High incidence of t(11;18)(q21;q21) in Helicobacter pylori-negative gastric MALT lymphoma

Hongtao Ye, Hongxiang Liu, Markus Raderer, Andreas Chott, Agnes Ruskone-Fourmestraux, Andrew Wotherspoon, Martin J S Dyer, Shih Sung Chuang, Ahmet Dogan, Peter G. Isaacson, Ming Qing Du

Research output: Contribution to journalArticle

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Abstract

In approximately 5% to 10% of gastric mucosa - associated lymphoid tissue (MALT) lymphomas, evidence of Helicobacter pylori infection is absent, and their pathogenesis is poorly understood. We reviewed the clinical data and histology, and we examined t(11;18)(q21;q21) and BCL10 expression pattern in 17 such cases. In each case, the absence of H pylori was confirmed by negative serology and histology/immunohistochemistry. Five cases with stage IE disease were first treated with antibiotics, and none of them showed any endoscopic or histologic response. Review of the histology failed to identify any apparent difference between gastric MALT lymphomas with and without H pylori infection. Reverse transcription-polymerase chain reaction (RT-PCR) showed t(11;18)(q21;q21) in 9 (53%) of 17 cases, more frequent in lymphomas at stage IIE or above (5 of 6) than those at stage IE (3 of 10). Two t(11;18)(q21;q21)-positive lymphomas were treated by partial gastrectomy and more than 16 years later showed lymphoma relapse in the gastric stump with dissemination to other mucosal sites, poorly responsive to therapy. BCL10 nuclear expression was observed in 7 of 8 t(11;18)(q21; q21)-positive cases and 4 of 7 t(11;18)(q21; q21)-negative cases, including one case suspicious for a BCL10-involved chromosomal translocation. Our results show that t(11;18)(q21;q21) occurs at a high frequency in H pylori-negative gastric MALT lymphomas. Translocation-positive gastric MALT lymphomas tend to be aggressive, and patients with such lymphomas might benefit from prompt treatment and close follow-up.

Original languageEnglish (US)
Pages (from-to)2547-2550
Number of pages4
JournalBlood
Volume101
Issue number7
DOIs
StatePublished - Apr 1 2003
Externally publishedYes

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Marginal Zone B-Cell Lymphoma
Gastric Mucosa
Helicobacter pylori
Histology
Lymphoma
Pylorus
Tissue
Incidence
Gastric Stump
Genetic Translocation
Polymerase chain reaction
Helicobacter Infections
Serology
Transcription
Gastrectomy
Reverse Transcription
Immunohistochemistry
Anti-Bacterial Agents
Recurrence
Polymerase Chain Reaction

ASJC Scopus subject areas

  • Hematology

Cite this

Ye, H., Liu, H., Raderer, M., Chott, A., Ruskone-Fourmestraux, A., Wotherspoon, A., ... Du, M. Q. (2003). High incidence of t(11;18)(q21;q21) in Helicobacter pylori-negative gastric MALT lymphoma. Blood, 101(7), 2547-2550. https://doi.org/10.1182/blood-2002-10-3167

High incidence of t(11;18)(q21;q21) in Helicobacter pylori-negative gastric MALT lymphoma. / Ye, Hongtao; Liu, Hongxiang; Raderer, Markus; Chott, Andreas; Ruskone-Fourmestraux, Agnes; Wotherspoon, Andrew; Dyer, Martin J S; Chuang, Shih Sung; Dogan, Ahmet; Isaacson, Peter G.; Du, Ming Qing.

In: Blood, Vol. 101, No. 7, 01.04.2003, p. 2547-2550.

