Antibodies to Helicobacter pylori and CagA protein are associated with the response to antibacterial therapy in patients with H. pylori-positive API2-MALT1-negative gastric MALT lymphoma.
The aim of this study was to clarify predictive factors for response to eradication therapy in cases of Helicobacter pylori (H. pylori)-positive API2-MALT1-negative gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Sixty-six patients who were examined for H. pylori infection and the presence of the API2-MALT1 chimeric transcript and who underwent H. pylori eradication therapy as first-line therapy, were enrolled in this study. Immunohistochemical markers (p53, Ki-67, and BCL10), microsatellite instability, loss of heterozygosity, serum levels of antibodies (anti-H. pylori and anti-CagA), and markers for gastritis (gastrin and pepsinogens) were examined, and the results were compared between patients whose tumors regressed completely after eradication therapy (responders) and patients whose tumors did not regress (non-responders). Of the 66 patients with localized gastric MALT lymphoma, 47 (71.2%) showed complete remission after eradication therapy. None of the H. pylori-negative (n = 9) and/or API2-MALT1-positive (n = 7) patients responded to antibacterial treatment. Of 44 patients with H. pylori-positive API2-MALT1-negative gastric MALT lymphoma, 38 (86.4%) showed complete remission after eradication therapy. Titers of antibodies against H. pylori and CagA protein were significantly higher in the responders than in the non-responders (P = 0.0235 and 0.0089, respectively). No significant difference between the groups was observed for the other factors. In conclusion, measurement of titers of serum antibodies to H. pylori and CagA protein may be useful for predicting the response to eradication therapy in patients with H. pylori-positive API2-MALT1-negative gastric MALT lymphoma.
Sumida
Tomonori
T
Department of Medicine and Molecular Science, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan.
Kitadai
Yasuhiko
Y
Hiyama
Toru
T
Shinagawa
Kei
K
Tanaka
Miwako
M
Kodama
Michiyo
M
Masuda
Hiroshi
H
Ito
Masanori
M
Tanaka
Shinji
S
Yoshihara
Masaharu
M
Chayama
Kazuaki
K
D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D000907:Antibodies, Bacterial / Q000187:drug effects; D000942:Antigens, Bacterial / Q000187:drug effects / Q000235:genetics*; D001426:Bacterial Proteins / Q000187:drug effects / Q000235:genetics*; D001706:Biopsy; D004273:DNA, Neoplasm / Q000235:genetics; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy; D016480:Helicobacter pylori / Q000235:genetics* / Q000276:immunology* / Q000302:isolation & purification; D006801:Humans; D007564:Japan; D018442:Lymphoma, B-Cell, Marginal Zone / Q000188:drug therapy / Q000382:microbiology*; D018895:Microsatellite Repeats; D015514:Oncogene Proteins, Fusion / Q000172:deficiency* / Q000235:genetics; D011706:Pyloric Antrum / Q000382:microbiology / Q000473:pathology; D012334:RNA, Neoplasm / Q000235:genetics; D012189:Retrospective Studies; D013270:Stomach / Q000382:microbiology / Q000473:pathology; D013274:Stomach Neoplasms / Q000188:drug therapy / Q000382:microbiology*; D014158:Transcription, Genetic
C415943:API2-MALT1 fusion protein, human; D000900:Anti-Bacterial Agents; D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D004273:DNA, Neoplasm; D015514:Oncogene Proteins, Fusion; D012334:RNA, Neoplasm; C080866:cagA protein, Helicobacter pylori