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Tumor heterogeneity due to mutator mutations may contribute to therapeutic resistance, and the degree of heterogeneity of tumors may need to be considered when therapeutic strategies are devised.
There was no significant correlation between the mutation frequencies and resistance levels in the resistant populations, indicating that other mutations may contribute to this variation.
Most scientists agree that most, if not all people, will have some sets of genetically distinct brain cells, but we are still learning about the extent of mosaicism in the human brain and how these mutations may contribute to disease.
These results, together with the suggestions that the residues at the tips of cardiotoxins' loop structure were involved in the manifestation of the biological activities of cardiotoxins, reflect that the preferential mutations may contribute to alterations in the function of cardiotoxin molecules.
These data suggest that heterogeneity in the expression of oncogenic EGFR mutations may contribute to therapy resistance and combining multiple EGFR inhibitors that act through different mechanisms may be required in glioblastoma patients who carry multiple EGFR variants.
Cancer-specific mitochondrial mutations may contribute to development of a malignant phenotype by direct genotoxic effects from increased reactive oxygen species production as well as induction of aerobic glycolysis and growth promotion.
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Conclusions: These results suggest that M6P/IGF2R functions as a growth suppressor and its loss or mutation may contribute to development and progression of cancer.
This mutation may contribute to the decline of blocking activity.
Therefore, the drop in brain copper levels induced by the Tg2576:sod2 double mutation may contribute to the increased amyloid burden in double mutants.
We quantified and visualized expression data for the subset of human genes containing these distinct alternative first exons (DAlFEs) to elucidate details of the "promoterome" regulating human gene expression and distinguish among alternative promoters whose mutation may contribute to disease phenotypes.
These results suggest that mitochondrial ND6 gene nonsense and missense mutation may contribute to the metastasis of lung adenocarcinoma.
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variations may contribute
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mutations may sensitize
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mutations may represent
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