Korean J Med.  2007 Feb;72(2):138-150.

The contribution of BCA-1 and apoptosis in gastric MALT lymphoma generation

  • 1Department of Gastroenterology and Genomic Research Center for Gastroenterology, Ajou University School of Medicine, Suwon, Korea.
  • 2Department of Anatomic Pathology, Ajou University School of Medicine, Suwon, Korea.
  • 3Digestive Disease center, Daejin Medical Center Jesaeng Hospital at Bundang, Seongnam, Korea. hahmkb@hotmail.com


BACKGROUND: In spite that several lines of evidence suggest that gastric MALT lymphoma arises from Helicobacter pylori (H. pylori)-associated acquired MALT(mucosa-associated lymphoid tissue), the exact underlying pathogenic mechanism has not yet been clearly exploited. The high expression of B cell attracting chemokine-1 (BCA-1) and modulation of cell death by apoptosis have been suggested as possible pathogenic determinants for whether the cases with H. pylori infection will develop MALToma or not.
We have studied the expression of BCA-1 and its receptor CXCR5 in gastric tissue samples obtained from patients suffering with H. pylori-positive gastritis, H. pylori-negative gastritis and H. pylori-positive low grade MALT lymphoma, respectively. TUNEL (Terminal deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling) staining for detecting apoptotic cells was also included. Furthermore, the changes of the BCA-1 and CXCR5 expressions before and after the complete remission of MALToma were compared. The in vitro influencing effect of H. pylori infection on the BCA-1 and CXCR5 expression was observed.
Significantly higher levels of BCA-1 and its receptor CXCR5 expression were observed in H. pylori-positive MALToma specimens as compared with either the H. pylori-positive gastritis or H. pylori-negative gastritis specimens; its levels were significantly reduced after the remission of MALToma. In contrast to the increased apoptotic activity after H. pylori infection, a significant reduction of epithelial apoptosis was observed in the H. pylori-positive MALToma specimens. H. pylori infection directly induced the expression of BCA-1 in the cultured gastric epithelial cells.
The up-regulated BCA-1 expression and the decreased apoptosis in H. pylori infected gastric epithelial cells might contribute to the development of MALT lymphoma.


Chemokine; BCA-1; CXCR5; Apoptosis; MALT lymphoma; Helicobacter pylori

MeSH Terms

Cell Death
DNA Nucleotidylexotransferase
Epithelial Cells
Helicobacter pylori
In Situ Nick-End Labeling
Lymphoma, B-Cell, Marginal Zone*
DNA Nucleotidylexotransferase
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