ReviewNature reviews. Urology2012
The complexity of prostate cancer: genomic alterations and heterogeneity.
Review in Nature reviews. Urology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
128 citing papers in PubMed, 4 syntheses or guidelines pooled it.
- Meta-analysis ofCancer imaging : the official publication of the International Cancer Imaging Society · 2023Pooled it
- A genetic study and meta-analysis of the genetic predisposition of prostate cancer in a Chinese population.Oncotarget · 2016Pooled it
- The role of CD147 expression in prostate cancer: a systematic review and meta-analysis.Drug design, development and therapy · 2016Pooled it
- The CYP19A1 (TTTA)n Repeat Polymorphism May Affect the Prostate Cancer Risk: Evidence from a Meta-Analysis.American journal of men's healthPooled it
- The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026Review
- Prostate Cancer Biomarkers with a Focus on Galectin-3: Emerging Clinical and Therapeutic Implications.Current oncology (Toronto, Ont.) · 2026Review
- Prostate Cancer: Dissecting Novel Immunosuppressive Mechanisms Through Context-Specific Transcriptomic Programs and MDSC Cells.International journal of molecular sciences · 2026Article
- Review
- PARP inhibitor response is enhanced in prostate cancer when XRCC1 expression is reduced.NAR cancer · 2025Article
- Mitochondrial SLC25A10 promotes prostate cancer progression by inhibiting ferritinophagy.Cell death discovery · 2025Article
- Heterogeneity of cancer-associated fibroblast subpopulations in prostate cancer: Implications for prognosis and immunotherapy.Translational oncology · 2025Article
- Overcoming drug resistance in castrate-resistant prostate cancer: current mechanisms and emerging therapeutic approaches.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Potential application of nanodelivery systems targeting ELAVL1 in prostate cancer treatment.Frontiers in oncology · 2025Review
- Role of MicroRNA-21 in Prostate Cancer Progression and Metastasis: Molecular Mechanisms to Therapeutic Targets.Annals of surgical oncology · 2024Review
- Metastatic Castration-Resistant Prostate Cancer: Advances in Treatment and Symptom Management.Current treatment options in oncology · 2024Review
- Therapeutic targets of formononetin for treating prostate cancer at the single-cell level.Aging · 2024Article
- Genomic evolution shapes prostate cancer disease type.Cell genomics · 2024Article
- Circulating tumor DNA and tissue complementarily detect genomic alterations in metastatic hormone-sensitive prostate cancer.iScience · 2024Article
- Cribiform and intraductal carcinoma in hereditary prostate cancer: clinical and pathological analysis of 20 cases.American journal of clinical and experimental urology · 2024Article
- Effect of subcutaneous adipose tissue-associated CSRP2 on the progression of prostate cancer via the WDR5/USP44 pathway.American journal of cancer research · 2024Article
68 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
3 authors.
Funding
Abstract
Although prostate cancer is the most common malignancy to affect men in the Western world, the molecular mechanisms underlying its development and progression remain poorly understood. Like all cancers, prostate cancer is a genetic disease that is characterized by multiple genomic alterations, including point mutations, microsatellite variations, and chromosomal alterations such as translocations, insertions, duplications, and deletions. In prostate cancer, but not other carcinomas, these chromosome alterations result in a high frequency of gene fusion events. The development and application of novel high-resolution technologies has significantly accelerated the detection of genomic alterations, revealing the complex nature and heterogeneity of the disease. The clinical heterogeneity of prostate cancer can be partly explained by this underlying genetic heterogeneity, which has been observed between patients from different geographical and ethnic populations, different individuals within these populations, different tumour foci within the same patient, and different cells within the same tumour focus. The highly heterogeneous nature of prostate cancer provides a real challenge for clinical disease management and a detailed understanding of the genetic alterations in all cells, including small subpopulations, would be highly advantageous.
Indexed as
Identifiers
23132303What 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.