Brad S Kahl1. 1. Department of Medicine, University of Wisconsin, Madison, USA. bsk@medicine.wisc.edu
Abstract
PURPOSE OF REVIEW: Gastric MALT lymphoma is a model malignancy for examination of how neoplasia may arise from chronic inflammation. It is also exemplifies the translation of biologic knowledge of a disease towards improved clinical practice. Several recent publications have furthered the understanding of gastric MALT lymphoma pathogenesis, clinical behavior, and treatment. RECENT FINDINGS: A substantial fraction of cases will harbor a balanced translocation between chromosomes 11 and 18. This translocation results in the generation of a novel fusion protein, aberrant nuclear BCL10 expression, and activation of the NF-kB pathway. The result is H. pylori-independent growth and a unique clinical picture characterized by a more advanced presentation and unresponsiveness to H. pylori eradication therapy. While more likely to require cytotoxic therapy, this subtype is paradoxically less likely to undergo large-cell transformation. Finally, clinical trials are helping define the optimal role for H. pylori eradication therapy and are demonstrating that therapeutic approaches incorporating stomach conservation are preferable for those cases unresponsive to eradication therapy. SUMMARY: The pathogenesis of gastric MALT lymphoma has been elucidated to a large degree in recent years. Understanding the biology of this disease will most certainly translate into clinical practice.
PURPOSE OF REVIEW: Gastric MALT lymphoma is a model malignancy for examination of how neoplasia may arise from chronic inflammation. It is also exemplifies the translation of biologic knowledge of a disease towards improved clinical practice. Several recent publications have furthered the understanding of gastric MALT lymphoma pathogenesis, clinical behavior, and treatment. RECENT FINDINGS: A substantial fraction of cases will harbor a balanced translocation between chromosomes 11 and 18. This translocation results in the generation of a novel fusion protein, aberrant nuclear BCL10 expression, and activation of the NF-kB pathway. The result is H. pylori-independent growth and a unique clinical picture characterized by a more advanced presentation and unresponsiveness to H. pylori eradication therapy. While more likely to require cytotoxic therapy, this subtype is paradoxically less likely to undergo large-cell transformation. Finally, clinical trials are helping define the optimal role for H. pylori eradication therapy and are demonstrating that therapeutic approaches incorporating stomach conservation are preferable for those cases unresponsive to eradication therapy. SUMMARY: The pathogenesis of gastric MALT lymphoma has been elucidated to a large degree in recent years. Understanding the biology of this disease will most certainly translate into clinical practice.