Loss of donor chimerism in remission after allogeneic stem cell transplantation of T-prolymphocytic leukemia patients following alemtuzumab induction therapy

Int J Hematol. 2014 Nov;100(5):425-8. doi: 10.1007/s12185-014-1678-8. Epub 2014 Sep 26.

Abstract

T-cell prolymphocytic leukemia is a rare aggressive malignancy with low susceptibility to conventional chemotherapy. The anti-CD52 antibody alemtuzumab induces remission, which requires consolidation by stem cell transplantation in eligible patients. In this case series, three chemotherapy-naïve T-PLL patients received alemtuzumab for remission induction and allogeneic SCT after reduced-intensity conditioning. While primary hematopoietic engraftment occurred in a timely fashion, donor chimerism declined in all patients between day 28 and day 290 post-transplantation. Loss of chimerism was not associated with disease recurrence, and full chimerisms were regained on donor leukocyte infusion. In six B-CLL patients, treated with identical regimens of alemtuzumab and SCT, a similar pattern of failing chimerism was not observed. We surmise that an accumulation of uncleared alemtuzumab in the plasma may impede the incoming graft after allogeneic SCT, which would indicate the need for close monitoring and management of engraftment to secure complete donor chimerism and putative cure in T-PLL patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alemtuzumab
  • Antibodies, Monoclonal, Humanized / administration & dosage
  • Antibodies, Monoclonal, Humanized / therapeutic use*
  • Antineoplastic Agents / administration & dosage
  • Antineoplastic Agents / therapeutic use*
  • Female
  • Graft vs Host Disease / etiology
  • Hematopoietic Stem Cell Transplantation* / adverse effects
  • Humans
  • Leukemia, Prolymphocytic, T-Cell / therapy*
  • Male
  • Middle Aged
  • Remission Induction
  • Tissue Donors
  • Transplantation Chimera*
  • Transplantation Conditioning
  • Transplantation, Homologous
  • Treatment Outcome

Substances

  • Antibodies, Monoclonal, Humanized
  • Antineoplastic Agents
  • Alemtuzumab