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E-GEOD-3648 - Histopathological stages of disease in Helicobacter-induced mucosa-associated lymphoid tissue lymphoma
Submitted on 22 November 2005, released on 22 November 2005, last updated on 27 March 2012
Long-term colonization of humans with Helicobacter pylori can cause the development of gastric B cell mucosa-associated lymphoid tissue lymphoma, yet little is known about the sequence of molecular steps that accompany disease progression. We used microarray analysis and laser microdissection to identify gene expression profiles characteristic and predictive of the various histopathological stages in a mouse model of the disease. The initial step in lymphoma development is marked by infiltration of reactive lymphocytes into the stomach and the launching of a mucosal immune response. Our analysis uncovered molecular markers of both of these processes, including genes coding for the immunoglobulins and the small proline-rich protein Sprr 2A. The subsequent step is characterized histologically by the antigen-driven proliferation and aggregation of B cells and the gradual appearance of lymphoepithelial lesions. In tissues of this stage, we observed increased expression of genes previously associated with malignancy, including the laminin receptor-1 and the multidrug-resistance channel MDR-1. Finally, we found that the transition to destructive lymphoepithelial lesions and malignant lymphoma is marked by an increase in transcription of a single gene encoding calgranulin A/Mrp-8. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed
unknown experiment type
Stanford Microarray Database <email@example.com>, Anne Mueller
Distinct gene expression profiles characterize the histopathological stages of disease in Helicobacter-induced mucosa-associated lymphoid tissue lymphoma. Mueller A, O'Rourke J, Grimm J, Guillemin K, Dixon MF, Lee A, Falkow S.