Taji S, Nomura K, Matsumoto Y, Sakabe H, Yoshida N, Mitsufuji S, Nishida K, Horiike S, Nakamura S, Morita M, Taniwaki M. Trisomy 3 may predict a poor response of gastric MALT lymphoma to Helicobacter pylori eradication therapy. World J Gastroenterol 2005; 11(1): 89-93 [PMID: 15609403 DOI: 10.3748/wjg.v11.i1.89]
Corresponding Author of This Article
Kenichi Nomura, M.D., Ph.D., Molecular Hematology and Oncology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kawaramachi Hirokoji, Kamigyo-ku, 602-8566 Kyoto, Japan. nomuken@sun.kpu-m.ac.jp
Article-Type of This Article
H Pylori
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Sawako Taji, Naohisa Yoshida, Shoji Mitsufuji, Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan
Kenichi Nomura, Yosuke Matsumoto, Kazuhiro Nishida, Shigeo Horiike, Molecular Hematology and Oncology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan
Hideaki Sakabe, Department of Internal Medicine, Kohka Public Hospital, Kohka, Rokusin 3-39, Kohka-Minakuchi, Shiga 528-0014, Japan
Shigeo Nakamura, Department of Pathology and Clinical Laboratories, Aichi Cancer Center Hospital, Chikusa-ku, Nagoya 464-8681, Japan
Masuji Morita, School of Nursing, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan
Masafumi Taniwaki, Clinical Molecular Genetics and Laboratory Medicine, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan
Author contributions: All authors contributed equally to the work.
Correspondence to: Kenichi Nomura, M.D., Ph.D., Molecular Hematology and Oncology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kawaramachi Hirokoji, Kamigyo-ku, 602-8566 Kyoto, Japan. nomuken@sun.kpu-m.ac.jp
Telephone: +81-75-2515521 Fax: +81-75-2510710
Received: April 30, 2004 Revised: May 2, 2004 Accepted: June 25, 2004 Published online: January 7, 2005
Abstract
AIM: To investigate the relation of the response to Helicobacter pylori eradication therapy to the depth of tumor invasion and chromosome abnormalities in patients with mucosa-associated lymphoid tissue (MALT) lymphoma and to determine the clinical value of aneuploidy.
METHODS: We studied 13 patients with localized gastric MALT lymphoma of stage E1. Before eradication therapy, the depth of tumor invasion was assessed by endoscopic ultrasonography in 8 patients and by endoscopic examination and gastrointestinal series in the remaining patients. To detect chromosomal abnormalities, paraffin-embedded tissue sections of diagnostic biopsy specimens underwent tissue-fluorescence in situ hybridization (FISH), using chromosome-specific α-satellite DNA probes for chromosomes 3,7,12, and 18 and YAC clones for t(11;18)(q21;q21).
RESULTS: Seven of the 13 patients had complete regression (CR) in response to H pylori eradication therapy. No patient with CR had submucosal tumor invasion. Trisomy 18 was seen in 1 patient with CR, and both trisomies 12 and 18 were present in another patient with CR. All patients with no response or progressive disease had deep submucosal tumor invasion and showed t(11;18)(q21;q21) or trisomy 3. Trisomy 7 was not detected in this series of patients.
CONCLUSION: The depth of tumor invasion is an accurate predictor of the response of stage E1 MALT lymphoma to H pylori eradication therapy and is closely associated with the presence of chromosomal abnormalities. Trisomy 3 may predict the aggressive development of MALT lymphoma.
