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J Clin Invest. 2012 Oct;122(10):3424-31. doi: 10.1172/JCI63186. Epub 2012 Oct 1.

Pathogenesis of follicular lymphoma.

Author information

1
Center for Lymphoid Cancer, BC Cancer Agency, Department of Pathology and Laboratory Medicine, and Division of Medical Oncology, University of British Columbia, Vancouver, British Columbia, Canada.

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.

PMID:
23023713
PMCID:
PMC3461914
DOI:
10.1172/JCI63186
[Indexed for MEDLINE]
Free PMC Article

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