nodes decreased in size and became impalpable. After discharge in February 1989, he was treated with maintenance chemotherapy every 3 months for 2 1 ⁄2 years. In October 1992, he had lt-inguinal lymph-node swelling and lymphocytosis. His leukocyte count was 10,000/l (neutrophils 23%, lymphocytes 72%), hemoglobin level of 10.2 g/dl, and platelet count of 9.2 × 10 4 /l. The peripheral blood and bone marrow were infiltrated by small to mediumsized lymphoid cells. Immunophenotypic analysis of the lymphoid cells showed a preponderance of CD5(+), CD19(+), CD20(+), and surface Ig(-) cells. In contrast, lt-cervical lymph-node biopsy showed NHL (diffuse, mixed-cell type). He was admitted to hospital and treated with remissioninduction chemotherapy (cytosine arabinoside, aclarubicin, and methyl prednisolone). Lt-inguinal lymph-node swelling disappeared, but lymphocytosis continued. In May 1994, his leukocyte count increased to 17,100/l (neutrophils 20%, lymphocytes 73%), and low-dose etoposide (25 mg/day) as started. This was continued intermittently until October 1995, when swelling of the lt-inguinal lymph node and interstitial pneumonia developed. Lt-inguinal lymph-node biopsy revealed the proliferation of small lymphoid cells, which were compatible with the pathological features of CLL. The patient died of respiratory failure on November 29, 1995.
Sequential immunogenotypic analysis was performed on lymphoid cells obtained from the lymph node (October 1992), peripheral blood (August 1994), and bone marrow (December 1994). DNA from these materials showed identical rearrangements with a J H gene probe (Fig. ). Analysis with kappa, lambda, and TCR- gene probes showed germline configuration.
In conclusion, the pathological and immunophenotypic analysis suggested that the patient had discordant lymphoma which consisted of CD5(-) NHL and CD5(+) CLL. The identical immunoglobulin gene rearrangement provided evidence for the evolution of two morphologically distinct neoplasms from the same clone.