Gastroenterology

Gastroenterology

Volume 122, Issue 5, May 2002, Pages 1286-1294
Gastroenterology

Clinical Research
T(11;18) is a marker for all stage gastric MALT lymphomas that will not respond to H. pylori eradication,☆☆,

https://doi.org/10.1053/gast.2002.33047Get rights and content

Abstract

Background & Aims: Eradication of Helicobacter pylori leads to cure of gastric mucosa-associated lymphoid tissue (MALT) lymphoma in 75% of localized cases. However, prolonged follow-up is necessary to determine whether a lymphoma responds to therapy. In a small series of cases, we showed that t(11;18)(q21;q21)-positive MALT lymphomas failed to respond to H. pylori eradication. The present study aimed to verify this finding in a large cohort and confirm whether the translocation predicts the response of stage IE tumors, for which clinical staging has little prognostic value. Methods: A total of 111 patients with H. pylori–positive gastric MALT lymphoma treated with antibiotics were studied. Clinical staging was undertaken before therapy. The response of lymphoma to H. pylori eradication was determined by histologic examination of gastric biopsy specimens. Diagnostic biopsy specimens were analyzed for t(11;18)(q21;q21) by reverse-transcription polymerase chain reaction of the API2-MALT1 transcript. Results: Forty-seven of the 48 patients who showed complete regression had lymphoma at stage IE, whereas 43 of the 63 nonresponsive cases were at stage IE and the remaining cases at stage IIE or above. t(11;18)(q21;q21) was detected in 2 of 48 complete-regression cases, and these positive cases showed relapse of lymphoma in the absence of H. pylori reinfection. In contrast, the translocation was present in 42 of the 63 nonresponsive cases, including 26 of 43 (60%) at stage IE. Conclusions: t(11;18)(q21;q21)-positive gastric MALT lymphomas, including those at stage IE, do not respond to H. pylori eradication. Detection of the translocation should help the clinical management of patients with gastric MALT lymphoma.

GASTROENTEROLOGY 2002;122:1286-1294

Section snippets

Patients and materials

A series of 111 patients with H. pylori–positive gastric MALT lymphoma who were treated with antibiotics alone was retrospectively recruited from the Groupe d'Etude des Lymphomes Digestifs, France (33 cases); Department of Pathology, The Netherlands Cancer Institute, The Netherlands (32 cases); Servizi di Anatomia Patologica e Gastroenterologia, Università degli Studi di Bologna, Italy (24 cases); the German MALT Lymphoma Study Group (18 cases); and Department of Histopathology, University

Clinical staging predicts treatment failure to H. pylori eradication in stage IIE or above but not stage IE gastric MALT lymphoma

A total of 111 patients with gastric MALT lymphoma were included in the present multicenter study (67 men and 44 women; mean age, 58 years [range, 25–88 years]). H. pylori infection was successfully cured in all cases as confirmed by histology and culture of gastric biopsy specimens taken after completion of the antibiotic therapy. After H. pylori eradication, patients were followed up by repeated endoscopy and biopsy. The mean period between H. pylori eradication and achievement of CR or

Discussion

H. pylori eradication leads to complete regression of gastric MALT lymphoma in 75% of cases and is widely accepted as the first-line treatment for this tumor.7, 8, 9, 10, 11, 12, 13 One of the major dilemmas in clinical management of patients with this disease is the identification of those that will not respond to H. pylori eradication and require chemotherapy or radiotherapy. At present, this requires prolonged follow-up with repeated endoscopy and gastric biopsy. Clinical staging is helpful

Acknowledgements

The authors thank J. Audouin, L. Bedenne, O. Bouche, Y. Bouhnik, J. Fournet, A. De Mascarel, Ph. Moreau, J. Lafon, and A. Pariente of the Groupe d'Etude des Lymphomes Digestifs, France, for contribution of part of the specimens used for this study, Dr. Tim C. Diss for critical reading of the manuscript, and M. Sisnaki for technical assistance.

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    Address requests for reprints to: Ming-Qing Du, Ph.D., Department of Histopathology, Royal Free and University College Medical School, University College London, Rockefeller Building, University Street, London WC1E 6JJ, England. e-mail: [email protected]; fax: (44) 20-7387-3674.

    ☆☆

    Supported by research grants from the Leukemia Research Fund, Cancer Research Campaign, Délégation à la Recherche Clinique, Assistance Publique-Hôpitaux de Paris, Associazioine Italiana per la Ricerca sul Cancro, and Deutsche Krebshilfe (grant 70-225I).

    H.L. and H.Y. contributed equally to this work.

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