[Chronic myeloid leukemia in the 21st century: biology and treatment]

Rev Invest Clin. 2009 May-Jun;61(3):221-32.
[Article in Spanish]

Abstract

Chronic Myeloid Leukaemia (CML) is a clonal disease, originated at the level of Hematopoietic Stem Cells (HSC) and characterized by the presence of the Philadelphia (Ph) chromosome and its oncogenic product p210(BcrAbl). Such a protein has been shown to be essential for malignant transformation, since it is capable of altering cell adhesion, proliferation and apoptosis. Historically, CML has been treated by using different approaches: arsenic (in the early days), a variety of chemical agents (busulfan, hydroxyurea, cytarabine), cytokines (IFN-alpha, IFNalpha-PEG), hematopoietic cell transplant (HCT), and more recently drugs generated by design (imatinib, nilotinib, dasatinib). All these molecules exert specific effects on HSC and lead to a variety of clinical and biological responses. In this article, we present an overview about hematopoiesis in CML and its implications in the treatment of this disease.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adult
  • Aged
  • Antineoplastic Agents / therapeutic use
  • Combined Modality Therapy
  • Drug Design
  • Fusion Proteins, bcr-abl / antagonists & inhibitors
  • Fusion Proteins, bcr-abl / genetics
  • Hematopoiesis / drug effects
  • Hematopoiesis / physiology
  • Hematopoietic Stem Cell Transplantation
  • Hematopoietic Stem Cells / drug effects
  • Hematopoietic Stem Cells / pathology
  • Humans
  • Immunologic Factors / therapeutic use
  • Incidence
  • Interferon-alpha / therapeutic use
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive* / drug therapy
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive* / epidemiology
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive* / genetics
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive* / physiopathology
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive* / surgery
  • Mexico / epidemiology
  • Middle Aged
  • Neoplastic Stem Cells / drug effects
  • Neoplastic Stem Cells / pathology
  • Protein Kinase Inhibitors / therapeutic use
  • United States / epidemiology

Substances

  • Antineoplastic Agents
  • Immunologic Factors
  • Interferon-alpha
  • Protein Kinase Inhibitors
  • Fusion Proteins, bcr-abl