Molecular Abnormalities in Benign Lymphoid Proliferations

The presence of a clonal B-cell population, by itself, does not establish a diagnosis of B-cell malignancy. Small B-cell clones may be detected by IGH PCR and SBA in benign lymphoid hyperplasias in the absence of other criteria for malignancy.40-42 This occurs in the setting of immune deficiencies, autoimmune diseases, and immunosuppres-sion, and reinforces the critical necessity for interpretation of these tests for B-cell clonality in conjunction with clinical, morphologic, and immunophenotypic information. Patients with immune dysfunction have an increased risk of non-Hodgkin lymphoma (NHL), in particular BCL, but many of these patients will never develop lymphomas,even without correction of the abnormal immune status.

Other types of BCL-associated genetic alterations have been described in benign settings and could result in a false-positive result. Rare B cells carry a t(14;18)(q32;q21) IGH/BCL2 translocation in normal individuals.43-46 PCR assays capable of detecting one IGH/BCL2 translocation-carrying cell in 105 to 106 normal cells will be positive in up to half of the tissue biopsies, bone marrow aspirates, and peripheral blood specimens from normal individuals. To date, there is no evidence that these individuals are at higher risk for development of FL. Diagnostic tests for FL must be designed with a sensitivity that avoids detection of the IGH/BCL2 translocation in normal individuals.

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