Sunshin Kim
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View article: VEGF Signal Complexity Confers Resistance to Atezolizumab, Bevacizumab, Carboplatin, and Paclitaxel in EGFR‐Tyrosine Kinase Inhibitor‐Resistant Non‐Small Cell Lung Cancer
VEGF Signal Complexity Confers Resistance to Atezolizumab, Bevacizumab, Carboplatin, and Paclitaxel in EGFR‐Tyrosine Kinase Inhibitor‐Resistant Non‐Small Cell Lung Cancer Open
Atezolizumab, bevacizumab, carboplatin, and paclitaxel (ABCP) therapy is beneficial for epidermal growth factor receptor‐tyrosine kinase inhibitor (EGFR‐TKI)‐resistant non‐small cell lung cancer (NSCLC); however, the resistance mechanisms …
View article: Overcoming MET-targeted drug resistance in MET-amplified lung cancer by aurora kinase B inhibition
Overcoming MET-targeted drug resistance in MET-amplified lung cancer by aurora kinase B inhibition Open
MET-targeted therapies are the most effective treatment for patients with MET-amplified lung cancer. However, acquired drug resistance is a significant challenge in MET-amplified lung cancer treatment. This study aimed to discover an effec…
View article: Single targeting of MET in EGFR-mutated and MET-amplified non-small cell lung cancer
Single targeting of MET in EGFR-mutated and MET-amplified non-small cell lung cancer Open
View article: Ataxia-Telangiectasia Mutated Is Involved in Autolysosome Formation
Ataxia-Telangiectasia Mutated Is Involved in Autolysosome Formation Open
Ataxia-telangiectasia mutated (ATM), a master kinase of the DNA damage response (DDR), phosphorylates a multitude of substrates to activate signaling pathways after DNA double-strand breaks (DSBs). ATM inhibitors have been evaluated as ant…
View article: Patient-derived cell-based pharmacogenomic assessment to unveil underlying resistance mechanisms and novel therapeutics for advanced lung cancer
Patient-derived cell-based pharmacogenomic assessment to unveil underlying resistance mechanisms and novel therapeutics for advanced lung cancer Open
View article: Additional file 2 of Patient-derived cell-based pharmacogenomic assessment to unveil underlying resistance mechanisms and novel therapeutics for advanced lung cancer
Additional file 2 of Patient-derived cell-based pharmacogenomic assessment to unveil underlying resistance mechanisms and novel therapeutics for advanced lung cancer Open
Additional file 2: Table S1. Clinical information and molecular subtypes of 102 lung cancer patients used to obtain PDCs. Table S2. The 48 drugs employed in the screening panel. We refer to the chemical or generic name of the drugs, and th…
View article: Patient-derived cell-based pharmacogenomic assessment to unveil underlying resistance mechanisms and novel therapeutics for advanced lung cancer
Patient-derived cell-based pharmacogenomic assessment to unveil underlying resistance mechanisms and novel therapeutics for advanced lung cancer Open
Background A pharmacogenomic platform using patient-derived cells (PDCs) was established to identify the underlying resistance mechanisms and tailored treatment for patients with advanced or refractory lung cancer. Methods Drug sensitivity…
View article: MYC amplification-conferred primary resistance to capmatinib in a MET-amplified NSCLC patient: a case report
MYC amplification-conferred primary resistance to capmatinib in a MET-amplified NSCLC patient: a case report Open
Concurrent MYC amplification could potentially confer primary resistance to capmatinib in highly MET amplified NSCLC patients. Further clinical studies are warranted to corroborate these findings, and treatment with MYC inhib…
View article: Oncogenic fusion of BCAR4 activates EGFR signaling and is sensitive to dual inhibition of EGFR/HER2
Oncogenic fusion of BCAR4 activates EGFR signaling and is sensitive to dual inhibition of EGFR/HER2 Open
We previously reported CD63-BCAR4 fusion as a novel oncogene that significantly enhanced cell migration and metastasis in lung cancer. To identify effective inhibitors of metastatic activity induced by BCAR4 fusion, we screened a drug libr…
View article: Early On-Treatment Prediction of the Mechanisms of Acquired Resistance to EGFR Tyrosine Kinase Inhibitors
Early On-Treatment Prediction of the Mechanisms of Acquired Resistance to EGFR Tyrosine Kinase Inhibitors Open
Background: Prediction of resistance mechanisms for epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) remains challenging. Thus, we investigated whether resistant cancer cells that expand shortly after EGFR-TKI treatm…
View article: ELF3 Is a Target That Promotes Therapeutic Efficiency in EGFR Tyrosine Kinase Inhibitor-Resistant Non-Small Cell Lung Cancer Cells via Inhibiting PKCί
ELF3 Is a Target That Promotes Therapeutic Efficiency in EGFR Tyrosine Kinase Inhibitor-Resistant Non-Small Cell Lung Cancer Cells via Inhibiting PKCί Open
(1) Background: Mutations in epidermal growth factor receptor (EGFR) proteins account for many non-small cell lung cancers (NSCLCs), and EGFR tyrosine kinase inhibitors (TKIs) are being used as targeted therapeutics. However, resistance to…
View article: A fusion of CD63–BCAR4 identified in lung adenocarcinoma promotes tumorigenicity and metastasis
A fusion of CD63–BCAR4 identified in lung adenocarcinoma promotes tumorigenicity and metastasis Open
