Chronic myeloid leukemia (CML) is a malignant cancer derived from hematopoietic stem cells. CML is induced by an oncogenic BCR-ABL1 fusion protein, which has constitutive tyrosine kinase activity. The BCR-ABL1 fusion protein is produced from the fused Philadelphia chromosome formed by the translocation of chromosomes 9 and 22 [1]. Multiple pharmaceutical companies have developed specific inhibi...

Chronic myeloid leukemia (CML) is a chronic myeloproliferative disease almost always caused by a genetic defect known as the Philadelphia (Ph) chromosome. Ph chromosome is associated with a BCR/ABL fusion gene expressed as an oncoprotein, which is generally considered as the initiator for the chronic phase of CML. Tyrosine kinase inhibitors (TKI) are targetspecific therapeutic agents that achie...

BACKGROUND Some reports have suggested that chronic myeloid leukemia (CML) patients have a higher prevalence of M-bcr than acute lymphoblastic leukemia (ALL) patients, which show a higher prevalence of m-bcr. However, the relationship between BCR-ABL subtypes and progression of CML and ALL remains unclear. MATERIALS AND METHODS 354 CML chronic phase (CML-CP) patients, 26 CML blastic phase (CM...

Chronic myeloid leukemia (CML) accounts for approximately 15% of adult leukemias. Forty percent of patients with CML are asymptomatic, in whom the disease is detected solely based on laboratory abnormalities. Since the introduction of tyrosine kinase inhibitor therapy in 2001, CML has become a chronic disease for the majority of patients. Primary care physicians may be the first to recognize a ...

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder. Current targeted therapies designed to inhibit the tyrosine kinase activity of the BCR-ABL oncoprotein have made a significant breakthrough in the treatment of CML patients. However, CML remains a chronic disease that a patient must manage for life. Although tyrosine kinase inhibitors (TKI) therapy has completely transforme...

Treatment of chronic myelogenous leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKI) fails to eliminate leukemia stem cells (LSC). Patients remain at risk for relapse, and additional approaches to deplete CML LSC are needed to enhance the possibility of discontinuing TKI treatment. We have previously reported that expression of the pivotal proinflammatory cytokine interleukin-1 (IL-1) ...

Abstract Natural killer (NK) cells have the capacity to recognize and clear cancer by releasing cytotoxic granules. In fact, NK cells’ mature phenotype abundance are associated with prolonged treatment-free remission in chronic myeloid leukemia (CML). However, cell anti-leukemic activity is suppressed during disease, environmental triggers of this impairment not fully characterized. Given role ...

Despite the unprecedented success of tyrosine kinase inhibitors (TKIs) in treating chronic myelogenous leukemia (CML), some patients nevertheless progress to advanced stages of the disease. Thus far, the biological basis leading to CML progression remains poorly understood. SH2-containing tyrosine phosphatase 1 (SHP-1) is reported to bind to p210BCR‑ABL1 and to function as a tumor suppressor. F...

Serial passage of axenically-cultured Leishmania chagasi promastigotes results in a progressive diminution in resistance to complement mediated lysis (CML), whereas high CML resistance is seen in infectious metacyclic promastigotes from the sandfly vector as well as metacyclic-like promastigotes within low passage cultures at stationary growth phase. As previously reported [94], in a screen see...

This paper investigates important problems involved in the design of a CML buffer as well as a chain of tapered CML buffers. A new design procedure to systematically design a chain of tapered CML buffers is proposed. The differential architecture of a CML buffer makes it functionally robust in the presence of environmental noise sources (e.g., crosstalk, power/ground noise). The circuit design ...