Concomitant Diagnosis of Chronic Myeloid Leukemia and B-Cell Chronic Lymphocytic Leukemia in a 57-Year-Old Female Patient, with Good Therapeutic Response Exclusively to Imatinib in Both Myeloid and Lymphoid Clones.

We describe the clinical, cytogenetic, hystopathologic, immunophenotypic and molecular findings of a rare case of Philadelphia positive chronic myeloid leukemia (Ph+ CML) and B-cell chronic lymphocytic leukemia (B-CLL) occurring simultaneously at diagnosis, in a 57-year-old female patient. In the present case, the patient showed at diagnosis leukocytosis (48.000/ul) with myelocytes and metamyelocytes along with well-differentiated neutrophils, but also with well differentiated lymphocytosis (28.992/ul) in peripheral blood (PB) and also in bone marrow (BM) aspirate cytology. FACS cytometry exhibited clearly two predominant separated cellular populations and the immunophenotype profile of the lymphoid component in BM and PB was CD5+, CD20+, CD23+, with light chain clonal restriction. The BM hystopathological analysis showed two distinct cellular populations, one lymphoid well differentiated CD5+/CD20+, and other myeloid, in several stages of differentiation. Cytogenetic analysis with unstimulated bone marrow culture confirmed the presence of Philadelphia chromosome but with additional translocation involving chromosomes 9, 10 and 22. Molecular studies showed the evidence of BCR-ABL positivity and the B-cell clone was documented by the presence of a clonal heavy chain immunoglobulin rearrangement. The patient was treated with imatinib mesylate 400mg/day, achieving complete cytogenetic response at the fourth month, and complete molecular response (nested PCR) of the BCR-ABL component at the sixth month of treatment. Besides, the absolute lymphocytosis was gradually reduced during the treatment exclusively with imatinib, achieving normal absolute values at the sixth month. This seldom described case of simultaneous occurrence of these two rare chronic hematological malignancies, brings interesting questions about the possible cellular origin and the correspondent mechanisms of clonal expansion. The therapeutic response of the B-cell lymphoid clone exhibited, brings also a possible relationship with the observation that the c-Abl could have enhanced expression in B-CLL cells, as described by Ke Lin et al, in which the c-Abl kinase activity could be inhibited by imatinib mesylate.