Does autologous transplantation directly increase the risk of secondary leukemia in lymphoma patients?

Bone Marrow Transplant. 2007 Jan;39(2):59-70. doi: 10.1038/sj.bmt.1705547. Epub 2006 Dec 4.

Abstract

Patients who undergo autologous stem cell transplantation (ASCT) for lymphoma have a significant risk of therapy-related acute myeloid leukemia and myelodysplasia (t-AML/MDS). Compared to that seen in other indications such as breast cancer, multiple myeloma or germ cell tumors, there is a substantially increased risk for t-AML/MDS following ASCT for lymphoma. This risk has largely been attributed to the extent of pre-transplant chemotherapy and radiation therapy. In many of the larger series to date, it has not been possible to directly implicate autologous transplantation itself as a risk factor for t-AML/MDS. Although pre-transplant therapy is certainly an important factor in the development of t-AML/MDS, specific components of the autologous transplantation procedure itself may also contribute to the risk of t-AML/MDS. Specifically, priming chemotherapy, total body irradiation, and the extensive cellular proliferation which occurs during engraftment may all play a role in the development of t-AML/MDS. Furthermore, there is an increasing body of evidence that certain inherited polymorphisms in genes governing drug metabolism, DNA repair and leukemogenesis may influence susceptibility to t-AML/MDS. In this paper, we review the evidence implicating the above risk factors for t-AML/MDS, present a potential mechanism for t-AML/MDS and propose interventions to reduce the rate of t-AML/MDS in lymphoma patients.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Bone Marrow Transplantation / adverse effects*
  • Humans
  • Incidence
  • Leukemia, Myeloid / epidemiology
  • Leukemia, Myeloid / etiology*
  • Lymphoma / surgery*
  • Myelodysplastic Syndromes / epidemiology
  • Myelodysplastic Syndromes / etiology
  • Transplantation, Autologous / adverse effects*