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.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antigen Presentation
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Apoptosis
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B-Lymphocytes / pathology*
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Cell Division
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Cell Transformation, Neoplastic / genetics*
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Chromosome Aberrations
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Chromosomes, Human, Pair 14 / genetics*
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Chromosomes, Human, Pair 14 / ultrastructure
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Chromosomes, Human, Pair 18 / genetics*
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Chromosomes, Human, Pair 18 / ultrastructure
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Disease Progression
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Genes, bcl-2
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Humans
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Lymphoma, Follicular / drug therapy
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Lymphoma, Follicular / etiology
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Lymphoma, Follicular / genetics*
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Lymphoma, Follicular / pathology
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Macrophages / pathology
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Models, Biological
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Molecular Targeted Therapy
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Neoplasm Proteins / biosynthesis
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Neoplasm Proteins / genetics*
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Neoplasm Proteins / physiology
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Neoplastic Stem Cells / pathology
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Proto-Oncogene Proteins c-bcl-2 / biosynthesis
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Proto-Oncogene Proteins c-bcl-2 / genetics*
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Proto-Oncogene Proteins c-bcl-2 / physiology
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Stem Cell Niche
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T-Lymphocytes / pathology
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Translocation, Genetic*
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Tumor Microenvironment / drug effects
Substances
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Neoplasm Proteins
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Proto-Oncogene Proteins c-bcl-2