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Abstract
B cell chronic lymphocytic leukemia (CLL) can evolve to several types of lymphoid proliferations, including large B cell lymphoma (Richter's syndrome), prolymphocytic transformation, and exceptionaly myeloma and acute lymphoblastic leukemia (ALL) (1). Analysis of genetic relation between the initial CLL and the subsequent lymphoid proliferation has shown that all prolymphocytic transformations and about one half of the cases of Richter's syndrome appear to evolve from the original CLL clone, whereas the remaining Richter's syndromes had genetically unrelated cancers (2) ALL accounts for only one third of acute leukemias developing during the course of CLL, the remaining cases being acute myeloid leukemia, probably related to the prolonged use of alkylating agents in most cases (3) In the 7 most recently reported cases of ALL developing during the course of CLL (4-9), in whom phenotypic documentation was done, ALL seemed to derive from clonal evolution of the initial CLL. In the six cases studied, similar immunoglobulin chain isotypes were found in the CLL and ALL cells, while identical cytogenetic abnormalities were present in CLL and ALL in the remaining patient (Table 1). In only one case, the blasts had L3 morphology (9), and all cases with available data had short survival.