Helicobacter pylori-related and -non-related gastric cancers do not differ with respect to chromosomal aberrations

• Published in: The Journal of pathology Vol. 192; no. 3; pp. 301 - 306
• Main Authors: van Grieken, Nicole C. T., Weiss, Marjan M., Meijer, Gerrit A., Hermsen, Mario A. J. A., Scholte, Ger H. A., Lindeman, Jan, Craanen, Mikael E., Bloemena, Elisabeth, Meuwissen, Stefan G. M., Baak, Jan P. A., Kuipers, Ernst J.
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01.11.2000; Wiley
• Subjects: Adult; Aged; Aged, 80 and over; Biological and medical sciences; chromosomal aberrations; Chromosome Aberrations; comparative genomic hybridization; DNA - analysis; Female; Flow Cytometry; gastric cancer; Gastroenterology. Liver. Pancreas. Abdomen; Helicobacter Infections - complications; Helicobacter pylori; Humans; Male; Medical sciences; Middle Aged; Nucleic Acid Hybridization; Stomach Neoplasms - etiology; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Tumors; Chromosomal aberration; Human; Flow cytometry; Stomach; Carcinoma; Spirillales; Spirillaceae; Malignant tumor; Carcinogenesis; Infection; Pathology; Helicobacter pylori; Comparative genomic hybridization; Bacteriosis; Cytogenetics; Digestive diseases; Bacteria; Molecular biology; Comparative study; Gastric disease
• ISSN: 0022-3417; 1096-9896
• DOI: 10.1002/1096-9896(2000)9999:9999<::AID-PATH697>3.0.CO;2-F

Gastric carcinogenesis is strongly associated with Helicobacter pylori infection, but the underlying genetic mechanisms are largely unknown. The aim of this study was to correlate chromosomal aberrations in gastric cancer to H. pylori status and its different strains, as well as to histological type and other clinico‐pathological variables. DNA from 46 gastric cancers (male/female 35/11, age 27–85 years) was extracted from formaldehyde‐fixed, paraffin‐embedded material and tested for chromosomal gains and losses by comparative genomic hybridization (CGH). Chromosomal aberrations with frequencies of 20% or higher were considered to be non‐random changes associated with gastric cancer. The mean number of chromosomal events per tumour was 9.7 (range 0–27), with a mean of 3.2 gains (range 0–16) and 6.5 losses (range 0–15). Gains were most frequently found at chromosomes 8q and 13q (24% and 26%, respectively). Losses were predominantly found on chromosome arms 2q, 9p, 12q, 14q, 15q, 16p, 16q, 17p, 17q, 19p, 19q, and 22q (22%, 30%, 43%, 22%, 33%, 50%, 28%, 50%, 39%, 33%, 39%, and 37%, respectively). Common regions of overlap narrowed down to 2q11–14, 8q23, 9p21, 12q24, 13q21–22, 14q24 and 15q11–15. The mean number of gains was higher in tumours with metastases than in localized tumours (4.1 vs. 1.9, p=0.04). Tumours with a loss at 17p showed a higher number of losses than tumours without a 17p loss (9.5 vs. 4.7 on average, p<0.001). Neither H. pylori status (+, n=25; −, n=21) nor H. pylori strain was correlated to the total number of events or to any specific chromosomal aberration, nor were there differences between intestinal (n=30) and diffuse (n=15) cancers or any other clinico‐pathological variable tested. In conclusion, a complex of chromosomal aberrations is involved in gastric cancer, but their pattern does not depend on H. pylori status or strain, nor on the histological type of the tumour. The exact biological meaning of these aberrations in carcinogenesis needs further clarification. Copyright © 2000 John Wiley & Sons, Ltd.