Monitoring molecular response in chronic myeloid leukemia

• Published in: Cancer Vol. 117; no. 6; pp. 1113 - 1122
• Main Authors: Cortes, Jorge, Quintás‐Cardama, Alfonso, Kantarjian, Hagop M.
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 15.03.2011; Wiley-Blackwell
• Subjects: Antineoplastic Agents - therapeutic use; BCR‐ABL; Biological and medical sciences; Biomarkers, Pharmacological - analysis; Biomarkers, Pharmacological - metabolism; Biomarkers, Tumor - analysis; Biomarkers, Tumor - genetics; chronic myeloid leukemia; Cytogenetic Analysis; Fusion Proteins, bcr-abl - genetics; Hematologic and hematopoietic diseases; Humans; imatinib; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - diagnosis; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - mortality; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis; Medical sciences; Molecular Diagnostic Techniques - methods; molecular response; Monitoring, Physiologic - methods; Prognosis; Protein Kinase Inhibitors - therapeutic use; Survival Analysis; Treatment Outcome; Tumors; tyrosine kinase inhibitor; Chromosomal aberration; Antineoplastic agent; Non-specific serine/threonine protein kinase; Myeloproliferative syndrome; Abnormal chromosome C9; Cancerology; Abnormal chromosome G22; chronic myeloid leukemia; Protein-tyrosine kinase; Hybrid gene; Chromosome translocation; Imatinib; Enzyme; Tyrosine kinase inhibitor; Transferases; BCR-ABL; Enzyme inhibitor; Chronic myelogenous leukemia; molecular response; Malignant hemopathy; Philadelphia chromosome; bcr gene; Surveillance; C-Onc gene; Abnormal chromosome; Cancer
• ISSN: 0008-543X; 1097-0142
• DOI: 10.1002/cncr.25527

Before the advent of tyrosine kinase inhibitor (TKI) therapy, the evaluation of hematologic and cytogenetic responses was sufficient to gauge treatment efficacy in patients with chronic myeloid leukemia. However, with more potent TKI therapies, the majority of patients achieve complete cytogenetic response. Furthermore, deeper molecular responses are now commonly achieved, necessitating a reliance on molecular monitoring to assess residual leukemic disease. The prognostic significance between molecular responses and duration of complete cytogenetic response, progression‐free survival, and event‐free survival is described herein. A discussion of the concept of complete molecular response is also provided, and the potential for imatinib treatment discontinuation is evaluated. The implications of rising BCR‐ABL1 transcript levels and caveats of molecular monitoring are also described. Cancer 2011. © 2010 American Cancer Society. Before the advent of tyrosine kinase inhibitor therapy, the evaluation of hematologic and cytogenetic responses was sufficient to gauge treatment efficacy in patients with chronic myeloid leukemia. Deeper molecular responses are now commonly achieved, necessitating a reliance on molecular monitoring to assess residual leukemic disease. Still, complete cytogenetic response remains the gold standard for an adequate response in CML.