Leucosis Quantum M-bcr – Chronic myelogenous (or myeloid) leukemia (CML), also known as chronic granulocytic leukemia (CGL), is a cancer of the white blood cells. It is a form of leukemia characterized by the increased and unregulated growth of predominantly myeloid cells in the bone marrow and the accumulation of these cells in the blood. CML is a clonal bone marrow stem cell disorder in which proliferation of mature granulocytes (neutrophils, eosinophils, and basophils) and their precursors are the main finding. It is a type of myeloproliferative disease associated with a characteristic chromosomal translocation called the Philadelphia chromosome. CML is now largely treated with tyrosine kinase inhibitors (TKIs), such as imatinib, dasatinib or nilotinib, which has led to dramatically improved survival rates since their introduction in the last decade. CML was the first malignancy to be linked to a clear genetic abnormality, the chromosomal translocation known as the Philadelphia chromosome. In this translocation, parts of two chromosomes (the 9th and 22nd by conventional karyotypic numbering) switch places. As a result, part of the BCR („breakpoint cluster region“) gene from chromosome 22 is fused with the ABL gene on chromosome 9. This abnormal „fusion“ gene generates a protein of p210 or sometimes p185 weight (p210 is short for 210 kDa protein, a shorthand used for characterizing proteins based solely on size). Because abl carries a domain that can add phosphate groups to tyrosine residues (a tyrosine kinase), the bcr-abl fusion gene product is also a tyrosine kinase. The fused BCR-ABL protein interacts with the interleukin 3 beta (c) receptor subunit. The bcr-abl transcript is continuously active and does not require activation by other cellular messaging proteins. In turn, BCR-ABL activates a cascade of proteins that control the cell cycle, speeding up cell division. Moreover, the BCR-ABL protein inhibits DNA repair, causing genomic instability and making the cell more susceptible to developing further genetic abnormalities. The action of the BCR-ABL protein is the pathophysiologic cause of chronic myelogenous leukemia. With improved understanding of the nature of the BCR-ABL protein and its action as a tyrosine kinase, targeted therapies (the first of them was imatinib mesylate) that specifically inhibit the activity of the BCR-ABL protein, have been developed. These tyrosine kinase inhibitors can induce complete remissions in CML, confirming the central importance of bcr-abl as the cause of CML. Clinically, leukemia is manifested in three distinct phases: chronic, accelerated, and blast. Most patients present in the chronic phase, a stage that is typically indolent in nature. Mature granulocytes are found, but patients typically have an increase in the number of myeloid progenitor cells found in the blood. Left untreated, the disease progresses to an accelerated phase followed by blast crisis, which is inevitably fatal. During blast phase, hematopoietic differentiation is blocked and blast cells accumulate in the bone marrow and peripheral blood. Expression of BCR-ABL onco-proteins in hematopoietic cells induces resistance to apoptosis, growth factor independence and leukemogenesis. AmpliSens Leucosis Quantum M-bcr-FRT PCR kit is an in vitro nucleic acid amplification test for qualitative and quantitative detection of the bcr-abl chimeric gene (M- bcr variant) mRNA and abl gene mRNA in the clinical materials (peripheral blood, bone marrow) by using real-time hybridization-fluorescence detection. AmpliSens Leucosis Quantum M-bcr-FRT PCR kit can be used for screening detection of CML (chronic myelogenous leukemia) associated with M-bcr-abl chromosomal rearrangement, confirmation of CML diagnosis, and monitoring of the minimal residual disease (MRD) and therapy efficiency.