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This confidence increases as more different mutations are tested.

Subsequently the immunogenicity of these mutations is defined, and finally, mutations are tested for their capability to elicit T-cell immunogenicity [ 22].

Single-gene testing is unlikely to be clinically useful for prognosis; although MSI immunohistochemistry is becoming routine and may confer prognostic significance in certain scenarios 28, it is notable that multiple mutations are tested simultaneously.

About 80% alleles from CF patients are identified if panels of the most frequent mutations are tested [ 56]; the analysis of mutations peculiar to specific ethnic-geographic groups may increase the detection rate [ 57], and the scanning of CFTR coding regions reveals mutations in up to 90% alleles [ 58, 59].

It is noteworthy that recent study showed a proof-of-concept in which somatic mutations are first detected using NGS, then the immunogenicity of these mutations is defined, and finally, mutations are tested for their capability to elicit T cell immunogenicity [ 15].

Similar(55)

The effects of these mutations were tested using neuropeptide Y receptors Y1R and Y2R.

Effects of those mutations were tested with the CPM assay and the affinity MS assay (Table 2).

The deleted mutations were tested in mice for attenuation in virulence and for growth in macrophages.

In the infection complementation assay, the A73D and A74D mutations were tested individually and in combination.

Piwi2/2, piwi3/3, and transheterozygous piwi3/2 mutations were tested in these experiments.

Differences in frequencies of different classes (transversions, insertions, insertions and deletions) or types (GC-TA, InsG, CG-TA) of mutations were tested using the hypergeometric test.

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