Background Recently, fusion variants of the breast cancer anti-oestrogen-resistance 4 (BCAR4) gene were recurrently discovered in lung adenocarcinoma from the genome-wide studies. However, the functional characterisation of BCAR4 fusion ha…
View article: Regulation of mRNA export through API5 and nuclear FGF2 interaction
Regulation of mRNA export through API5 and nuclear FGF2 interaction Open
API5 (APoptosis Inhibitor 5) and nuclear FGF2 (Fibroblast Growth Factor 2) are upregulated in various human cancers and are correlated with poor prognosis. Although their physical interaction has been identified, the function related to th…
View article: NEDD4L downregulates autophagy and cell growth by modulating ULK1 and a glutamine transporter
NEDD4L downregulates autophagy and cell growth by modulating ULK1 and a glutamine transporter Open
In mammals, autophagosome formation is initiated by ULK1 via the posttranslational modification of this protein. However, the precise role of ULK1 ubiquitination in modulating autophagy is unknown. Here, we show that NEDD4L, an E3 ubiquiti…
View article: GenomomFF: Cost-Effective Method to Measure Fetal Fraction by Adaptive Multiple Regression Techniques With Optimally Selected Autosomal Chromosome Regions
GenomomFF: Cost-Effective Method to Measure Fetal Fraction by Adaptive Multiple Regression Techniques With Optimally Selected Autosomal Chromosome Regions Open
The accurate measure of fetal fraction is important to ensure the results of noninvasive prenatal testing. However, measuring fetal fraction could require a substantial amount of data and additional costs. Therefore, this study proposes an…
View article: EI24, as a Component of Autophagy, Is Involved in Pancreatic Cell Proliferation
EI24, as a Component of Autophagy, Is Involved in Pancreatic Cell Proliferation Open
Autophagy is a highly conserved cellular process in which cytoplasmic materials are degraded and recycled as energy sources when nutrient supplies are lacking. Established tumor cells require autophagy for cell growth and tumor promotion. …
View article: Development of zebrafish medulloblastoma-like PNET model by TALEN-mediated somatic gene inactivation
Development of zebrafish medulloblastoma-like PNET model by TALEN-mediated somatic gene inactivation Open
Genetically engineered animal tumor models have traditionally been generated by the gain of single or multiple oncogenes or the loss of tumor suppressor genes; however, the development of live animal models has been difficult given that ca…
View article: C-terminally mutated tubby protein accumulates in aggresomes
C-terminally mutated tubby protein accumulates in aggresomes Open
The tubby protein (Tub), a putative transcription factor, plays important roles in the maintenance and function of neuronal cells. A splicing defect-causing mutation in the 3'-end of the tubby gene, which is predicted to disrupt the carbox…
View article: Fanconi anemia protein <scp>FANCD</scp>2 is activated by <scp>AICAR</scp>, a modulator of <scp>AMPK</scp> and cellular energy metabolism
Fanconi anemia protein <span>FANCD</span>2 is activated by <span>AICAR</span>, a modulator of <span>AMPK</span> and cellular energy metabolism Open
FANCD 2 is a pivotal molecule in the pathogenesis of Fanconi anemia ( FA ), an autosomal recessive human syndrome with diverse clinical phenotypes, including cancer predisposition, short stature, and hematological abnormalities. In our pre…
View article: The Effectiveness of Ferritin as a Contrast Agent for Cell Tracking MRI in Mouse Cancer Models
The Effectiveness of Ferritin as a Contrast Agent for Cell Tracking MRI in Mouse Cancer Models Open
Ferritin could be a good candidate as an endogenous MR contrast agent and a potential reporter gene that is capable of maintaining cell labeling stability and cellular safety.
View article: Histone variant H3F3A promotes lung cancer cell migration through intronic regulation
Histone variant H3F3A promotes lung cancer cell migration through intronic regulation Open
View article: AMP-activated protein kinase is involved in the activation of the Fanconi anemia/BRCA pathway in response to DNA interstrand crosslinks
AMP-activated protein kinase is involved in the activation of the Fanconi anemia/BRCA pathway in response to DNA interstrand crosslinks Open
Fanconi anemia complementation group (FANC) proteins constitute the Fanconi Anemia (FA)/BRCA pathway that is activated in response to DNA interstrand crosslinks (ICLs). We previously performed yeast two-hybrid screening to identify novel F…
View article: Aurora A kinase is required for activation of the Fanconi anemia/<scp>BRCA</scp> pathway upon <scp>DNA</scp> damage
Aurora A kinase is required for activation of the Fanconi anemia/<span>BRCA</span> pathway upon <span>DNA</span> damage Open
Previous studies have linked the DNA damage response to mitotic progression machinery. Mitotic kinases, such as Aurora A kinase and Polo‐like kinase, are involved in the phosphorylation of cell cycle regulators in response to DNA damage. H…
View article: DDRI-9: a novel DNA damage response inhibitor that blocks mitotic progression
DDRI-9: a novel DNA damage response inhibitor that blocks mitotic progression Open
The DNA damage response (DDR) is an emerging target for cancer therapy. By modulating the DDR, including DNA repair and cell cycle arrest, the efficacy of anticancer drugs can be enhanced and side effects reduced. We previously screened a …