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-  2018 

Immature CML cells implement a BMP autocrine loop to escape TKI treatment

DOI: 10.21037/22385

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Abstract:

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder emanating from a reciprocal translocation between BCR on chromosome 22 and ABL kinase on chromosome 9, generally known as the Philadelphia chromosome. Although activity level of ABL kinase in the resting condition is preserved and regulated by a hydrophobic pocket, in CML, this pocket substitute with BCR that engenders in incessant activation of ABL and culminates in actuation of downstream signaling pathways (1,2). Introduction of tyrosine kinase inhibitors (TKIs), revolutionized the response criteria, progression free survival and overall survival in CML patients in contrast with the previous form of treatment comprise of interferon-α and cytarabine combination (3). Even though a sizable proportion of cells respond to TKIs in a highly efficient manner, a strong intimation of resistance has been received from a minority group called leukemic stem cells (LSCs), responsible for disease progression (4). Impervious to TKIs whether by the acquisition of some features such as domain mutations or inheritance hallmarks, come to pass in a spatial structure called bone marrow niche. So, acts as a shield in the way of targeting LSCs and plays an indispensable role in the development of leukemia (5)

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