ArticleProceedings of the National Academy of Sciences of the United States of America1990
Allelic loss of chromosomes 16q and 10q in human prostate cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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
97 citing papers in PubMed, 457 citations in OpenAlex.
- Loss of CYLD on Chromosome 16q Impairs Homologous Recombination and Genomic Stability Through TIRR Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ProstaMine: a bioinformatics tool for identifying subtype-specific co-alterations associated with aggressiveness in prostate cancer.Frontiers in pharmacology · 2024Article
- Analysis of genetic biomarkers, polymorphisms in ADME-related genes and their impact on pharmacotherapy for prostate cancer.Cancer cell international · 2023Review
- Therapeutic Implications of PTEN in Non-Small Cell Lung Cancer.Pharmaceutics · 2023Review
- The evolving landscape of prostate cancer somatic mutations.The Prostate · 2022Review
- Cadherin 13 Inhibits Pancreatic Cancer Progression and Epithelial-mesenchymal Transition by Wnt/β-Catenin Signaling.Journal of Cancer · 2020Article
- The Genomics of Prostate Cancer: A Historic Perspective.Cold Spring Harbor perspectives in medicine · 2019Review
- Alterations of COX-2, HER-2/neu and E-Cadherin protein expression in the prostatic adenocarcinoma: preliminary findings.American journal of translational research · 2019Article
- Novel Homozygous Mutation in the WWOX Gene Causes Seizures and Global Developmental Delay: Report and Review.Translational neuroscience · 2018Article
- Systems pharmacology using mass spectrometry identifies critical response nodes in prostate cancer.NPJ systems biology and applications · 2018Article
- Review
- RUNX3 regulates renal cell carcinoma metastasis via targeting miR-6780a-5p/E-cadherin/EMT signaling axis.Oncotarget · 2017Article
- Crossed wires: 3D genome misfolding in human disease.The Journal of cell biology · 2017Review
- Upregulation of T-cadherin suppresses cell proliferation, migration and invasion of gastric cancerExperimental and therapeutic medicine · 2017Article
- RUNX3 regulates hepatocellular carcinoma cell metastasis via targeting miR-186/E-cadherin/EMT pathway.Oncotarget · 2017Article
- Article
- Host nucleotide polymorphism in hepatitis B virus-associated hepatocellular carcinoma.World journal of hepatology · 2016Review
- Alteration of WWOX in human cancer: a clinical view.Experimental biology and medicine (Maywood, N.J.) · 2015Review
- Prolonged exposure to acid and bile induces chromosome abnormalities that precede malignant transformation of benign Barrett's epithelium.Molecular cytogenetics · 2012Article
- Genetic alterations of the WWOX gene in breast cancer.Medical oncology (Northwood, London, England) · 2012Article
37 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
8 authors at 1 institution in 1 country.
Funding
Abstract
Recent advances in understanding the molecular genetics of common adult tumors have indicated that multiple genetic alterations including the activation of oncogenes and the inactivation of tumor suppressor genes are important in the pathogenesis of these tumors. Loss of heterozygosity is a hallmark of tumor suppressor gene inactivation and has been used to identify chromosomal regions that contain these genes. We have examined allelic loss in the most common tumor in men, prostate cancer. Twenty-eight prostate cancer specimens have been examined for loss of heterozygosity at 11 different chromosomal arms including 3p, 7q, 9q, 10p, 10q, 11p, 13q, 16p, 16q, 17p, and 18q. Fifty-four percent (13/24) of clinically localized tumors and 4 of 4 metastatic tumors showed loss of heterozygosity on at least one chromosome. Chromosomes 16q and 10q exhibited the highest frequency of loss of heterozygosity with 30% of tumors showing loss at these chromosomes. These data demonstrate that allelic loss is a common event in prostate cancer and suggest that chromosomes 16q and 10q may contain the sites of tumor suppressor genes important in the pathogenesis of human prostate cancer.
Indexed as
Identifiers
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.