Affiliations: [a] Department of Biochemistry and Molecular Biology, Wright State University, Dayton, OH, USA | [b] Department of Dermatology, Wright State University Boonshoft School of Medicine, Dayton, OH, USA | [c] Dermatopathology Laboratory of Central States, Dayton, OH, USA
Correspondence:
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Corresponding author: Michael Markey, Department of Biochemistry and Molecular Biology, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Tel.: +1 937 775 4536; Fax: +1 937 775 4494; E-mail:michael.markey@wright.edu
Abstract: BACKGROUND: Skin melanocytes can give rise to benign and malignant
neoplasms. Discrimination of an early melanoma from an unusual/atypical
benign nevus can represent a significant challenge. However, previous
studies have shown that in contrast to benign nevi, melanoma demonstrates
pervasive chromosomal aberrations. OBJECTIVE: This substantial difference between melanoma and benign nevi can
be exploited to discriminate between melanoma and benign nevi. METHODS: Array-comparative genomic hybridization (aCGH) is an approach that
can be used on DNA extracted from formalin-fixed paraffin-embedded (FFPE)
tissues to assess the entire genome for the presence of changes in DNA copy
number. In this study, high resolution, genome-wide single-nucleotide
polymorphism (SNP) arrays were utilized to perform comprehensive and
detailed analyses of recurrent copy number aberrations in 41 melanoma
samples in comparison with 21 benign nevi. RESULTS: We found statistically significant copy number gains and losses
within melanoma samples. Some of the identified aberrations are previously
implicated in melanoma. Moreover, novel regions of copy number alterations
were identified, revealing new candidate genes potentially involved in
melanoma pathogenesis. CONCLUSIONS: Taken together, these findings can help improve melanoma
diagnosis and introduce novel melanoma therapeutic targets.
