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    The routes for transformation of follicular lymphoma 
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    The routes for transformation of follicular lymphoma

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    Published version
    Embargoed until: 2100-01-01
    Reason: author cannot archive publisher's version
    Volume
    23
    Pagination
    385 - 391
    Publisher
    Lippincott, Williams & Wilkins
    DOI
    10.1097/MOH.0000000000000255
    Journal
    CURRENT OPINION IN HEMATOLOGY
    Issue
    4
    ISSN
    1065-6251
    Metadata
    Show full item record
    Abstract
    Aggressive transformation, a frequent event in the natural history of follicular lymphoma, is associated with increased lymphoma-related mortality and yet the underlying biology remains poorly defined. This review outlines recent advances in our understanding of the genetic basis and evolutionary process leading to transformation. Recent findings Both the antecedent indolent and transformed follicular lymphoma (tFL) arise through branched divergent evolution with tumors emerging from a founder precursor population, the common progenitor cell. Although the majority of tFLs maintain a germinal center B-cell gene expression signature, an activated B-cell-type (ABC-type) profile appears to predominate in BCL2-translocation negative cases. It does not appear that a single unifying genetic or epigenetic event promotes a fitter and more aggressive clone. Summary Transformed follicular tumors are genetically heterogeneous perhaps reflecting the varying clinical behavior and outcomes of this disease event. Follicular lymphoma and tFL remain incurable tumors highlighted by our inability to eradicate the founder common progenitor cell population with current therapies. Progress has now been made in defining the genetic events and evolutionary pathways responsible for transformation. Although more research is required in predicting and understanding the biology of transformation, there are opportunities to improve outcomes by preferentially directing targeted therapies toward ‘actionable’ early and transformation-specific aberrations
    Authors
    Okosun, J; Montoto, S; Fitzgibbon, J
    URI
    https://qmro.qmul.ac.uk/xmlui/handle/123456789/61361
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    • Centre for Haemato-Oncology [91]
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    All rights reserved
    Copyright statements
    2016 Wolters Kluwer Health, Inc.
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