Research output: Contribution to journalArticle

Ye, H, Liu, H, Raderer, M, Chott, A, Ruskone-Fourmestraux, A, Wotherspoon, A, Dyer, MJS, Chuang, SS, Dogan, A, Isaacson, PG & Du, MQ 2003, 'High incidence of t(11;18)(q21;q21) in Helicobacter pylori-negative gastric MALT lymphoma', Blood, vol. 101, no. 7, pp. 2547-2550. https://doi.org/10.1182/blood-2002-10-3167
Ye H, Liu H, Raderer M, Chott A, Ruskone-Fourmestraux A, Wotherspoon A et al. High incidence of t(11;18)(q21;q21) in Helicobacter pylori-negative gastric MALT lymphoma. Blood. 2003 Apr 1;101(7):2547-2550. https://doi.org/10.1182/blood-2002-10-3167
Ye, Hongtao ; Liu, Hongxiang ; Raderer, Markus ; Chott, Andreas ; Ruskone-Fourmestraux, Agnes ; Wotherspoon, Andrew ; Dyer, Martin J S ; Chuang, Shih Sung ; Dogan, Ahmet ; Isaacson, Peter G. ; Du, Ming Qing. / High incidence of t(11;18)(q21;q21) in Helicobacter pylori-negative gastric MALT lymphoma. In: Blood. 2003 ; Vol. 101, No. 7. pp. 2547-2550.
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abstract = "In approximately 5{\%} to 10{\%} of gastric mucosa - associated lymphoid tissue (MALT) lymphomas, evidence of Helicobacter pylori infection is absent, and their pathogenesis is poorly understood. We reviewed the clinical data and histology, and we examined t(11;18)(q21;q21) and BCL10 expression pattern in 17 such cases. In each case, the absence of H pylori was confirmed by negative serology and histology/immunohistochemistry. Five cases with stage IE disease were first treated with antibiotics, and none of them showed any endoscopic or histologic response. Review of the histology failed to identify any apparent difference between gastric MALT lymphomas with and without H pylori infection. Reverse transcription-polymerase chain reaction (RT-PCR) showed t(11;18)(q21;q21) in 9 (53{\%}) of 17 cases, more frequent in lymphomas at stage IIE or above (5 of 6) than those at stage IE (3 of 10). Two t(11;18)(q21;q21)-positive lymphomas were treated by partial gastrectomy and more than 16 years later showed lymphoma relapse in the gastric stump with dissemination to other mucosal sites, poorly responsive to therapy. BCL10 nuclear expression was observed in 7 of 8 t(11;18)(q21; q21)-positive cases and 4 of 7 t(11;18)(q21; q21)-negative cases, including one case suspicious for a BCL10-involved chromosomal translocation. Our results show that t(11;18)(q21;q21) occurs at a high frequency in H pylori-negative gastric MALT lymphomas. Translocation-positive gastric MALT lymphomas tend to be aggressive, and patients with such lymphomas might benefit from prompt treatment and close follow-up.",
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AU - Ruskone-Fourmestraux, Agnes

AU - Wotherspoon, Andrew

AU - Dyer, Martin J S

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AU - Isaacson, Peter G.

AU - Du, Ming Qing

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AB - In approximately 5% to 10% of gastric mucosa - associated lymphoid tissue (MALT) lymphomas, evidence of Helicobacter pylori infection is absent, and their pathogenesis is poorly understood. We reviewed the clinical data and histology, and we examined t(11;18)(q21;q21) and BCL10 expression pattern in 17 such cases. In each case, the absence of H pylori was confirmed by negative serology and histology/immunohistochemistry. Five cases with stage IE disease were first treated with antibiotics, and none of them showed any endoscopic or histologic response. Review of the histology failed to identify any apparent difference between gastric MALT lymphomas with and without H pylori infection. Reverse transcription-polymerase chain reaction (RT-PCR) showed t(11;18)(q21;q21) in 9 (53%) of 17 cases, more frequent in lymphomas at stage IIE or above (5 of 6) than those at stage IE (3 of 10). Two t(11;18)(q21;q21)-positive lymphomas were treated by partial gastrectomy and more than 16 years later showed lymphoma relapse in the gastric stump with dissemination to other mucosal sites, poorly responsive to therapy. BCL10 nuclear expression was observed in 7 of 8 t(11;18)(q21; q21)-positive cases and 4 of 7 t(11;18)(q21; q21)-negative cases, including one case suspicious for a BCL10-involved chromosomal translocation. Our results show that t(11;18)(q21;q21) occurs at a high frequency in H pylori-negative gastric MALT lymphomas. Translocation-positive gastric MALT lymphomas tend to be aggressive, and patients with such lymphomas might benefit from prompt treatment and close follow-up.

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