serican journal of medicine · 2026Article
- Active Substances from the Micro-Immunotherapy Medicine 2LC1International journal of molecular sciences · 2025Article
- EphB4-ephrin-B2 are targets in castration resistant prostate cancer.British journal of cancer · 2025Article
- The dual HDAC/PI3K inhibitor CUDC-907 inhibits the growth and proliferation of MYC-driven Group 3 medulloblastoma.Cell death discovery · 2025Article
- TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathways.Communications biology · 2025Article
- CRIPTO's multifaceted role in driving aggressive prostate cancer unveiled by in vivo, organoid, and patient data.Oncogene · 2025Article
- Genomic clustering tendency of transcription factors reflects phase-separated transcriptional condensates at super-enhancers.Nucleic acids research · 2025Article
- Antisense RNAs (asRNAs) as key players in gallbladder cancer progression: a bioinformatics analysis.Gastroenterology and hepatology from bed to bench · 2025Article
- Efficacy of Next-Generation Sequencing in Identifying Genetic Markers for Prostate Cancer Risk.Journal of pharmacy & bioallied sciences · 2024Article
- Convergent alterations in the tumor microenvironment of MYC-driven human and murine prostate cancer.Nature communications · 2024Article
- Glutamine Metabolism and Prostate Cancer.Cancers · 2024Review
126 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Prostate cancer, the majority of which is adenocarcinoma, is the most common epithelial cancer affecting a majority of elderly men in Western nations. Its manifestation, however, varies from clinically asymptomatic insidious neoplasms that progress slowly and do not threaten life to one that is highly aggressive with a propensity for metastatic spread and lethality if not treated in time. A number of somatic genetic and epigenetic alterations occur in prostate cancer cells. Some of these changes, such as loss of the tumor suppressors PTEN and p53, are linked to disease progression. Others, such as ETS gene fusions, appear to be linked more with early phases of the disease, such as invasion. Alterations in chromosome 8q24 in the region of MYC have also been linked to disease aggressiveness for many years. However, a number of recent studies in human tissues have indicated that MYC appears to be activated at the earliest phases of prostate cancer (e.g., in tumor-initiating cells) in prostatic intraepithelial neoplasia, a key precursor lesion to invasive prostatic adenocarcinoma. The initiation and early progression of prostate cancer can be recapitulated in genetically engineered mouse models, permitting a richer understanding of the cause and effects of loss of tumor suppressors and activation of MYC. The combination of studies using human tissues and mouse models paints an emerging molecular picture of prostate cancer development and early progression. This picture reveals that MYC contributes to disease initiation and progression by stimulating an embryonic stem cell-like signature characterized by an enrichment of genes involved in ribosome biogenesis and by repressing differentiation. These insights pave the way to potential novel therapeutic concepts based on MYC biology.
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What OpenQuestion holds
Registered trials
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.