Cytogenetic studies in primary gastric cancer

Ochi, Hisako; Douglass, Harold O.; Sandberg, Avery A.

doi:10.1016/0165-4608(86)90022-1

Cited by 86 publications

(32 citation statements)

References 18 publications

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“…The detection of frequent LOH at lIpiS is consistent with a cytogenetic study detailing Ilpl3-15 rearrangements in seven out of eight cases of primary adenocarcinoma of the oesophagus and gastric cardia (Rodriguez et al, 1990). In contrast to these observations, other cytogenetic studies failed to detect lIp rearrangements in gastric carcinoma (Ochi et al, 1986;Seruca et al, 1993) (Sano et al, 1991;Uchino et al, 1992 (Becker et al, 1994). In contrast, intestinal-type carcinomas demonstrated silent mutations in 2 out of 20 tumours, indicating that E-cadherin gene mutations may contribute to the development of diffusely growing gastric carcinomas (Becker et al, 1994 Additional studies have suggested that allele loss at a number of loci may be specific to the development of particular subtypes of gastric carcinoma (Sano et al, 1991).…”

Section: Resultsmentioning

confidence: 45%

“…Allelic imbalance may also represent the amplification of a mutant allele without concomitant loss of the wild-type allele. Furthermore, cytogenetic and flow cytometric studies have indicated that gains in chromosome copy number occur frequently in gastric adenocarcinoma (Ochi et al, 1986;Ferti-Passantonopoulou et al, 1987;Flejou et al, 1994). Polymorphic DNA markers will British Journal of Cancer (1997) 76(11), 1455-1465 Compared with histological subtype, a higher incidence of Al was detected on 16q in tumours of the diffuse type relative to those of the intestinal type (7 out of 9 vs 7 out of 26; P = 0.02, Fisher's exact test).…”

Section: Resultsmentioning

confidence: 99%

“…In contrast, the genetic events underlying the development of gastric cancer remain poorly characterized. Cytogenetic studies of gastric adenocarcinoma have reported complex karyotypes, with multiple numerical and/or structural abnormalities (Ochi et al, 1986;Ferti-Passantonopoulou et al, 1987;Seruca et al, 1993). Loss of heterozygozity studies have identified a number of chromosomal regions that demonstrate allele loss in primary gastric tumours.…”

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confidence: 99%

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Allelotype analysis of adenocarcinoma of the gastric cardia

Gleeson

Sloan²,

McGuigan³

et al. 1997

Br J Cancer

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Summary To identify chromosomal loci involved in the development of proximal gastric adenocarcinoma, this study delineated the pattern of allelic imbalance in a series of 38 adenocarcinomas arising in the gastric cardia. A total of 137 microsatellite markers covering all autosomal arms, excluding acrocentric arms, were analysed. A mean of 35 out of a total of 39 chromosomal arms studied were informative for each patient. The tumour group demonstrated a high level of allelic imbalance, with an observed median fractional allelic imbalance of 0.47 for the 29 intestinal-type adenocarcinomas and 0.54 for the nine diffuse-type adenocarcinomas. Allelic imbalance was detected in >50% of informative cases in both histological subtypes on a number of chromosomal arms. In the intestinal subtype, these included, 3p (61%), 4q (71%), 5q (59%), 8p (60%), 9p (65%), 9q (83%), 12q (52%), 13q (52%), 17p (78%) and 18q (70%). A higher incidence of allelic imbalance was detected on chromosome 16q in tumours of the diffuse type relative to those of the intestinal type. A more detailed mapping on chromosomes 4q and 6q identified a number of cases with subchromosomal breakpoints. In conclusion, this analysis has indicated regions of the genome potentially involved in the development of proximal gastric carcinomas.

