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D.All of the above
Follicular lymphoma typically follows an indolent clinical course and yet remains largely incurable. Recent advances in the understanding of the biology and complex pathogenesis of follicular lymphoma have shown that this disease begins in the bone marrow.
Although incurable, follicular lymphoma's indolent clinical path and sometimes-dramatic responses to chemoimmunotherapy translate to significantly improved survival time, now reaching a median of approximately 20 years. Patients typically experience multiple relapse events, each associated with more pronounced resistance to chemotherapy. Despite its indolent behavior, follicular lymphoma becomes more aggressive over time.
Approximately 90% of follicular lymphoma cases harbor the t(14;18)(q32;q21) chromosomal translocation. The pathobiology of t(14;18)-negative follicular lymphoma has been less-thoroughly studied and is not as well understood. BCL2 amplification mutations appear to occur only in t(14;18)-positive follicular lymphoma's. t(8;14) translocations are found in Burkitt lymphoma/leukemia. t(2;5) occurs in anaplastic large-cell lymphoma and acute and chronic myeloid leukemias.
D.All of the above
Follicular lymphoma is a prototype of epigenetic alterations’ roles in malignancy, frequently harboring mutations in chromatin-modifying genes that disrupt normal expression of histone methyltransferases, histone acetyltransferases, and linker histone proteins. It is suspected that multiple such mutations triggering widespread transcriptional changes work together to drive follicular lymphoma lymphomagenesis.
Reported mutation frequencies include KMT2D and CREBBP mutations in more than 60% of follicular lymphoma samples, compared to ≤ 10% gene mutation rates for TP53, TCF3 and dozens of other loci. BCL2 mutations occur in approximately half of follicular lymphoma cases.