Research ArticleOpen Access

FLT3 Receptor Heterogeneity Strictly Specifies the Dimensions of Malignant Transformation Events in Acute Myeloid Leukemia

Volume 1 - Issue 5

*Lawrence M Agius

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- Department Of Pathology, University Of Malta Medical School, Europe
*Corresponding author: Lawrence M Agius, Department Of Pathology, Mater Dei Hospital, Tal-Qroqq, University Of Malta Medical School, Msida, Malta Europe, 27 “Ballarat” Guzeppe Caruana Street, Tal-Virtu, Rabat, Rbt09, Malta, Europe

Received: October 25, 2017; Published: October 31, 2017

DOI: 10.26717/BJSTR.2017.01.000479

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Abstract

Qualitative mutational events act synergistically with increases in mutated FLT3 receptors in the plasma-membrane in inducing constitutive activation of the receptors in terms of such indices as auto phosphorylation of the tyrosine kinase domains. Dimerization of the FLT3 sub-units and diminished “repulsive” dysfunctions of the juxtamembrane domain allow for permissive receptor activation. Incremental numbers of mutated receptors may strictly characterize the nature of origin of the malignant transformation event in terms of both synergic and compensatory mechanisms that directly modulate and further impact the hematopoietic progenitor cell subpopulations and also renewal of the hematopoietic stem populations in the bone marrow. Blast cell generation proliferation and impaired differentiation programs come to account for a great degree of heterogeneity in hematopoietic ally-related cell types in response to agents with tyrosine kinase inhibitory action.

Abbreviations: AML: Acute Myeloid Leukemia; ITDs: Internal Tandem Duplications; TKIs: Tyrosine kinase inhibitors; WT: Wild Type; GFI: Growth Factor Independence; SKY: Spleen Tyrosine kinase