Concomitant gastrin and ERBB2 gene amplifications at 17q12-q21 in the intestinal type of gastric cancer

Vidgren, Virve; Varis, Asta; Kokkola, Arto; Monni, Outi; Puolakkainen, Pauli; Nordling, Stig; Forozan, Farahnaz; Kallioniemi, Anne; Vakkari, Marja-Leena; Kivilaakso, Eero; Knuutila, Sakari

doi:10.1002/(sici)1098-2264(199901)24:1<24::aid-gcc4>3.0.co;2-h

Cited by 35 publications

(11 citation statements)

References 19 publications

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“…Strong amplification of the region 17q12-21 was reported in the intestinal type of gastric cancer. 59 Amplification and/or overexpression of some genes on chromosome 17q21.1, such as ERBB-2 (HER2/ neu) 8,9,60,61 and TOP2A (for topoisomerase IIa), 62 have been reported in gastric cancer and breast cancer, and might represent prognostic factors. Recently, an antineoplastic drug that targets the HER2 gene has been used to treat breast cancer and there are reports of overexpression of the HER2/neu gene in gastric cancer.…”

Section: Genetic Alterations In Gastric Cancermentioning

confidence: 99%

“…The chromosome localization of about 26 000 genes in the human genome have already been mapped accurately. 2 The expression or amplification of various genes, for example, genes for p53, 3 p27, 4 smad4, 5 c-met, 6,7 c-erbB2, 8,9 c-myc, l-myc, 10,11 K-sam, 12 E-cadherin, 13 b-catenin, 13 VEGF, 14 and FHIT 15 and mutations in the genes for TP53, 16 APC, 17 K-ras 18,19 and E-cadherin 20 have been associated with gastric carcinogenesis. There also have been reports of loss of heterozygosity (LOH) on chromosomes 1p, 2q, 3p, 4p, 5q, 7q, 8p, 9p, 11q, 13q, 14q, 17p, and 18q, suggesting a relationship between carcinogenesis and potential tumor suppressor genes.…”

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confidence: 99%

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Genetic alterations in 102 primary gastric cancers by comparative genomic hybridization: gain of 20q and loss of 18q are associated with tumor progression

et al. 2004

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Gastric cancer is one of the most common cancers. Molecular events in the carcinogenesis of gastric cancer remain, however, largely undefined. We investigated changes in DNA copy number in 102 gastric cancers by CGH. We found changes in DNA copy number in all cases, with frequent (^30% of patients) gains at 20q, 8q, 20p, 7q, 17q, 5p, and 13q. Frequent (^20%) losses were found at 19p, 18q, 5q, 21q, 4p, 4q, 15q, and 17p. The mean number of total alterations was significantly lower in grade 3 and scirrhous-type carcinomas (10.81 in grade 3 vs 13.98 in grade 1 and grade 2, 9.31 in scirrhous-type vs 13.18 in medullary-and intermediate-type). The mean number of losses and total alterations were higher in tumors at pT2, pT3 and pT4 (4.68 and 12.77 in pT2, pT3, and pT4 vs 2.55 and 9.22 in pT1). The mean number of losses was higher in carcinomas with lymph node metastasis (4.83). The mean number of gains and total alterations were higher in carcinomas with venous invasion (8.44 and 13.28). Several chromosomal alterations were linked in a statistically significant manner to specific clinicopathological parameters. Gain of 17q, 20p, and 20q and loss of 4p were associated with the pattern of the cancer-stroma relationship; loss of 18q was associated with pT category; gain of 5p was associated with pN category; loss of 4q and loss of 21q were associated with lymphatic invasion; gain of 7p and loss of 4q and 18q were associated with venous invasion; and loss of 18q was associated with pathological stage. These data suggest that gain of 20q and loss of 18q might play an important role in the development and progression of gastric cancer. Moreover, some genes on 20q and 18q might be target genes of gastric cancer.

