Jorge E. Cortes, MD

Myelodysplastic syndromes (MDS) are a group of hematologic malignancies of the pluripotent hematopoietic stem cells. These disorders are characterized by ineffective hematopoiesis, including abnormalities in proliferation, differentiation, and apoptosis. The overall clinical phenotype is peripheral cytopenias in the setting of a normocellular or hypercellular bone marrow and an increased risk for transformation to acute leukemia.

The introduction of imatinib mesylate (Gleevec) has dramatically changed the management and prognostic outlook of patients with chronic myeloid leukemia (CML).

Myelodysplastic syndromes (MDS) are a group of hematologic malignanciesof the pluripotent hematopoietic stem cells. These disorders arecharacterized by ineffective hematopoiesis, including abnormalities inproliferation, differ­entiation, and apoptosis.

Chronic lymphocytic leukemia (CLL) is a clonal malignancy that results from expansion of the mature lymphocyte compartment. This expansion is a ­consequence of prolonged cell survival, despite a varied cell turnover. The affected lymphocytes are of B-cell lineage in 95% of cases, and the remaining cases involve T lymphocytes, representing a distinct disorder. CLL is the most common leukemia in adults in Western countries, accounting for approximately 25%-30% of all leuke­mias. The proportion of cases diag­nosed with the early stages of the disease (Rai stage 0) has risen from 10% to 50%, probably because of earlier diagnosis (routine automated blood counts).  

Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disor­der resulting from the neoplastic transformation of the primitive hemato­poie­tic stem cell. The disease is monoclonal in origin, affecting myeloid, mono­cytic, erythroid, megakaryocytic, B-cell, and, sometimes, T-cell linea­ges. Bone marrow stromal cells are not involved.

The development of imatinib mesylate (Gleevec), a tyrosine kinase inhibitor targeted against the causative Bcr-Abl protein in chronic myeloid leukemia (CML), has resulted in hematologic and cytogenetic remissions in all phases of CML. Following imatinib treatment, more than 90% of patients obtain complete hematologic response, and 70% to 80% achieve a complete cytogenetic response. With 5 years of follow-up, the data are very encouraging, exhibiting a major change in the natural history of the disease. The understanding of at least some of the mechanisms of resistance to imatinib has led to a rapid development of new agents that may overcome this resistance. Combination strategies are currently being investigated in preliminary clinical studies and may prove to be useful. Overall, there are an increasing number of treatment options now available for patients with CML.

Biologic therapy for cancer may be defined as the use of compounds, or their derivatives, that can be found within the body to treat malignancy. The recent era of biologic therapy began with the identification and isolation of interferon (IFN)[1] and has been expanded with interleukin-2 (IL-2, aldesleukin [Proleukin]), the hematopoietic growth factors, and the retinoids.

Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder resulting from the neoplastic transformation of the primitive hemopoietic stem cell [1-4]. The disease is monoclonal in origin, affecting myeloid, monocytic, erythroid, megakaryocytic, B-cell, and, sometimes, T-cell lineages [4,5].

Chronic lymphocytic leukemia (CLL) is a clonal malignancy that results fromexpansion of the mature lymphocyte compartment. This expansion is aconsequence of prolonged cell survival, despite a low proliferative index. Theaffected lymphocytes are of B-cell lineage in 95% of cases, and the remainingcases involve T lymphocytes, likely representing a distinct disorder.

Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disorderresulting from the neoplastic transformation of the primitive hematopoietic stemcell. The disease is monoclonal in origin, affecting myeloid, monocytic, erythroid,megakaryocytic, B-cell, and, sometimes, T-cell lineages. Bone marrowstromal cells are not involved.

Acute lymphocytic leukemia (ALL) is a malignant disorder resulting from the clonal proliferation of lymphoid precursors with arrested maturation [1]. The disease can originate in lymphoid cells of different lineages, thus giving rise to B- or T-cell leukemias or sometimes mixed-lineage leukemia.