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Sug Hyung Lee

Researcher at Catholic University of Korea

Publications -  463
Citations -  23933

Sug Hyung Lee is an academic researcher from Catholic University of Korea. The author has contributed to research in topics: Frameshift mutation & Germline mutation. The author has an hindex of 64, co-authored 454 publications receiving 21552 citations. Previous affiliations of Sug Hyung Lee include Chung-Ang University & The Catholic University of America.

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Mutational analysis of the CASP6 gene in colorectal and gastric carcinomas.

TL;DR: The data indicate that the CASP6 gene is occasionally mutated in gastric and colorectal carcinomas, and the data suggest the possibility that deficiency of caspase‐6 expression might contribute to the pathogenesis of gastric cancers.
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The mutational burdens and evolutionary ages of early gastric cancers are comparable to those of advanced gastric cancers.

TL;DR: The results suggest that the genetic makeup for gastric cancer may already be achieved in EGC genomes and that the time required for transition to AGC may be relatively short, and suggest a possibility that the mutational profiles obtained from early biopsies may be useful in the clinical settings for the molecular diagnosis and therapeutics of gastric patients.
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Somatic mutations of BECN1, an autophagy-related gene, in human cancers.

TL;DR: The first report on BECN1 gene mutations in human cancer tissues is reported, and the data suggest that point mutations are a rare event in common human cancers and probably do not play a major role in cancer pathogenesis.
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Immunohistochemical analysis of NF‐κB signaling proteins IKKε, p50/p105, p52/p100 and RelA in prostate cancers

TL;DR: Immunohistochemical analysis of NF‐κB signaling proteins IKKε, p50/p105, p52/p100 and RelA in prostate cancers shows positive associations with disease progression in men and women.
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Laminin gene LAMB4 is somatically mutated and expressionally altered in gastric and colorectal cancers.

TL;DR: The data show that frameshift mutations of LAMA1, LAMA3, LAMB1 and LAMb4, and loss of L AMB4 may be features of GC and CRC with MSI‐H.