Sentence examples for sensitivity to therapy from inspiring English sources

That is, it cannot otherwise be predicted whether the autophagy induced by radiation or chemotherapy is associated with resistance and the circumstances under which autophagy inhibition might be a useful strategy for enhancing sensitivity to therapy.

It is important to think clinical lipidomics as the part of clinical trans-omics which was coined as a new emerging scientific discipline where clinical phenomes are integrated with molecular multiomics, in order to further understand molecular mechanisms of disease pathogenesis and progression, patient sensitivity to therapy and prognosis, and therapy design and development [3].

With such data, it will be possible to relate the extent of diversity to clinically important covariates like survival, proliferation indices, invasiveness, sensitivity to therapy, etc.

Higher inter-patient viral genetic diversity correlated with successful treatment, implying that there are HCV genotype 1 strains with intrinsic differences in sensitivity to therapy.

In particular, these biomarkers typically each depend on a number of physiological factors that when altered by tumor therapy may lead to opposing effects on the biomarker response, thereby minimizing the biomarker sensitivity to therapy.

Wild-type IDH1 was associated with resistance, whereas mutant-IDH1 showed enhanced sensitivity to therapy [ 94].

However, understanding the mechanisms underlying the physiological effects of this important hormone and how their deregulation impacts on sensitivity to therapies directed at the ER remains a significant challenge.

At the cell differentiation level, there appears to be a hierarchy of clonally related cells that have different clonogenic potential and sensitivity to therapies.

Transformation of the tumor correlates with the difference between small-cell lung cancer and adenocarcinoma in sensitivity to therapies, so repeated biopsies are beneficial for choosing appropriate treatments.

Cross-talk between ER and HER2 pathways may result in synergistic tumor progression, differential sensitivity to therapies, and differential sites of tumor relapse [ 9].

Future modeling work will build upon the model developed here, in the continued effort to identify clinically-relevant drug targets or determine how levels of different components of growth factor systems influence sensitivity to therapies [ 85].