Hagop M. Kantarjian, MD

Jorge E. Cortes, MD and Hagop Kantarjian, MD share a summary on ponatinib in CML and ALL and exploration of potential future studies.

Experts review future implications such as using ponatinib in earlier lines of therapy and in patients with Ph-positive ALL.

Jorge E. Cortes, MD and Hagop Kantarjian, MD debate optimal dosing and discuss how they use ponatinib in patients with CML.

Hagop Kantarjian, MD responds to a review of dosing options in patients with CML treated with ponatinib.

Dr. Cortes reviews ponatinib dosing strategies based on patient profiles and mutational status.

Hematologic oncologists summarize the dose ranging study of ponatinib in patients with CML and discuss clinical implications of this work.

Jorge E. Cortes, MD, presents data from a dose ranging study of ponatinib in patients with chronic-phase chronic myeloid leukemia.

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.

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder resulting from the neoplastic transformation of the primitive hematopoietic stem cell.

In this review, we will discuss the management of ALL in the adult population, in the context of the recently published guidelines from the NCCN. We will focus in particular on the strides being made in salvage and targeted approaches.

CancerNetwork speaks with Hagop Kantarjian, MD, M.D. Anderson Cancer Center, who shares his impressions of some of the highlights of this year’s ASCO meeting with regard to hematologic malignancies.

Chronic myeloid 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.

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.

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 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.

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 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.

Chronic myelogenous leukemia (CML) is a myeloproliferative disorder that follows a characteristic clinical course in which a chronic phase of variable duration precedes an accelerated, and ultimately blastic, phase,

Drs. Enright and McGlave succinctly review the biology of chronic myelogenous leukemia (CML) and highlight the therapeutic role of allogeneic stem-cell transplantation. Two points, however, warrant further discussion. The first is that a regimen containing interferon-alfa (Intron A, Roferon-A) is optimal front-line therapy for the great majority of CML patients.[1] The second is that use of an interferon-alfa-based regimen prior to allogeneic stem-cell transplantation does not adversely affect post-transplant mortality, morbidity, or anti-CML efficacy.

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.