ArticleInternational journal of cancer2016
A comprehensive genome-wide analysis of melanoma Breslow thickness identifies interaction between CDC42 and SCIN genetic variants.
Article in International journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.
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Who cites it
10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 15 citations in OpenAlex.
- Integrative transcriptome-wide analysis of atopic dermatitis for drug repositioning.Communications biology · 2022Pooled it
- Novel pleiotropic risk loci for melanoma and nevus density implicate multiple biological pathways.Nature communications · 2018Pooled it
- Article
- Novel Tubeimoside I liposomal drug delivery system in combination with gemcitabine for the treatment of pancreatic cancer.Nanomedicine (London, England) · 2024Article
- Scinderin Promotes Hydrogen Peroxide-induced Lens Epithelial Cell Injury in Age-related Cataract.Current molecular medicine · 2024Article
- Germline variants are associated with increased primary melanoma tumor thickness at diagnosis.Human molecular genetics · 2021Article
- MiR-301a-5p/SCIN promotes gastric cancer progression via regulating STAT3 and NF-κB signaling.Journal of Cancer · 2021Article
- A novel immune-related genes prognosis biomarker for melanoma: associated with tumor microenvironment.Aging · 2020Article
- Host Characteristics and Risk of Incident Melanoma by Breslow Thickness.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019Article
- Genetic variants in the metzincin metallopeptidase family genes predict melanoma survival.Molecular carcinogenesis · 2018Article
Corrections and comments
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Authors and funding
15 authors at 10 institutions in 3 countries.
Funding
Abstract
Breslow thickness (BT) is a major prognostic factor of cutaneous melanoma (CM), the most fatal skin cancer. The genetic component of BT has only been explored by candidate gene studies with inconsistent results. Our objective was to uncover the genetic factors underlying BT using an hypothesis-free genome-wide approach. Our analysis strategy integrated a genome-wide association study (GWAS) of single nucleotide polymorphisms (SNPs) for BT followed by pathway analysis of GWAS outcomes using the gene-set enrichment analysis (GSEA) method and epistasis analysis within BT-associated pathways. This strategy was applied to two large CM datasets with Hapmap3-imputed SNP data: the French MELARISK study for discovery (966 cases) and the MD Anderson Cancer Center study (1,546 cases) for replication. While no marginal effect of individual SNPs was revealed through GWAS, three pathways, defined by gene ontology (GO) categories were significantly enriched in genes associated with BT (false discovery rate ≤5% in both studies): hormone activity, cytokine activity and myeloid cell differentiation. Epistasis analysis, within each significant GO, identified a statistically significant interaction between CDC42 and SCIN SNPs (pmeta-int =2.2 × 10(-6) , which met the overall multiple-testing corrected threshold of 2.5 × 10(-6) ). These two SNPs (and proxies) are strongly associated with CDC42 and SCIN gene expression levels and map to regulatory elements in skin cells. This interaction has important biological relevance since CDC42 and SCIN proteins have opposite effects in actin cytoskeleton organization and dynamics, a key mechanism underlying melanoma cell migration and invasion.
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