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• W1980794013 abstract "BACKGROUND The incidence of skin cancer has been rising since the 1950s. About 75% of skin cancer−associated deaths are caused by malignant melanoma. Nodular malignant melanoma accounts for 20% of melanocytic malignant tumors and is associated with a relatively poor prognosis. Extensive research has been undertaken, but a molecular marker that can predict a more aggressive course of melanoma still has not been found. METHODS The authors applied cytogenetic and molecular genetic techniques to a case of nodular malignant melanoma. They used comparative genomic hybridization (CGH) to identify chromosomal regions affected by genomic changes and interphase fluorescence in situ hybridization (FISH) on touch preparations of the tissue to elucidate the CGH findings further. To investigate the functionality of the affected c-MYC gene, the authors detected its transcript via reverse transcription and polymerase chain reaction. RESULTS CGH revealed a copy number gain in the 6p and 8q24-8qter region. FISH with c-MYC and centromere eight specific probes revealed that the tumor, in contrast to unaffected skin, was characterized by a gain in copy numbers of the c-MYC gene. The c-MYC gene transcript was detected at higher levels in the tumor than in the tissue taken from the safety margin. CONCLUSIONS The WAF1 gene located on chromosome 6p, which in this case had a copy number gain, might be involved in melanoma pathogenesis. The authors suggest that the c-MYC gene plays an important role in melanoma development and progression. The c-MYC gene seems to be affected by gaining functional copies, leading to a change in the normally regulated gene-dose effect. Cancer 2000;89:97–103. © 2000 American Cancer Society." @default.
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• W1980794013 date "2000-07-01" @default.
• W1980794013 modified "2023-10-18" @default.
• W1980794013 title "c-MYC and nodular malignant melanoma" @default.
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• W1980794013 doi "https://doi.org/10.1002/1097-0142(20000701)89:1<97::aid-cncr14>3.0.co;2-0" @default.
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