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Section: Genetic Alterations In Gastric Cancermentioning

confidence: 99%

mentioning

confidence: 99%

Genetic alterations in 102 primary gastric cancers by comparative genomic hybridization: gain of 20q and loss of 18q are associated with tumor progression

et al. 2004

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“…Although amplifications at 17q12-21 and 20q and losses at 8p and 9p are more frequently observed in iGC, 8p and 12q gains are associated with dGC (12,13), arguing that iGC and dGC may represent molecularly distinct entities. Furthermore, ERBB2/HER2 amplifications are observed in iGC but not dGCs, raising the possibility that only the former may be candidates for Trastuzumab (anti-HER2) therapy (14). Identifying additional genetic and genomic aberrations specifically associated with iGC or dGC might further elucidate the mechanistic basis of their morphologic differences, and identify potential avenues for iGC or dGC-specific treatments.…”

Section: Introductionmentioning

confidence: 99%

Integrative Genomics IdentifiesRAB23as an Invasion Mediator Gene in Diffuse-Type Gastric Cancer

Hou

Grabsch

et al. 2008

Cancer Research

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Recurrent genomic amplifications and deletions are frequently observed in primary gastric cancers (GC). However, identifying specific oncogenes and tumor suppressor genes within these regions can be challenging, as they often cover tens to hundreds of genes. Here, we combined high-resolution array-based comparative genomic hybridization (aCGH) with gene expression profiling to target genes within focal high-level amplifications in GC cell lines, and identified RAB23 as an amplified and overexpressed Chr 6p11p12 gene in Hs746T cells. High RAB23 protein expression was also observed in some lines lacking RAB23 amplification, suggesting additional mechanisms for up-regulating RAB23 besides gene amplification. siRNA silencing of RAB23 significantly reduced cellular invasion and migration in Hs746T cells, whereas overexpression of RAB23 enhanced cellular invasion in AGS cells. RAB23 amplifications in primary gastric tumors were confirmed by both fluorescence in situ hybridization and genomic qPCR, and in two independent patient cohorts from Hong Kong and the United Kingdom RAB23 expression was significantly associated with diffuse-type GC (dGC) compared with intestinal-type GC (iGC). These results provide further evidence that dGC and iGC likely represent two molecularly distinct tumor types, and show that investigating focal chromosomal amplifications by combining highresolution aCGH with expression profiling is a powerful strategy for identifying novel cancer genes in regions of recurrent chromosomal aberration. [Cancer Res 2008;68(12): 4623-30]

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“…LOH studies have demonstrated frequent imbalances at 1p, 1q, 5q, 7p, 7q, 11p, 12q, 16p, 17p, 18q, and 21q (Sano et al, 1991;Kuniyasu et al, 1994;Baffa et al, 1996;Ezaki et al, 1996;Sakata et al, 1997;Yustein et al, 1999). Comparative genomic hybridization (CGH) studies on GC have identified a complex pattern of gains and losses of many chromosomes (Koizumi et al, 1997;Kokkola et al, 1997Kokkola et al, , 1998El-Rifai et al, 1998;Larramendy et al, 1998;Moskaluk et al, 1998;Nessling et al, 1998;Sakakura et al, 1999;van Dekken et al, 1999;Vidgren et al, 1999), but studies simultaneously comparing various histopathological parameters and other genetic alterations remain limited.…”

Section: Introductionmentioning

confidence: 99%

Correlation of histologic subtypes and replication error phenotype with comparative genomic hybridization in gastric cancer

Chang

Huang

et al. 2000

Genes Chromosom. Cancer

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Concomitant gastrin and ERBB2 gene amplifications at 17q12-q21 in the intestinal type of gastric cancer

Cited by 35 publications

References 19 publications

Genetic alterations in 102 primary gastric cancers by comparative genomic hybridization: gain of 20q and loss of 18q are associated with tumor progression

Genetic alterations in 102 primary gastric cancers by comparative genomic hybridization: gain of 20q and loss of 18q are associated with tumor progression

Integrative Genomics IdentifiesRAB23as an Invasion Mediator Gene in Diffuse-Type Gastric Cancer

Correlation of histologic subtypes and replication error phenotype with comparative genomic hybridization in gastric cancer

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