Abstract
B cell tumors in man include a group of heterogenous diseases with varying natural histories and responsiveness to therapy. Classic examples of B cell tumors are the chronic lymphocytic leukemia (CLL), Burkitt’s lymphoma and multiple myeloma. These tumors express the conventional B cell marker, that is, surface and/or cytoplasmic immunoglobulins. Malignant transformation, however, can affect precursors of the “mature” B lymphocytes as exemplified by the non-T cell acute lymphoblastic leukemia (ALL). Such cases demonstrate immunoglobulin gene rearrangements and react with monoclonal antibodies to B cell differentiation antigens. B cell tumors, therefore, represent a spectrum of disorders extending from the immature “stem cell” to the most mature “plasma cell” of the B lineage. It has been long hypothesized that disturbance in the differentiation pathway is important in the pathophysiology of malignancy (1). Phenotypic analysis of the B cell lineage has identified a malignant counterpart phenotype for each stage of the normal B cell differentiation pathway (3).
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Al-Katib, A.M., Mohammad, R. (1996). Differentiation of Human B-Cell Tumors: A Preclinical Model for Differentiation Therapy. In: Valeriote, F.A., Nakeff, A., Valdivieso, M. (eds) Basic and Clinical Applications of Flow Cytometry. Developments in Oncology, vol 77. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1253-6_12
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DOI: https://doi.org/10.1007/978-1-4613-1253-6_12
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