Sentence examples for mutations have defined from inspiring English sources

Exact(1)

Current models of carcinogenesis are dominated by the assumption that oncogenic mutations have defined advantageous fitness effects on recipient stem and progenitor cells, promoting and rate-limiting somatic evolution.

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Indeed, there is evidence that BIBN4096BS acts allosterically [10] and it is interesting that neither of the mutations that have defined the two known contact sites for these non-peptide antagonists disrupt CGRP binding.

Early studies on these genetic alterations copy number variations, mutations, gene rearrangements—have defined mechanisms of oncogenesis, led to the creation of targeted therapies, and improved patient outcomes for certain cancers.

Some of these LRs, such as the 5 BRCA1 mutations in the LRP, have defined endpoints and were previously characterized as founder mutations.

Future therapy options include the utilization of induced pluripotent stem cells that might be beneficial for patients that have defined mutations in telomerase components such as TERC [ 5]. mTOR is a protein kinase that promotes cell growth in response to nutrient supplies and growth signals, and can be specifically inhibited by rapamycin [ 27].

Wright (1964) and Kimura (1990) have defined compensatory mutations as those masking the deleterious effect of another mutation or as mutations that are independently deleterious but neutral when combined [ 12, 13].

Haplogroup, M18 was previously characterized by only the HVS I mutation (16318T), but now we have defined this haplogroup by two coding region mutations (12498 and 15942), and an additional control region mutation (194) (Fig. 1 and also see Additional file 1).

In the past, we have defined specific point mutations in the translation initiation factor eIF2B based upon phenotypic resistance/sensitivity to high concentrations of exogenously added n-butanol.

Re-sequence studies have investigated candidate genes based on prior genetic observations (changes in copy number or regions of genetic instability) or other laboratory observations and have defined critical somatic mutations in genes such as TP53 and PIK3CA.

Initial re-sequence studies examined individual candidate genes based on prior genetic observations (changes in copy number or regions of genetic instability) or those identified in animal or in vitro laboratory studies and have defined critical somatic mutations in genes such as TP53 and PIK3CA [ 4- 11].

Such sentiments have defined L.S.U.

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