ArticleNeoplasia (New York, N.Y.)2008
Loss of heterozygosity and copy number abnormality in clear cell renal cell carcinoma discovered by high-density affymetrix 10K single nucleotide polymorphism mapping array.
Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Significance of chromosome 9p status in renal cell carcinoma: a systematic review and quality of the reported studies.BioMed research international · 2014Pooled it
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- HIF-2α expression and metabolic signaling require ACSS2 in clear cell renal cell carcinoma.The Journal of clinical investigation · 2024Article
- Synergistic Antitumor Activity of Talazoparib and Temozolomide in Malignant Rhabdoid Tumors.Cancers · 2024Article
- PRKDC-Mediated NHEJ May Play a Crucial Role in Aneuploidy of Chromosome 8-Driven Progression of Ovarian Cancer.International journal of molecular sciences · 2024Article
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- Therapeutic potential of parkin as a tumor suppressor via transcriptional control of cyclins in glioblastoma cell and animal models.Theranostics · 2021Article
- Mitophagy-associated genes PINK1 and PARK2 are independent prognostic markers of survival in papillary renal cell carcinoma and associated with aggressive tumor behavior.Scientific reports · 2020Article
- Genomic profiling in renal cell carcinoma.Nature reviews. Nephrology · 2020Review
- Allelic Switching ofInternational journal of genomics · 2019Article
- Epigenome Aberrations: Emerging Driving Factors of the Clear Cell Renal Cell Carcinoma.International journal of molecular sciences · 2017Review
- Mutant allele specific imbalance in oncogenes with copy number alterations: Occurrence, mechanisms, and potential clinical implications.Cancer letters · 2017Review
- Stratification of clear cell renal cell carcinoma (ccRCC) genomes by gene-directed copy number alteration (CNA) analysis.PloS one · 2017Article
- Tumor Suppressor Genes within Common Fragile Sites Are Active Players in the DNA Damage Response.PLoS genetics · 2016Review
- Tumour suppressor gene (CDKNA2) status on chromosome 9p in resected renal tissue improves prognosis of localised kidney cancer.Oncotarget · 2016Article
- Article
- Expression of FOXP1 in epithelial ovarian cancer (EOC) and its correlation with chemotherapy resistance and prognosis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- WWOX, large common fragile site genes, and cancer.Experimental biology and medicine (Maywood, N.J.) · 2015Review
- FOXP1 potentiates Wnt/β-catenin signaling in diffuse large B cell lymphoma.Science signaling · 2015Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic aberrations are crucial in renal tumor progression. In this study, we describe loss of heterozygosity (LOH) and DNA-copy number abnormalities in clear cell renal cell carcinoma (cc-RCC) discovered by genome-wide single nucleotide polymorphism (SNP) arrays. Genomic DNA from tumor and normal tissue of 22 human cc-RCCs was analyzed on the Affymetrix GeneChip Human Mapping 10K Array. The array data were validated by quantitative polymerase chain reaction and immunohistochemistry. Reduced DNA copy numbers were detected on chromosomal arm 3p in 91%, on chromosome 9 in 32%, and on chromosomal arm 14q in 36% of the tumors. Gains were detected on chromosomal arm 5q in 45% and on chromosome 7 in 32% of the tumors. Copy number abnormalities were found not only in FHIT and VHL loci, known to be involved in renal carcinogenesis, but also in regions containing putative new tumor suppressor genes or oncogenes. In addition, microdeletions were detected on chromosomes 1 and 6 in genes with unknown impact on renal carcinogenesis. In validation experiments, abnormal protein expression of FOXP1 (on 3p) was found in 90% of tumors (concordance with SNP array data in 85%). As assessed by quantitative polymerase chain reaction, PARK2 and PACRG were down-regulated in 57% and 100%, respectively, and CSF1R was up-regulated in 69% of the cc-RCC cases (concordance with SNP array data in 57%, 33%, and 38%). Genome-wide SNP array analysis not only confirmed previously described large chromosomal aberrations but also detected novel microdeletions in genes potentially involved in tumor genesis of cc-RCC.
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