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Updated: May 18, 2026

Tumor Engraftment in a Xenograft Mouse Model of Human Mantle Cell Lymphoma
Published on: March 30, 2018
Pathogenesis of follicular lymphoma
Robert Kridel1, Laurie H Sehn, Randy D Gascoyne
1Center 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.
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