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  • Title: Hematological and molecular response evaluation of CML patients on imatinib.
    Author: Gupta A, Prasad K.
    Journal: J Assoc Physicians India; 2007 Feb; 55():109-13. PubMed ID: 17571739.
    Abstract:
    BACKGROUND: The BCR-ABL tyrosine kinase is a well-validated therapeutic target in Chronic Myeloid Leukemia (CML). Imatinib mesylate (formerly STI-571), a tyrosine kinase inhibitor is highly effective at the hematological, cytogenetic and molecular level in CML. AIMS: To evaluate hematological and molecular response in CML patients on Imatinib and also the side effects of the therapy if any. METHODS AND MATERIALS: Sixteen patients were diagnosed as having chronic phase CML at Kasturba Medical College Hospital, Attavar, Mangalore during the period of two years from January 2004 to January 2006 and were given Imatinib at 400 mg/day orally. They were followed closely over a period of 1 year using the following parameters: (1) monthly clinical examination, (2) monthly peripheral blood smear examination, (3) real time reverse transcriptase quantitative polymerase chain reaction (RT Q-PCR) for BCR-ABL at the end of every 6 months. The findings were evaluated after one year for hematological and molecular response achieved. RESULTS: Fifteen (93.75%) patients achieved complete hematological response within three months of therapy. Six (37.5%) patients achieved complete molecular response(CMR) within six months of therapy as measured by real time RT Q-PCR. None of the patients who did not achieve CMR within first six months of therapy achieved it after one year of therapy. No patient lost the initial response. The median BCR--ABL/ABL value at the end of the six months was 11% and at the end of the one year was 3.38%. CONCLUSION: Imatinib mesylate is highly effective in the treatment of chronic phase CML and so should be considered as the drug of first choice in CML. Molecular response evaluation after six months can predict the subsequent molecular response and can also be usedas a surrogate monitor of the marrow cytogenetic response to imatinib therapy in CML.
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