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.
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