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Section: Resultsmentioning

confidence: 45%

Section: Resultsmentioning

confidence: 99%

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confidence: 99%

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Allelotype analysis of adenocarcinoma of the gastric cardia

Gleeson

Sloan²,

McGuigan³

et al. 1997

Br J Cancer

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“…Loss of heterozygosity at 19p13 is frequently seen in adult acute lymphocytic leukemia (Pabst et al, 1996). Some types of cancer, including ovarian (Sato et al, 1991), familial breast carcinoma (Lindblom et al, 1993), malignant ®brous histiocytoma (Mandahl et al, 1989), and gastric cancer (Ochi et al, 1986) are associated with either allelic losses with 19p or chromosomal translocations involving 19p13. These ®ndings, together with data relating to cytocidal activity, support the view that the gene encoding antizyme could be a candidate tumor suppressor gene.…”

Section: Discussionmentioning

confidence: 99%

Anti-tumor activity of antizyme which targets the ornithine decarboxylase (ODC) required for cell growth and transformation

et al. 1999

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Cell proliferation and transformation induced by growth factor stimulation or by carcinogens, viruses, or oncogenes are characterized by an associated increase in polyamine levels, which is mediated by increased polyamine biosynthesis and enhanced uptake of polyamines. Polyamine biosynthesis is catalyzed particularly, in the level of ornithine decarboxylase (ODC). The elevation of cellular polyamine levels on the other hand accelerates the induction of ornithine decarboxylase antizyme (antizyme), which is involved not only in ODC-degradation, but in the negative regulation of polyamine transport. Taking advantage of these characteristics of antizyme, the potential of antizyme as a factor having anti-cell growth and anti-tumor activity was investigated. We show that antizyme can induce cell death associated with a rapid decline of intracellular polyamine contents. The possible anti-tumor activities of ectopically expressed antizyme were tested in p21H-ras (Val 12)-transformed NIH3T3 cells and several human malignant cell lines including a line with loss of p53 expression, and they were shown to be as sensitive as nontransformed NIH3T3 cells in vitro. The in vivo antitumor activity was also tested using nude mice inoculated with H-ras transformed NIH3T3 cells that had been transfected with inducible antizyme expression vector and the results showed that antizyme expression in vivo blocks tumor formation in these mice. These results suggest that ectopic antizyme expression is of possible therapeutic bene®t in the treatment of cancer, which is mediated by ODC inactivation and intracellular polyamine depletion.

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“…Selection criteria were based on literature data considering numerical (and structural) aberrations in esophageal and other gastrointestinal tumors (2,10,11,21,41). The (peri)centromeric repetitive satellite DNA probes were labeled with biotin-14-dATP by nick translation of complete plasmid DNAaccording to manufacturer's directions (BRL, Gaithersburg, MD).…”

Section: Methodsmentioning

confidence: 99%

Detection of genetic changes in Barrett's adenocarcirioma and Barrett's esophagus by DNA in situ hybridization and immunohistochemistry

Krishnadath

Tilanus

Alers³

et al. 1994

Cytometry

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We have investigated the occurrence of chromosomal DNA and cell cycle‐related protein changes in Barrett's epithelium and adenocarcinoma. The presence of numerical chromosomal aberrations was studied by applying nonisotopic in situ hybridization (ISH) with (peri‐)centromeric DNA probes, specific for chromosomes 7, 8, 17, and Y, to routinely processed tissue sections of five cases (4 male, 1 female) of Barrett's adenocarcinoma and adjacent Barrett's epithelium. Cell cycle‐related protein expression was studied by immunohistochemistry (IHC) for p53 protein and the Ki‐67 antigen (Mib‐1) in subsequent sections. P53 protein overexpression was found in 3 of the 5 tumors. Overrepresentation of chromosome 8 and loss of chromosome 17 were found in 2 adenocarcinomas, both also negative for p53 protein overexpression. Y‐loss, mostly clonal, was detected in 3 of the 4 male adenocarcinomas and 2 cases of adjacent Barrett's epithelium. One tumor had both areas of overrepresentation and loss of the Y chromosome. All Barrett's adenocarcinomas appeared to contain aneuploid cell populations. No relation was found between cell proliferation characteristics and chromosomal aberrations. We conclude that ISH with chromosome specific DNA probes can be applied for the assessment of potentially important numerical chromosome changes in Barrett's esophagus. Further, the combination of IHC and ISH is useful for evaluation of specific genetic events. © 1994 Wiley‐Liss, Inc.

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Cytogenetic studies in primary gastric cancer

Cited by 86 publications

References 18 publications

Allelotype analysis of adenocarcinoma of the gastric cardia

Allelotype analysis of adenocarcinoma of the gastric cardia

Anti-tumor activity of antizyme which targets the ornithine decarboxylase (ODC) required for cell growth and transformation

Detection of genetic changes in Barrett's adenocarcirioma and Barrett's esophagus by DNA in situ hybridization and immunohistochemistry

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