“…In our samples, the most frequent losses of DNA sequence copy number were located at 13q13q31, which agree well with the results by others. 30,32,33 We observed recurrent losses, albeit infrequently, affecting chromosome 4 (with the minimal common region 4q) and in chromosome 8 (minimal common region 8p). So far, no tumor suppressor gene has been identified on chromosome 4.…”
Comparative genomic hybridization (CGH) was used to search for gains, high-level amplifications and losses of DNA sequences along all chromosome arms in 19 primary Merkel cell carcinomas (MCC). Extensive genetic aberrations, with a mean value of 5.571.1 changes per tumor were detected in 13 out of the 19 samples analyzed. Our CGH results reveal several new and other previously known chromosomal regions that are involved in the pathogenesis of MCC. The majority of the alterations were gains of whole chromosomes or whole chromosome arms. Compared to losses, the frequency of DNA copy number gains was two-fold. DNA sequence copy number gains were most common in chromosomes 6 (42%), 1 (37%), and 5 (32%). The most frequent minimal common regions of gains were 6pterqter (42%), 1q11q31 (32%), and 5p (32%). No recurrent high-level amplifications were observed. High-level amplifications of small chromosomal regions were found in four samples out of the 19 tumors analyzed (21%). Amplifications affected 1q22q24 (5%), 4p (5%), and 5p (5%). Losses most frequently affected chromosomes 13 (21%) and 4 (16%). Minimal common regions with the most frequent losses were 13q13q31 (21%), 4q (16%), and 16q (11%). No significant statistical correlation between genomic aberrations and clinicopathological factors was revealed, despite the fact that there was an obvious tendency towards it. Primary MCC expressing DNA alterations were predominantly distinguished in large tumors, and risk of metastatic dissemination was three-fold compared to tumors with no DNA alterations.
“…In our samples, the most frequent losses of DNA sequence copy number were located at 13q13q31, which agree well with the results by others. 30,32,33 We observed recurrent losses, albeit infrequently, affecting chromosome 4 (with the minimal common region 4q) and in chromosome 8 (minimal common region 8p). So far, no tumor suppressor gene has been identified on chromosome 4.…”
Comparative genomic hybridization (CGH) was used to search for gains, high-level amplifications and losses of DNA sequences along all chromosome arms in 19 primary Merkel cell carcinomas (MCC). Extensive genetic aberrations, with a mean value of 5.571.1 changes per tumor were detected in 13 out of the 19 samples analyzed. Our CGH results reveal several new and other previously known chromosomal regions that are involved in the pathogenesis of MCC. The majority of the alterations were gains of whole chromosomes or whole chromosome arms. Compared to losses, the frequency of DNA copy number gains was two-fold. DNA sequence copy number gains were most common in chromosomes 6 (42%), 1 (37%), and 5 (32%). The most frequent minimal common regions of gains were 6pterqter (42%), 1q11q31 (32%), and 5p (32%). No recurrent high-level amplifications were observed. High-level amplifications of small chromosomal regions were found in four samples out of the 19 tumors analyzed (21%). Amplifications affected 1q22q24 (5%), 4p (5%), and 5p (5%). Losses most frequently affected chromosomes 13 (21%) and 4 (16%). Minimal common regions with the most frequent losses were 13q13q31 (21%), 4q (16%), and 16q (11%). No significant statistical correlation between genomic aberrations and clinicopathological factors was revealed, despite the fact that there was an obvious tendency towards it. Primary MCC expressing DNA alterations were predominantly distinguished in large tumors, and risk of metastatic dissemination was three-fold compared to tumors with no DNA alterations.
“…This observation could be the result of genetic heterogeneity within the tumor biopsy as evidenced by presence of mitoses with and without monosomy for chromosome 10. 17 CGH clearly demonstrated loss of the 10q region in this tumor. 10 In addition, all samples were screened for homozygous PTEN deletions by multiplex PCR.…”
Section: Screening For Pten Mutations and Homozygous Deletions In MCCmentioning
confidence: 99%
“…LOH and CGH data for these tumors have been reported previously. 10,17 Morphological characterization and cytogenetic data of the MCC cell lines have been published previously 18 -21 except for MCC26 and T95-45, which will be published elsewhere (Van Gele et al, in preparation). Genomic DNA was extracted from cell lines and frozen sections of tumor samples by using standard proteinase-K digestion, phenol/chloroform extraction and ethanol precipitation protocols.…”
“…We have previously examined six MCC biopsies for cytogenetic abnormalities (Leonard et al, 1993b). None of these cases, or another 10 cases in the literature (Kusyk and Romsdahl, 1986;Rosen et al, 1987;Sandbrick et al, 1988;Sozzi et al, 1988;Shabatai et al, 1989;Smadja et al, 1991), demonstrated any deletion of the short arm of chromosome 3.…”
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