Acquired resistance develops through various mechanisms including secondary mutations of the targeted oncogene or activation of alternative proliferative signaling pathways.
Late resistance can be associated with several mechanisms, including secondary KIT mutations, genomic KIT amplification, the activation of alternative survival pathways, altered pharmacokinetics or the elevated expression of drug efflux proteins., Therefore, the overexpression of wild-type KIT presents another challenge for therapy.
Other possible masking mechanisms include RNA secondary structures, which can mask AUG codons within helices and may restrict their use.
Common mechanisms of acquired resistance include secondary mutation in the target gene, activation of alternative pathway or feedback loop, and induction of EMT [ 23, 30].
These phytochemicals include secondary metabolites viz.
MR can become exaggerated during TAVR for several reasons, including direct mechanical damage to the mitral valve leaflets or subvalvular apparatus by the guidewire or prosthetic valve; secondary mechanisms include new-onset LBBB, myocardial ischemia, systolic anterior motion of the mitral valve leaflet, significant paravalvular leakage, and cardiac tamponade [2].
Supports Thrift interface Secondary indexing mechanisms include column families, super-columns, collections.
Such mechanisms include antibody-dependent enhancement of a secondary infection or cross-reactivity with proteins such as endothelial cell or coagulation proteins [ 4– 8].
Other possible mechanisms include endorphin release, exercise protection against secondary fibromyalgia, increased resistance to musculoskeletal micro-injury, psychologically based increase in pain threshold, innately high pain threshold influencing decision to exercise vigorously, or other psychological mechanisms.
