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Further large studies on HFE association with breast cancer susceptibility in populations lacking the C282Y mutation may need to include markers from HLA loci, loci between the HLA complex and HFE and other variants of the HFE gene for more meaningful results than our preliminary study has shown.
Noting that the difference in the baseline level of ROS in HN31 was two- to threefold higher than in HN30, we decided to investigate the possibility that cells with a partially functional TP53 mutation may need a higher exposure to ROS, higher than the level produced using 4 Gy, in order to achieve a senescent state.
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However, RNASEL does not account for a significant number of familial prostate cancers in Germany, and the penetrance of deleterious mutations may need further evaluation.
Of note, cases with EMG mutations may need further enhanced therapy such as high dose anthracyclines and regulatory agents for DNA methylation and/or histone modification to improve their clinical outcome.
These studies have highlighted that the accuracy of mutation detection may need to be improved in order for NGS to become a prudent option for clinical genetic testing [ 1, 6].
To account for subpopulations without distinguishing mutations, we may need to add auxiliary frequencies to L ∼ that correspond to the missing subpopulation frequencies.
If alleles carry multiple mutations, you may need to perform site-directed mutagenesis to create single amino acid substitution alleles and test their ability to confer drug resistance.
These results show synergistic pathogenic effects between the presence of defective PPARγ and AngII-induced hypertension and suggest that patients with PPARγ mutation and hypertension may need more aggressive therapeutic measures to reduce the risk of accelerated cardiac fibrosis.
The Border Collie breed is also affected by the ABCB1/MDR1-gene mutation (nt230 (del4)), which may need to be considered in dogs with acute seizures and potential previous exposure to neurotoxic P-gp substrates.
Meanwhile, the apparently dominant effects of the p53γ isoform influencing the p53 network may provide an explanation for the conflicting literature regarding the clinical associations between mutant p53 and breast cancer and issue a warning that clinical decisions made on the basis of p53 mutation status alone may need to be approached with caution.
Due to recombination between indirect markers and causative mutations, the marker effects may need to be re-estimated from time to time.
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