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Until recently, the knowledge of the mutational processes that cause these somatic mutations has been very limited.
Over the last few decades, the term "nearly neutral mutations" has been used in various ways.
Pharmacologic restoration of the trafficking defects of HERG missense mutations has been documented.
Clustering of mutations has been observed in cancer genomes as well as for germline de novo mutations (DNMs).
A wide spectrum of androgen receptor (AR) gene mutations has been reported in complete androgen insensitivity syndrome (CAIS).
Apparently, in breast cancer the involvement of c-kit gene mutations has been considered as a rare phenomenon.
Identification of genetic mutations has been of burgeoning importance in amyotrophic lateral sclerosis (ALS) in recent years.
The technical difficulty of engineering mtDNA mutations has been a major handicap in furthering our understanding of the mitochondrial genetic system.
While identification of cancer somatic mutations has been serendipitous, genome sequencing has provided an unbiased approach to systematically catalog somatic mutations and elucidate the mechanisms of tumourigenesis.
A similar result of the gene mutations has been reported previously in other literatures (Table 2).
Increased frequency of p53 mutations has been generally observed in advanced stage CaP and metastatic prostate cancer cell lines.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com