Abstract:
:Chronic myelogenous leukemia (CML) results from clonal proliferation of malignant hematologic progenitor cells and is responsible for 7% to 15% of all adult leukemias. The hallmark of CML is a genetic translocation between chromosomes 9 and 22 (the Philadelphia chromosome), which creates the abnormal bcr-abl gene and a continuously activated Bcr-Abl protein. Bcr-Abl tyrosine kinase activity leads to signal transduction and cell growth. Traditional therapies for CML include allogeneic stem cell transplantation, interferon alfa, and oral chemotherapeutic agents. However, because Bcr-Abl is the causative abnormality in CML, it represents an ideal target for rational biologic therapy. Imatinib mesylate is an orally available tyrosine kinase inhibitor that specifically blocks Bcr-Abl function. Clinical trials have demonstrated that imatinib mesylate produces rapid responses in patients with all stages of CML, including those who were resistant to interferon alfa therapy or intolerant of it. When imatinib mesylate therapy was initiated early in the course of CML, there was a complete hematologic response in 98% of the patients and a complete cytogenetic response in 72% of the patients. Although long-term safety and survival data are not yet available, imatinib mesylate is a promising new treatment option for CML that targets the molecular cause of the disease.
journal_name
Cancer Nursjournal_title
Cancer nursingauthors
Duffy KMdoi
10.1097/00002820-200312001-00007subject
Has Abstractpub_date
2003-12-01 00:00:00pages
26S-31Sissue
6 Suppleissn
0162-220Xissn
1538-9804journal_volume
26pub_type
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