作者: Franklin R. Moore , Carole B. Rempfer , Richard D. Press
DOI: 10.1007/978-1-62703-357-2_1
关键词: Cancer research 、 Myelogenous 、 Chronic myelogenous leukemia 、 Philadelphia chromosome 、 Imatinib 、 Minimal residual disease 、 Leukemia 、 Myeloid leukemia 、 ABL 、 Medicine
摘要: The reciprocal Philadelphia translocation between chromosomes 9 and 22 [t(9;22)(q34;q11)] creates a BCR-ABL1 fusion protein that occurs in approximately 95% of cases chronic myelogenous leukemia (CML), 15% adult acute lymphoblastic leukemia, 5% myeloid leukemia. is constitutively activated tyrosine kinase induces maintains the neoplastic phenotype these leukemias. PCR-based methods to identify quantitate tumor-specific RNA have been shown be an ultrasensitive diagnostic/prognostic tool for Philadelphia-positive A novel inhibitor (TKI), imatinib, has confirmed as effective targeted treatment most CML patients. consensus goal TKI achieve major molecular response (MMR), defined 3-log (1,000-fold) reduction transcripts. Patients who MMR significantly reduced risk disease progression. Conversely, increasing post-therapy levels convey increased early identification high-risk patients may allow changes therapeutic strategy, before frank relapse. Thus, quantitative measurement transcripts blood bone marrow both aids initial diagnosis essential routine minimal residual monitoring. We describe here method quantitating peripheral or using real-time reverse transcription PCR (RQ-PCR).