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Nam Jin Yoo

Researcher at Catholic University of Korea

Publications -  405
Citations -  13537

Nam Jin Yoo 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 63, co-authored 403 publications receiving 12692 citations. Previous affiliations of Nam Jin Yoo include Catholic University College, Kensington & The Catholic University of America.

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Expression of AIMP1, 2 and 3, the scaffolds for the multi-tRNA synthetase complex, is downregulated in gastric and colorectal cancer.

TL;DR: Investigation of the expression status of AIMP members in gastric cancer and colorectal cancer tissues suggested that downregulation of these proteins may be related to inactivation of the tumor suppressor functions of A IMP proteins and might play a role in the development of GC and CRC.
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Novel somatic frameshift mutations of genes related to cell cycle and DNA damage response in gastric and colorectal cancers with microsatellite instability.

TL;DR: The results of this study suggest that the mutations might contribute to the development of GC and CRC with MSI by deregulation of the cell cycle and DNA damage signaling/repair.
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Mutational analysis of TTK gene in gastric and colorectal cancers with microsatellite instability.

TL;DR: The data suggest that frameshift mutations of TTK might alter cell cycle control in the affected cells and contribute to pathogenesis of cancers with MSI-H, and that the mutations occur not only in the A9 repeat but also in theA7 repeat.
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Frameshift mutations of axon guidance genes ROBO1 and ROBO2 in gastric and colorectal cancers with microsatellite instability.

TL;DR: Frameshift mutations of ROBO1 and ROBO2 genes and alteration ofROBO2 expression in GC and CRC suggest that both genes might play roles in the pathogenesis ofGC and CRC.
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Mutational and expressional analysis of RFC3, a clamp loader in DNA replication, in gastric and colorectal cancers.

TL;DR: The data indicate RFC3 mutation and loss of RFC3 expression occur in large fractions of GC and CRC and suggest that these alterations may contribute to the cancer pathogenesis by deregulating DNA repair and replication.