Gastric MALT lymphoma: a model of chronic inflammation-induced tumor development.
Mucosa-associated lymphoid tissue (MALT) lymphoma, or extranodal marginal zone lymphoma of MALT, is an indolent B-cell non-Hodgkin lymphoma arising in lymphoid infiltrates that are induced by chronic inflammation in extranodal sites. The stomach is the most commonly affected organ, in which MALT lymphoma pathogenesis is clearly associated with Helicobacter pylori gastroduodenitis. Gastric MALT lymphoma has attracted attention because of the involvement of genetic aberrations in the nuclear factor kappaB (NFkappaB) pathway, one of the most investigated pathways in the fields of immunology and oncology. This Review presents gastric MALT lymphoma as an outstanding example of the close pathogenetic link between chronic inflammation and tumor development, and describes how this information can be integrated into daily clinical practice. Gastric MALT lymphoma is considered one of the best models of how genetic events lead to oncogenesis, determine tumor biology, dictate clinical behavior and represent viable therapeutic targets. Moreover, in view of the association of gastric MALT lymphoma with dysregulation of the NFkappaB pathway, this signaling pathway will be discussed in depth in both normal and pathological conditions, highlighting strategies to identify new therapeutic targets in this lymphoma.
Sagaert
Xavier
X
Department of Pathology, University Hospitals of K. U. Leuven, Minderbroederstraat 12, B-3000 Leuven, Belgium. xavier.sagaert@uz.kuleuven.ac.be
Van Cutsem
Eric
E
De Hertogh
Gert
G
Geboes
Karel
K
Tousseyn
Thomas
T
D000075747:Baculoviral IAP Repeat-Containing 3 Protein; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000276:immunology; D018450:Disease Progression; D051858:Forkhead Transcription Factors / Q000235:genetics; D005753:Gastric Mucosa / Q000276:immunology; D015972:Gene Expression Regulation, Neoplastic / Q000276:immunology; D016481:Helicobacter Infections / Q000276:immunology; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D007150:Immunohistochemistry; D051034:Inhibitor of Apoptosis Proteins / Q000235:genetics; D018442:Lymphoma, B-Cell, Marginal Zone / Q000175:diagnosis / Q000235:genetics* / Q000276:immunology* / Q000382:microbiology / Q000473:pathology / Q000628:therapy; D016403:Lymphoma, Large B-Cell, Diffuse / Q000235:genetics; D016328:NF-kappa B / Q000502:physiology; D015514:Oncogene Proteins, Fusion / Q000276:immunology; D012097:Repressor Proteins / Q000235:genetics; D015398:Signal Transduction; D013274:Stomach Neoplasms / Q000175:diagnosis / Q000235:genetics* / Q000276:immunology* / Q000382:microbiology / Q000473:pathology / Q000628:therapy; D051841:Transcription Factor RelB / Q000276:immunology; D014178:Translocation, Genetic; D044767:Ubiquitin-Protein Ligases
C486626:FOXP1 protein, human; D051858:Forkhead Transcription Factors; D051034:Inhibitor of Apoptosis Proteins; D016328:NF-kappa B; D015514:Oncogene Proteins, Fusion; C497593:RELB protein, human; D012097:Repressor Proteins; D051841:Transcription Factor RelB; C494832:BIRC3 protein, human; D000075747:Baculoviral IAP Repeat-Containing 3 Protein; D044767:Ubiquitin-Protein Ligases