Pathogenesis of follicular lymphoma.
review · Level V
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- Record sourced from PubMed, PMID 23023713.
- Also identified by DOI 10.1172/JCI63186 and PMC identifier 3461914.
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Abstract
The hallmark t(14;18)(q32;q21) in follicular lymphoma (FL) results in constitutive overexpression of the BCL2 protein, allowing B cells to abrogate the default germinal center apoptotic program. Most tumors are characterized by recurrent secondary genetic alterations including genomic gains, losses, and mutations, some providing a growth advantage, including alterations in MLL2, EPHA7, TNFRSF14, and EZH2. The sequence in which these events occur and how they contribute to progression and ultimately to transformation is unclear. Lastly, crosstalk between neoplastic B cells and non-neoplastic immune and stromal cells in the microenvironment plays an important role in sustaining tumor cell growth, cultivating immune privilege, and promoting transformation.
Medical subject headings
- B-Lymphocytes
- Cell Transformation, Neoplastic
- Chromosomes, Human, Pair 14
- Chromosomes, Human, Pair 18
- Lymphoma, Follicular
- Neoplasm Proteins
- Proto-Oncogene Proteins c-bcl-2
- Translocation, Genetic