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Tumor Engraftment in a Xenograft Mouse Model of Human Mantle Cell Lymphoma
Published on: March 30, 2018
The pathogenesis of MALT lymphomas: where do we stand?
X Sagaert1, C De Wolf-Peeters, H Noels
1Department of Morphology and Molecular Pathology, University of Leuven, Leuven, Belgium. xavier.sagaert@uz.kuleuven.ac.be
Leukemia
|January 19, 2007
Summary
Mucosa-associated lymphoid tissue (MALT) lymphoma, a B-cell non-Hodgkin's lymphoma, often involves the gastrointestinal tract. Specific translocations activate the nuclear factor-kappaB (NF-kappaB) pathway, linking inflammation to oncogenesis.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Mucosa-associated lymphoid tissue (MALT) lymphoma is a diverse B-cell non-Hodgkin's lymphoma.
- It characteristically presents with extranodal involvement, most commonly in the gastrointestinal tract.
- Other organ systems can also be affected.
Purpose of the Study:
- To review the genetic landscape of MALT lymphoma.
- To elucidate the role of specific translocations in MALT lymphoma pathogenesis.
- To present MALT lymphoma as a model for inflammation-induced oncogenesis.
Main Methods:
- Review of scientific literature on MALT lymphoma.
- Analysis of genetic translocations associated with MALT lymphoma.
- Examination of the nuclear factor-kappaB (NF-kappaB) signaling pathway.
Main Results:
- Four specific translocations, t(11;18), t(1;14), t(14;18), and t(3;14), are uniquely linked to MALT lymphoma.
- At least three of these translocations target genes within the same pathway.
- This pathway activation leads to the dysregulation of nuclear factor-kappaB (NF-kappaB).
Conclusions:
- MALT lymphoma pathogenesis involves specific genetic alterations.
- Sustained inflammation can promote genotoxic events leading to MALT lymphoma.
- MALT lymphoma serves as a paradigm for understanding oncogenesis driven by inflammation and genetic insults.
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