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Soo Jung Kim

Researcher at Inha University

Publications -  25
Citations -  854

Soo Jung Kim is an academic researcher from Inha University. The author has contributed to research in topics: Pancreatic cancer & PI3K/AKT/mTOR pathway. The author has an hindex of 13, co-authored 23 publications receiving 608 citations.

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Methylation-dependent loss of RIP3 expression in cancer represses programmed necrosis in response to chemotherapeutics

TL;DR: This work shows that programmed necrosis is activated in response to many chemotherapeutic agents and contributes to chemotherapy-induced cell death, and proposes that RIP3-deficient cancer patients may benefit from receiving hypomethylating agents to induce RIP3 expression prior to treatment with conventional Chemotherapeutics.
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NQO1 inhibits proteasome-mediated degradation of HIF-1α

TL;DR: A previously undescribed function for NQO1 is shown in stabilizing HIF-1α, a master transcription factor of oxygen homeostasis that has been implicated in the survival, proliferation and malignant progression of cancers.
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Tumor vessel normalization by the PI3K inhibitor HS-173 enhances drug delivery.

TL;DR: Findings indicate that vessel normalization by PI3K inhibitors restrained tumor growth and metastasis while improving chemotherapy by enhancing drug delivery into the tumor, suggesting that HS-173 may have a therapeutic value as an enhancer or an anticancer drug.
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A novel imidazopyridine PI3K inhibitor with anticancer activity in non-small cell lung cancer cells.

TL;DR: Investigation of the anticancer effects of a novel phosphatidylinositol 3-kinase α (PI3Kα) inhibitor in human NSCLC cell lines demonstrates that HS-173 exhibits anticancer activities, including the induction of apoptosis, by blocking the PI3K/Akt/mTOR pathway in human lung cancer cell lines, and suggests that this novel drug could potentially be used for targetedNSCLC therapy.
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KRAS targeting antibody synergizes anti-cancer activity of gemcitabine against pancreatic cancer.

TL;DR: It is suggested that RT11-i and gemcitabine be viewed a potential combination treatment option for pancreatic cancer patients with KRAS mutation because of the synergistic anticancer activity shown.