Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the development of imatinib mesylate, an ABL tyrosine kinase inhibitor (TKI), the treatment of chronic myeloid leukemia (CML) has made remarkable progress. Second and third generation TKIs have also become available for clinical use. Considering the improved treatment outcomes, chronic phase CML has become manageable, with a low mortality rate. Furthermore, clinical trials such as STIM and DADI have shown that TKI can be discontinued safely in certain CML patients. However, some CML patients, especially those in accelerated phase (AP) or blast phase (BP), require more aggressive forms of treatment such as allogenic hematopoietic stem cell transplantation. Next-generation sequencing technology and other novel technologies allow us to investigate the cause of CML and the molecular biology of progression to AP/BP in more detail. Based on these data, an increasing number of novel therapeutic agents for CML are being developed, which will improve the prognosis of CML.
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PMID:Molecular biology and treatment of CML. 2897 34

Chronic Myeloid Leukemia (CML) is a stem cell cancer that arises when t(9;22) translocation occurs in a hematopoietic stem cells. This event results in the expression of the BCR-ABL1 fusion gene, which codes for a constitutively active tyrosine kinase that is responsible for the transformation of a HSC into a CML stem cell, which then gives rise to a clonal myeloproliferative disease. The introduction of Tyrosine Kinase Inhibitors (TKIs) has revolutionized the management of the disease. However, these drugs do not seem to be able to eradicate the malignancy. Indeed, discontinuation trials (STIM; TWISER; DADI) for those patients who achieved a profound molecular response showed 50% relapsing within 12 months. We performed a comparative analysis on 15 CML patients and one B-ALL patient, between the standard quantitative reverse-transcriptase PCR (qRT-PCR) and our genomic DNA patient-specific quantitative PCR assay (gDNA qPCR). Here we demonstrate that gDNA qPCR is better than standard qRT-PCR in disease monitoring after an average follow-up period of 200 days. Specifically, we statistically demonstrated that DNA negativity is more reliable than RNA negativity in indicating when TKIs therapy can be safely stopped.
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PMID:gDNA qPCR is statistically more reliable than mRNA analysis in detecting leukemic cells to monitor CML. 2950 Mar 81