ArticleCancer research2011
Integrative genomics identifies molecular alterations that challenge the linear model of melanoma progression.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 68 citations in OpenAlex.
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- Comparative Expression Profiling Reveals Molecular Markers Involved in the Progression of Cutaneous Melanoma towards Metastasis.International journal of molecular sciences · 2023Article
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- GRASP55 restricts early-stage autophagy and regulates spatial organization of the early secretory network.Biology open · 2021Article
- Screening and identification of potential biomarkers and therapeutic drugs in melanoma via integrated bioinformatics analysis.Investigational new drugs · 2021Article
- Primary Melanoma Histologic Subtype: Impact on Survival and Response to Therapy.Journal of the National Cancer Institute · 2019Article
- CarcinogenicMolecular & cellular proteomics : MCP · 2019Article
- DIS3 isoforms vary in their endoribonuclease activity and are differentially expressed within haematological cancers.The Biochemical journal · 2018Article
- MicroRNA-125a promotes resistance to BRAF inhibitors through suppression of the intrinsic apoptotic pathway.Pigment cell & melanoma research · 2017Article
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- Functional characterization of a chr13q22.1 pancreatic cancer risk locus reveals long-range interaction and allele-specific effects on DIS3 expression.Human molecular genetics · 2016Article
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Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Superficial spreading melanoma (SSM) and nodular melanoma (NM) are believed to represent sequential phases of linear progression from radial to vertical growth. Several lines of clinical, pathologic, and epidemiologic evidence suggest, however, that SSM and NM might be the result of independent pathways of tumor development. We utilized an integrative genomic approach that combines single nucleotide polymorphism array (6.0; Affymetrix) with gene expression array (U133A 2.0; Affymetrix) to examine molecular differences between SSM and NM. Pathway analysis of the most differentially expressed genes between SSM and NM (N = 114) revealed significant differences related to metabolic processes. We identified 8 genes (DIS3, FGFR1OP, G3BP2, GALNT7, MTAP, SEC23IP, USO1, and ZNF668) in which NM/SSM-specific copy number alterations correlated with differential gene expression (P < 0.05; Spearman's rank). SSM-specific genomic deletions in G3BP2, MTAP, and SEC23IP were independently verified in two external data sets. Forced overexpression of metabolism-related gene MTAP (methylthioadenosine phosphorylase) in SSM resulted in reduced cell growth. The differential expression of another metabolic-related gene, aldehyde dehydrogenase 7A1 (ALDH7A1), was validated at the protein level by using tissue microarrays of human melanoma. In addition, we show that the decreased ALDH7A1 expression in SSM may be the result of epigenetic modifications. Our data reveal recurrent genomic deletions in SSM not present in NM, which challenge the linear model of melanoma progression. Furthermore, our data suggest a role for altered regulation of metabolism-related genes as a possible cause of the different clinical behavior of SSM and NM.
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