Literature DB >> 9408755

Comparative genomic hybridization reveals frequent gains of 20q, 8q, 11q, 12p, and 17q, and losses of 18q, 9p, and 15q in pancreatic cancer.

E H Mahlamäki1, M Höglund, L Gorunova, R Karhu, S Dawiskiba, A Andrén-Sandberg, O P Kallioniemi, B Johansson.   

Abstract

Comparative genomic hybridization (CGH) was used to screen for genomic imbalances in 24 exocrine pancreatic carcinomas, including II low-passage cell lines (4-8 subcultures) and 13 uncultured samples. Aberrations were found in all cell lines and in seven of the 13 biopsies. The most frequent changes in the cell lines were gains of 20q (91%), 11q (64%), 17q (64%), 19q (64%), 8q, 12p, 14q, and 20p (55%), and losses of 18q (100%), 9p (91%), 15q(73%), 21q (64%), 3p (55%), and 13q (55%). High-levels gains (tumor to normal ratio over 1.5) were detected at 3q, 6p, 7q, 8q, 12p, 19q, and 20q. Among the tumor biopsies, overrepresentations of 7p and 8q were most common (31%), followed by 5p, 5q, 11p, 11q, 12p, and 18q (23%), whereas the most frequent losses involved 18p and 18q (31%) and 6q and 17p (23%). The genetic changes in nine samples obtained from metastatic lesions did not differ significantly from those in 15 primary carcinomas. Most of the gains and losses detected in this CGH study correspond well to those identified in previous cytogenetic and molecular genetic investigations of pancreatic carcinomas. However, frequent gain of 12p and loss of 15q have not been previously reported. Molecular genetic analyses of these chromosome arms are warranted, and may lead to the discovery of novel genes important in pancreatic carcinogenesis.

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Year:  1997        PMID: 9408755     DOI: 10.1002/(sici)1098-2264(199712)20:4<383::aid-gcc10>3.0.co;2-o

Source DB:  PubMed          Journal:  Genes Chromosomes Cancer        ISSN: 1045-2257            Impact factor:   5.006


  30 in total

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3.  Bayesian Hidden Markov Modeling of Array CGH Data.

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Journal:  J Am Stat Assoc       Date:  2008-06-01       Impact factor: 5.033

Review 4.  Genomics of pancreatic cancer: does it make any improvement in diagnosis, prognosis and therapy?

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5.  Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma.

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6.  Loss of heterozygosity predicts poor survival after resection of pancreatic adenocarcinoma.

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7.  High-resolution characterization of the pancreatic adenocarcinoma genome.

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8.  Reduced level of the spindle checkpoint protein BUB1B is associated with aneuploidy in colorectal cancers.

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9.  The reg4 gene, amplified in the early stages of pancreatic cancer development, is a promising therapeutic target.

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10.  Genetic alterations in intrahepatic cholangiocarcinoma as revealed by degenerate oligonucleotide primed PCR-comparative genomic hybridization.

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