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No significant differences were detected between normal thyroid, nonneoplastic lesions, and PTC (or any PTC variant) regarding expression/activation of TrkA, thus suggesting that by itself and in contrast to p75 NTR, TrkA is not altered during PTC development.
We compared cases with and without a given variant regarding their exposure to THMs using unconditional logistic regression.
Genetic counselling is very useful for explaining in detail the meaning of the possible genotypes that can be identified and the usefulness of the knowledge of its own variant regarding the procreative risk.
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However, we found no evidence for significant gene-gene interactions between these variants regarding CD susceptibility.
We therefore hypothesized that there may be epistasis between CD-associated NOD2 and ATG16L1 variants regarding susceptibility to CD.
Although inversions are generally considered as neutral variants regarding phenotype, there are several exceptions where specific genes at the breakpoints are interrupted [41] [46].
Overall, these studies confirm IL23R as a CD susceptibility gene, but demonstrate differences for certain IL23R variants regarding the strength of their disease-modifying effect in different populations.
The specific actions of OPN splice variants regarding non-small-cell lung cancer angiogenesis and VEGF have been investigated [ 55].
No important differences were found between TTO variants regarding values for EQ-5D-5L health states, suggesting that they could be equivalent variants.
During our genome-wide analysis, we found some genes with remarkable alternative splicing variants regarding the size or number of excluded introns and exons.
Databases such as dbSNP, COSMIC, and clinVAR [ 63] provide annotation information for DNA variants regarding their frequency within the population and potential associations with disease and clinical phenotype.
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