SECONDARY MALIGNANCIES AFTER BONE-MARROW TRANSPLANTATION IN ADULTS

Purpose: The records of 557 consecutive adult recipients of allogeneic -related and -unrelated and syngeneic bone marrow transplants (BMTs) w ere reviewed to determine the incidence of secondary cancers. Patients and Methods: Four hundred fifty-six patients were transplanted for ac ute lymphocytic leukemia (ALL; n = 79), acute myelogenous leukemia (AM L; n = 182), and chronic myelogenous leukemia (CML; n = 195); 42 patie nts were transplanted for aplastic anemia (AA) and 59 for a variety of other hematologic and nonhematologic disorders, malignant and nonmali gnant. Conditioning regimens included high-dose chemotherapy with or w ithout total-body irradiation (TBI). Statistical analyses determined t he cumulative incidence of developing a secondary cancer and elucidate d the associated risk factors. Complete records (1 to 24 years of foll ow-up) on all patients were available. Results: Nine patients develope d 10 secondary cancers for a cumulative actuarial risk of 12% (95% con fidence interval [CI], 4.3 to 23.0) 11 years ether transplant. The age -adjusted incidence of secondary cancer was 4.2 times higher than that of primary cancer in the general population. Eight of the 10 were epi thelial in origin and three were cutaneous. TBI and acute graft-versus -host disease (GVHD) with a severity greater than or equal to grade II were associated with the development of any secondary cancer. On the other hand, chronic GVHD wets a risk factor only for the development o f secondary skin neoplasms. Conclusion: Adult recipients of BMT face a significant risk of developing a secondary malignancy. Their risk is similar to that of other patients with hematologic malignancies who ar e treated with chemoradiotherapy only. Epithelial rumors, rather than the more commonly reported Epstein-Barr virus (EBV)-associated lymphom as, were most common. The fact that we did not routinely use T-cell-de pleted marrow grafts nor anti-T-cell immunoglobulin for the treatment of acute GVHD may explain this variance. (C) 1994 by American Society of Clinical Oncology.