Chronic myelogenous leukemia: molecule to man

Henry Ford Hosp Med J. 1991;39(2):108-11.

Abstract

Chronic myelogenous leukemia (CML) is the best understood human cancer. The molecular basis of CML involves activation of a cellular proto-oncogene--ABL. The consequence is to increase tyrosine kinase activity. This results in a marked clonal increase in the myeloid mass. Later on, cellular maturation is blocked and the decrease eventuates in acute leukemia. Abnormalities of other proto-oncogenes or antioncogenes, like P53, may be involved in leukemia progression. Treatment of CML involves chemotherapy and, more recently, interferon. Whether this treatment prolongs survival or increases the likelihood of cure is unknown but either result seems unlikely. Bone marrow transplants which cure about 50% of persons with CML are most effective when performed in chronic phase.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use
  • Bone Marrow Transplantation
  • Combined Modality Therapy
  • Genes, abl / genetics
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / physiopathology
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • Molecular Biology*
  • Proto-Oncogene Mas
  • Translocation, Genetic

Substances

  • Antineoplastic Agents
  • MAS1 protein, human
  • Proto-Oncogene Mas