| 1. |
- Hallén, Magnus, et al.
(författare)
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Cytogenetic abnormalities in a hemangiopericytoma of the spleen.
- 2002
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Ingår i: Cancer Genetics and Cytogenetics. - 0165-4608. ; 136:1, s. 62-65
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Tidskriftsartikel (refereegranskat)abstract
- To date, only 16 cytogenetically abnormal hemangiopericytomas (HP) have been reported. Despite this low number, some characteristic karyotypic features have already emerged: most HP are near-diploid and breakpoints in 12q13, 12q24, and 19q13 seem to be common, with t(12;19)(q13;q13) being a recurrent translocation. Here, we report the first case of a probably benign splenic HP with chromosomal abnormalities. The abnormal karyotype was 47,XX,t(5;22;11)(q31;q11;q13),+10. None of these abnormalities have previously been reported in HP, suggesting that the karyotypic pattern of splenic HP may differ from soft tissue HP.
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| 2. |
- Heidenblad, Markus, et al.
(författare)
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Detailed genomic mapping and expression analyses of 12p amplifications in pancreatic carcinomas reveal a 3.5-Mb target region for amplification.
- 2002
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Ingår i: Genes, Chromosomes and Cancer. - : Wiley. - 1045-2257. ; 34:2, s. 211-223
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Tidskriftsartikel (refereegranskat)abstract
- Previous cytogenetic and comparative genomic hybridization (CGH) analyses have shown that the gain of chromosome arm 12p is frequent in pancreatic carcinomas. We investigated 15 pancreatic carcinoma cell lines using CGH, fluorescence in situ hybridization (FISH), and semiquantitative polymerase chain reaction (PCR) to characterize 12p amplifications in detail. The CGH analysis revealed gains of 12p in four of the cell lines and local amplification within 12p11-12 in six cell lines. By FISH analysis, using precisely mapped YAC clones, the commonly amplified region was found to be approximately 5 Mb. The amplified segment extended from YAC 753f12, covering the KRAS2 locus, to YAC 891f1, close to the centromere. A semiquantitative PCR methodology was used to estimate genomic copy numbers of 14 precisely mapped expressed sequence tags (ESTs) and sequence-tagged sites, located within this interval. The level of amplification ranged from two- to 12-fold. The produced gene copy profiles revealed a 3.5-Mb segment with various local amplifications. This region includes KRAS2 and ranges from D12S1617 to sts-N38796. Two of the cell lines (primary and metastatic tumor from the same patient) showed amplification peaks within the distal region of this segment, two had peaks within the proximal region, one showed subpeaks in both regions, and one displayed amplification of the entire region. Chromosome segment-specific cDNA array analysis of 29 expressed sequences within the whole interval between D12S1617 and sts-N38796 indicated overexpression of four ESTs, two corresponding to DEC2 and PPFIBP1, and two to ESTs with unknown function. Expression analysis of these and of KRAS2 showed specific overexpression in the six cell lines with local 12p amplifications. These findings indicate two target regions within the 3.5-Mb segment in 12p11-12, one proximal including PPFIBP1, and one distal including KRAS2.
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| 3. |
- Mahlamaki, EH, et al.
(författare)
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Frequent amplification of 8q24, 11q, 17q, and 20q-specific genes in pancreatic cancer
- 2002
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Ingår i: Genes, Chromosomes and Cancer. - : Wiley. - 1045-2257. ; 35:4, s. 353-358
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Tidskriftsartikel (refereegranskat)abstract
- Genetic changes involved in the development and progression of pancreatic cancer are still partly unknown, despite the progress in recent years. In this study, comparative genomic hybridization analysis in 31 pancreatic cancer cell lines showed that chromosome arms 8q, 11q, 17q, and 20q are frequently gained in this tumor type. Copy number analysis of selected genes from these chromosome arms by fluorescence in situ hybridization showed amplification of the MYC oncogene in 54% of the cell lines, whereas CCNDI was amplified in 28%. In the 17q arm, the ERB82 oncogene was amplified in 20% of the cell lines, TBX2 in 50%, and BIRC5 in 58%, indicating increased involvement toward the q telonnere of chromosome 17. In the 20q arm, the amplification frequencies varied from 32% to 83%, with the CTSZ gene at 20q 13 being most frequently affected. These results illustrate that amplification of genes from the 8q, 11q, 17q, and 20q chromosome arms is common in pancreatic cancer.
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