![]() ![]() However, the process is iterative, and once the underlying molecular cause is known, we gain access to new diagnostic tools that help better define the borderlines of the disease ( Figure 1). This paradigm is exemplified by both mantle cell lymphoma (MCL) 3, 4 and anaplastic large cell lymphoma (ALCL), 5 in which careful pathologic descriptions preceded the recognition of CCND1 and ALK, respectively, as genes critical to their pathogenesis. However, progress in identifying the molecular pathogenesis of lymphoid malignancies has in most instances followed an accurate description of the disease by pathologists, based on morphologic, immunophenotypic and clinical parameters ( Table 1). Thus, the normal counterpart of the neoplastic cell cannot at this time be the sole basis for classification.Ĭancers are increasingly recognized as genetic diseases, with precise molecular alterations often defining entities. ![]() However, some neoplasms-for example, hairy cell leukemia-do not clearly correspond to a normal B-cell differentiation stage, and some clinically distinctive neoplasms may exhibit immunophenotypic heterogeneity, such as hepatosplenic T-cell lymphoma, which is derived from either α/β or γ/δ T cells. A recent review by Kyle and Rajkumar in this series comprehensively discussed plasma cell myeloma, 2 and thus we will not include it further in this review.Īs immunologists and pathologists have come to understand the ontogeny of lymphoid cells, it has been tempting to base the classification of lymphoid malignancies strictly on the corresponding normal stage. In addition, plasma cell neoplasms often have been treated separately from other lymphoid neoplasms, but this segregation is equally artificial, and the World Health Organization (WHO) classification of lymphoid neoplasms 1 includes plasma disorders. ![]() However, as the precursor neoplasms-lymphoblastic lymphomas/leukemias and acute myeloid leukemias-are closely related from a clinical and biological perspective, they will not be covered in this review. Although classifications of lymphoid malignancies have historically treated lymphomas and leukemias separately, this distinction is now appreciated as artificial. Mature B-cell and T/natural killer (NK)–cell neoplasms are clonal tumors of B cells, T cells, or NK cells that in many respects recapitulate stages of normal B-cell or T-cell differentiation. In addition, accurate and precise classification of disease entities facilitates the discovery of the molecular basis of lymphoid neoplasms in the basic science laboratory. The multiparameter approach to classification adopted by the World Health Organization (WHO) classification has been validated in international studies as being highly reproducible, and enhancing the interpretation of clinical and translational studies. The clinical manifestations of lymphomas likewise reflect the normal function of lymphoid cells in vivo. Likewise, the molecular mechanisms involved the pathogenesis of lymphomas and lymphoid leukemias are often based on the physiology of the lymphoid cells, capitalizing on deregulated normal physiology by harnessing the promoters of genes essential for lymphocyte function. B-cell, T-cell, and natural killer (NK)–cell neoplasms in many respects recapitulate normal stages of lymphoid cell differentiation and function, so that they can be to some extent classified according to the corresponding normal stage. In the past 50 years, we have witnessed explosive growth in the understanding of normal and neoplastic lymphoid cells. ![]()
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