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These findings provide evidence that the 2 novel FHL2 variants could increase cardiac function in HCM.
Instead, our data support the view that FHL2 genetic variants could increase cardiac function in HCM.
Thus, HVR1 heterogeneity could facilitate treatment failure since coexistence of multiple antigenic variants could increase the probability of positive selection of those effectively evading immune pressure induced by treatment [ 15, 16].
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These results suggested that LMP7 genetic variant could increase the susceptibility to ovarian cancer development; especially increase the risk of lymph node and tumor distant metastasis.
Several hypotheses have been proposed to explain how the genetic variants in TCF7L2 could increase T2D risk.
In population level, we found that individuals with variant C allele could increase cancer susceptibility in Asians but not in Europeans, suggesting a possible role of ethnic differences in genetic background and the environment they lived in [36].
Since Fralying et al. found that the variant of rs9939609 could increase the risk of developing obesity by 31%, numerous studies covering multiple populations subsequently focused on this SNP [ 40- 42].
In our theoretical model of cis-regulated alternative splicing, PS genes are simply genes with more than a single splicing variant, and MS genes have a single splicing variant because newly created splicing variants could not increase in frequency or because a new variant had fixed in a population.
An alternative possibility could be that the increased expression of H2A.Z-1 wouleadead to an altered association of this histone variant with chromatin which could increase the plasticity of castration resistant cancer cells.
However, other variants in the same gene could increase risk for diseases in these populations.
Sustained NKG2D-mediated activation of alloreactive CD8+ T cells would be expected if only a MICA-129Val variant is present, and this could increase the risk of cGVHD.
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