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To determine whether these similarities may indicate common genetic alterations, we studied the genetic profile of 10 MCCs and analyzed 6 derived cell lines and 5 skin SCC lines by comparative genomic hybridization (CGH) and molecular genetic analyses. Although the MCCs were highly divergent\u2014only 3 of the 10 tumors exhibited common gains and losses\u2014they shared gain of 8q21\u2010q22 and loss of 4p15\u2010pter with the genetically much more homogeneous SCC lines. In addition, 2 of 5 SCC and 2 of 6 MCC lines exhibited UV\u2010B\u2010type\u2010specific mutations in the <jats:italic>p53<\/jats:italic> tumor\u2010suppressor gene and a high frequency (9\/11) of CC\u2192TT double base changes in codon 27 of the <jats:italic>Harvey (Ha)\u2010ras<\/jats:italic> gene. Since 45% of the tumor lines were homozygous for this nucleotide substitution compared to 14% of the controls and in 1 MCC patient the wild\u2010type allele was lost in the tumor, this novel polymorphism may contribute to tumor development. On the other hand, loss of 3p, characteristic for SCCs, was rare in MCCs. Although in 2 of 3 SCC lines 3p loss was correlated with reduced expression of the <jats:italic>FHIT<\/jats:italic> (fragile histidine triad) gene, the potential tumor suppressor mapped to 3p14.2 and 2 MCC lines with normal 3p showed aberrant or no <jats:italic>FHIT<\/jats:italic> transcripts. Taken together, in addition to the common UV\u2010B\u2010specific mutations in the <jats:italic>p53<\/jats:italic> and <jats:italic>Ha\u2010ras<\/jats:italic> gene, MCCs and SCCs also share chromosomal imbalances that may point to a common environmental\u2010derived (<jats:italic>e.g.,<\/jats:italic> UV\u2010A) oxidative damage. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.10321","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T23:45:33Z","timestamp":1030319133000},"page":"352-360","source":"Crossref","is-referenced-by-count":167,"title":["UV\u2010B\u2010type mutations and chromosomal imbalances indicate common pathways for the development of Merkel and skin squamous cell carcinomas"],"prefix":"10.1002","volume":"99","author":[{"given":"Susanne","family":"Popp","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Waltering","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christel","family":"Herbst","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ingrid","family":"Moll","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petra","family":"Boukamp","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2002,4,25]]},"reference":[{"key":"e_1_2_6_2_2","first-page":"37","article-title":"Epidemiology of nonmelanoma skin cancer: a review","volume":"32","author":"Corona R","year":"1996","journal-title":"Ann 1st Super 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