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Jung-Sik Kim

Researcher at Georgetown University

Publications -  42
Citations -  3718

Jung-Sik Kim is an academic researcher from Georgetown University. The author has contributed to research in topics: Mutation & PTEN. The author has an hindex of 24, co-authored 41 publications receiving 3336 citations. Previous affiliations of Jung-Sik Kim include Children's Hospital at Westmead.

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Synthetic lethal targeting of PTEN mutant cells with PARP inhibitors

TL;DR: The data presented here now suggests that the clinical assessment of PARP inhibitors should be extended beyond those with BRCA mutations to a larger group of patients with PTEN mutant tumours.
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Mutational Inactivation of STAG2 Causes Aneuploidy in Human Cancer

TL;DR: Studying a near-diploid human cell line with a stable karyotype, it is found that targeted inactivation of STAG2 led to chromatid cohesion defects and aneuploidy, whereas in two aneuPLoid human glioblastoma cell lines, targeted correction of the endogenous mutant alleles of STAE led to enhanced chromosomal stability.
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The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation

TL;DR: The largest genomic survey to date of 101 EFT (65 tumors and 36 cell lines) is reported, finding that EFT has a very low mutational burden but frequent deleterious mutations in the cohesin complex subunit STAG2 and that 11% of tumors pathologically diagnosed as EFT lack a typical EWSR1 fusion oncogene and these tumors do not have a characteristic Ewing sarcoma gene expression signature.
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Pharmacologic inhibition of cyclin-dependent kinases 4 and 6 arrests the growth of glioblastoma multiforme intracranial xenografts

TL;DR: The results support clinical trial evaluation of PD-0332991 against newly diagnosed as well as recurrent GBM, and indicate that Rb status is the primary determinant of potential benefit from this therapy.
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Radiation-induced Akt activation modulates radioresistance in human glioblastoma cells

TL;DR: Akt may be a central player in a feedback loop whereby activation of Akt induced by IR increases radioresistance of GBM cells, and targeting the Akt signaling pathway may have important therapeutic implications when used in combination with IR.