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Chronic myeloid leukemia (CML) is a slowly-progressing cancer characterized by the clonal myeloproliferative expansion of pluripotent hematopoietic stem cells resulting from acquisition of the fusion oncogene BCR-ABL1.
The Genmark Leukemia assay offers a very simple procedure for testing the most relevant mutations implicated
BCR-ABL1 translocation can be observed in myeloproliferative neoplasms, acute leukemia of ambiguous lineage and precursor lymphoid neoplasms class as chronic myeloid leukemia (CML), acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
Somatic mutation of the JAK2 gene (JAK2 p.V617F) can be detected in a variable proportion of patients with myeloproliferative neoplasms.
Myeloproliferative Leukemia Virus (MPL) appears distinctly associated with polycythemia vera (PV), essential thrombocythemia (ET) and Primary myelofibrosis (PMF).
The calcium-binding endoplasmic reticulin chaperone protein, calreticulin (CALR), is somatically mutated in approximately 70% of patients with JAK2-negative essential thrombocythemia (ET) and 60% to 88% of patients with JAK2-negative primary myelofibrosis (PMF).
Mutations within exon 12 of the JAK2 gene occur in most cases of JAK2 V617F-mutation negative polycythemia vera.
Nucleophosmin-1 (NPM1) mutations represent the most frequent gene alteration in acute myeloid leukemia (AML).
Mutation of the fms-like tyrosine kinase 3 gene consisting of internal tandem duplication (FLT3-ITD), which is one of the most frequent genetic alterations, occurs in 15–35% of adults with acute myeloid leukemia (AML).