The evolving role of etoposide in the management of lymphomas and hodgkin's disease

✍ Scribed by Susan E. O';Reilly; P. Klimo; Joseph M. Connors

• Publisher: John Wiley and Sons
• Year: 1991
• Tongue: English
• Weight: 902 KB
• Volume: 67
• Category: Article
• ISSN: 0008-543X
• DOI: 10.1002/1097-0142(19910101)67:1+<271::aid-cncr2820671311>3.0.co;2-l

✦ Synopsis

Etoposide, a derivative of epipodophyllotoxin, is one of the most important new drugs that was introduced into the management of the malignant lymphomas during the past decade. A growing number of specific protocols include this useful agent in the management of malignant lymphoma, both at the time of primary treatment and at relapse. The broad activity of etoposide across several histologic subtypes of malignant lymphoma and Hodgkin's disease indicates a potential that is only now being fully exploited. Used according to optimal doses and schedules, etoposide has single-agent activity that rivals earlier drugs such as the alkylating agents and doxorubicin. Functioning as a protein synthesis and topoisomerase I1 inhibitor, it offers the potential for non-cross-resistant cytotoxicity. After a brief comment on the single-agent activity of etoposide, this report will focus on the integration of etoposide into multiagent protocols used in the primary treatment of malignant lymphoma and Hodgkin's disease. The specific findings from protocols such as prednisone, methotrexate, doxorubicin, cyclophosphamide, etoposide-cytarabine, bleomycin, vincristine, and methotrexate (Pro-MACE-CytaBOM) (US National Cancer Institute [NCI]) and etoposide, doxorubicin, cyclophosphamide, vincristine, prednisone, and bleomycin [VACOP-B) [Vancouver) for the primary treatment of malignant lymphoma, and vinblastine, etoposide, cyclophosphamide, doxorubicin, bleomycin, vincristine, and prednisone (VECABOP) [Vancouver) for the treatment of previously untreated patients with advanced Hodgkin's disease will be discussed. cancer 67271-280, 1991. TOWSIDE (VP-16), a phase-sensitive cytocidal drug E that preferentially affects cells in S or G2, first un-