Treatment of T-cell prolymphocytic leukemia with human CD52 antibody.

Abstract

CAMPATH-1H is an effective agent in T-PLL and represents a significant improvement over other types of therapy. However, CAMPATH-1H alone is not sufficient for long-term remissions, and the role of autologous stem-cell transplantation needs further investigation.

Low-dose alemtuzumab (Campath®) in myeloablative allogeneic stem cell transplantation for CD52-positive malignancies: decreased incidence of acute graft-versus-host-disease with unique pharmacokinetics

“…6,7 In B-cell and T-cell prolymphocytic leukemias, response rates as high as 76% have been reported. [8][9][10] Other malignancies that express CD52 are potential targets for alemtuzumab therapy, including acute lymphocytic leukemia (ALL), hairy cell leukemia, and Waldenstro¨m's macroglobulinemia. 11 Within the setting of allogeneic stem cell transplantation (ASCT) for hematologic malignancies, alemtuzumab has been used extensively, both in vivo and ex vivo, to deplete T cells in the graft and in the recipient, a simple procedure that is effective in controlling graft-versus-host disease (GVHD), one of the major causes of post transplant morbidity and mortality.…”

T-cell prolymphocytic leukemia: a report of two cases with review of literature

“…Approximately one-third patients respond to CHOP but most responses are partial [8]. More recently, Campath-1H has been shown to be effective in T-PLL [9]. Both of our patients were lost to follow up, so the clinical course could not be defi ned in them.…”

Cardiac complications after haploidentical HLA-mismatched hematopoietic stem cell transplantation using in vivo alemtuzumab

“…[10][11][12][13] However, a high incidence of cardiac complications was reported in four of Cardiac complications after HLA-mismatched HSCT using alemtuzumab K Oshima et al eight patients who received alemtuzumab for mycosis fungoides or Se´zary syndrome. 14 The expression of CD52 was not observed on cardiac myocytes and, thus, cytokine-release syndrome after alemtuzumab infusion was considered to be responsible for the cardiac complications, 14 because inflammatory cytokines such as tumor necrosis factor (TNF), interleukin-1 (IL-1) and interleukin-6 (IL-6) have been reported to be responsible for the development and progression of heart failure.…”