title: New insights into biology of chronic myeloid leukemia: implications in therapy.
abstract: Over the past decades the prognosis of patients with Chronic Myeloid Leukemia (CML) has radically changed due to groundbreaking scientific and translational studies that have revealed the biologic basis of such a hematologic malignancy. These studies have led to the rapid development of many BCR-ABL specific tyrosine kinase inhibitors (TKIs), such as Imatinib, Nilotinib and Dasatinib, which have improved 10-years survival to more than 80%. Although these therapies represent a landmark step in the race for the cure of CML, they did not change the progression in advanced phase of disease. Therefore unravel the molecular mechanisms and the biological basis of CML, especially during the advanced stage, is of seminal importance as this would result in the design of more effective and less toxic therapies. In such a scenario, several novel drugs designed to specifically target biological features of CML cells are currently in clinical trials with promising results that would provide not only improve the therapeutic armamentarium but also to overcome drug resistance of this tumor. Here we review recent advances in biology of CML and their therapeutic implications.
authors.affiliation: Department of Medical Oncology, Dana-Farber Cancer Institute, M551, 450 Brookline Avenue, Boston, MA 02115, USA. michele_cea@dfci.harvard.edu.
authors.forename: Michele
authors.initials: M
authors.lastname: Cea
authors.forename: Antonia
authors.initials: A
authors.lastname: Cagnetta
authors.forename: Alessio
authors.initials: A
authors.lastname: Nencioni
authors.forename: Marco
authors.initials: M
authors.lastname: Gobbi
authors.forename: Franco
authors.initials: F
authors.lastname: Patrone
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000009:adverse effects / Q000737:chemistry / Q000627:therapeutic use*; D018450:Disease Progression; D015195:Drug Design; D019008:Drug Resistance, Neoplasm; D016044:Fusion Proteins, bcr-abl / Q000037:antagonists & inhibitors / Q000235:genetics; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D058990:Molecular Targeted Therapy; D014411:Neoplastic Stem Cells / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D047428:Protein Kinase Inhibitors / Q000009:adverse effects / Q000737:chemistry / Q000627:therapeutic use*; D015398:Signal Transduction / Q000187:drug effects; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; D047428:Protein Kinase Inhibitors; D016044:Fusion Proteins, bcr-abl