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Alemtuzumab in T-cell malignancies


Alemtuzumab is a humanized monoclonal antibody directed against the CD52 antigen, which is abundantly expressed on all normal and most malignant T-lymphocytes. We summarize the results of our experience using alemtuzumab to treat a range of clinically aggressive, mature, post-thymic, T-cell malignancies, including T-cell prolymphocytic leukemia (T-PLL), cutaneous T-cell lymphoma (CTCL), T-cell large granular lymphocyte (T-LGL) leukemia, and human T-cell lymphotropic virus I (HTLV-I) associated adult T-cell leukemia-lymphoma (ATLL). Alemtuzumab was administered at a dose of 30 mg, three times a week until maximum response. Apart from first-dose reactions, which were common, treatment was well tolerated, the main complication being infection and viral reactivation associated with the prolonged lymphopenia. Overall response rates were 76% (60% complete response) in 39 patients with T-PLL and 100% in 3 patients with CTCL, of duration up to 4 yr. Experience in T-LGL and ATLL is limited to single cases only and further studies are required to better define the role of alemtuzumab in these subgroups. Our results indicate that alemtuzumab has activity in T-cell malignancies, particularly in T-PLL and in patients with predominantly blood and bone marrow disease. It may be possible to prolong response duration by the use of high-dose therapy and stem cell transplantation. Alemtuzumab may also have a role in purging minimal residual disease following other chemotherapy and prior to transplantation. We conclude that treatment with alemtuzumab may offer new hope to patients who otherwise have a bleak prognosis.

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  1. Matutes, E., et al. (1991). Clinical and laboratory features of 78 cases of T-prolymphocytic leukemia. Blood 78:3269–3274.

    PubMed  CAS  Google Scholar 

  2. Yuille, M.A., et al. (1998). ATM is usually rearranged in T-cell prolymphocytic leukaemia. Oncogene 16:789–796.

    Article  PubMed  CAS  Google Scholar 

  3. Stoppa-Lyonnet, D., et al. (1998). Inactivation of the ATM gene in T-cell prolymphocytic leukemias. Blood 91:3920–3926.

    PubMed  CAS  Google Scholar 

  4. Garand, R., et al. (1998). Indolent course as a relatively frequent presentation in T-prolymphocytic leukaemia. Groupe Francais d’Hematologie Cellulaire. Br. J. Haematol. 103:488–494.

    Article  PubMed  CAS  Google Scholar 

  5. Matutes, E., Brito-Babapulle, V., Yuille, M., Catovsky, D., and Dearden, C. Prolymphocytic leukaemia of B- and T-cell types, in Chronic Lymphoid Leukaemias (Cheson, B., ed.), Marcel Dekker, New York.

  6. Dyer, M.J.S., Hale, G., Hayhoe, F.G.J. and Waldmann, H. (1989). Effects of CAMPATH-1H antibodies in vivo in patients with lymphoid malignancies: influence of antibody isotype. Blood 73:1431–1439.

    PubMed  CAS  Google Scholar 

  7. Pawson, R., et al. (1997). Treatment of T-cell prolymphocytic leukaemia with human CD52 antibody. J. Clin. Oncol. 15:2667–2672.

    PubMed  CAS  Google Scholar 

  8. Dearden, C.E., et al. (2001). High remission rate in T-cell prolymphocytic leukemia with Campath-1H. Blood 98:1721–1726.

    Article  PubMed  CAS  Google Scholar 

  9. Mercieca, J., Matutes, E., Dearden, C., MacLennan, K. and Catovsky, D. (1994). The role of pentostatin in the treatment of T-cell malignancies: analysis of response rate in 145 patients according to disease subtype. J. Clin. Oncol. 12:2588–2593.

    PubMed  CAS  Google Scholar 

  10. Lundin, J., et al. (1998). CAMPATH-1H monoclonal antibody in therapy for previously treated low-grade non-Hodgkin’s lymphomas: a phase II multicenter study. European Study Group of CAMPATH-1H Treatment in Low-Grade Non-Hodgkin’s Lymphoma. J. Clin. Oncol. 16:3257–3263.

    PubMed  CAS  Google Scholar 

  11. Dyer, M.J.S., Hale, G., Marcus, R.E. and Waldmann, H. (1990). Remission induction in patients with lymphoid malignancies using unconjugated CAMPATH-1 monoclonal antibodies. Leuk. Lymphoma 2:179–190.

    Google Scholar 

  12. Lim, S.H., Davey, G. and Marcus, R. (1993). Differential response in a patient treated with Campath-1H monoclonal antibody for refractory non-Hodgkin lymphoma. Lancet 341:432–433.

    Article  PubMed  CAS  Google Scholar 

  13. Osterborg, A., et al. (1997). Phase II multicenter study of human CD52 antibody in previously treated chronic lymphocytic leukemia. European Study Group of CAMPATH-1H Treatment in Chronic Lymphocytic Leukemia. J. Clin. Oncol. 15:1567–1574.

    PubMed  CAS  Google Scholar 

  14. Armitage, J.O. (1998). Emerging applications of recombinant human granulocyte-macrophage colony-stimulating factor. Blood 92:4491–4508.

    PubMed  CAS  Google Scholar 

  15. Ginaldi, L., et al. (1998). Levels of expression of CD52 in normal and leukemic B and T cells: correlation with in vitro therapeutic responses to Campath-1H. Leuk. Res. 22:1185–1191.

    Article  Google Scholar 

  16. Dyer, M.J.S., et al. (1997). In vivo ‘purging’ of residual disease in CLL with Campath-1H. Br. J. Haematol. 97:669–672.

    Article  PubMed  CAS  Google Scholar 

  17. Bowen, A.L., et al. (1997). Subcutaneous CAMPATH-1H in fludarabine-resistant/relapsed chronic lymphocytic and B-prolymphocytic leukaemia. Br. J. Haematol. 96:617–619.

    Article  PubMed  CAS  Google Scholar 

  18. Gilleece, M.H. and Dexter, T.M. (1993). Effects of CAMPATH-1H antibody on human haemopoietic progenitors in vitro. Blood 82:807–812.

    PubMed  CAS  Google Scholar 

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Correspondence to Claire E. Dearden.

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Dearden, C.E., Matutes, E. & Catovsky, D. Alemtuzumab in T-cell malignancies. Med Oncol 19 (Suppl 2), S27–S32 (2002).

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Key Words

  • Campath-1H
  • leukemia
  • prolymphocytic
  • T-cell
  • lymphoma
  • alemtuzumab