Mei-Kuang Chen

发表

H2O2 induces nuclear transport of the receptor tyrosine kinase c-MET in breast cancer cells via a membrane-bound retrograde trafficking mechanism

M. Hung, Lin-lin Sun, J. Hsu, 2019, The Journal of Biological Chemistry.

Selective small molecule PARG inhibitor causes replication fork stalling and cancer cell death

J. Tainer, J. Houl, M. Hung, 2019, Nature Communications.

Inhibition of c-MET upregulates PD-L1 expression in lung adenocarcinoma.

M. Hung, Yun-Ju Lai, Li-Chuan Chan, 2020, American journal of cancer research.

Exploiting induced vulnerability to overcome PARPi resistance and clonal heterogeneity in BRCA mutant triple-negative inflammatory breast cancer.

K. Do, M. Hung, W. J. Zheng, 2022, American journal of cancer research.

Efficacy of PARP inhibition combined with EZH2 inhibition depends on BRCA mutation status and microenvironment in breast cancer

Mei-Kuang Chen, 2021, The FEBS journal.

Targeting the ALK–CDK9-Tyr19 kinase cascade sensitizes ovarian and breast tumors to PARP inhibition via destabilization of the P-TEFb complex

G. Hortobagyi, M. Hung, A. Sood, 2022, Nature Cancer.

PARP Inhibitor Upregulates PD-L1 Expression and Enhances Cancer-Associated Immunosuppression

G. Hortobagyi, M. Hung, Seung-Oe Lim, 2017, Clinical Cancer Research.

Synergism of PARP inhibitor fluzoparib (HS10160) and MET inhibitor HS10241 in breast and ovarian cancer cells.

G. Hortobagyi, L. Nie, M. Hung, 2019, American journal of cancer research.

Blocking c-Met-mediated PARP1 phosphorylation enhances anti-tumor effects of PARP inhibitors

Chien-Liang Liu, Morag Park, Hirohito Yamaguchi, 2016, Nature Medicine.

Definition of PKC-α, CDK6, and MET as therapeutic targets in triple-negative breast cancer.

G. Mills, Jun Yao, G. Hortobagyi, 2014, Cancer research.

Definition of PKC-α , CDK 6 , and MET as therapeutic targets in triple-negative breast cancer

G. Mills, Jun Yao, G. Hortobagyi, 2014 .

Therapeutics , Targets , and Chemical Biology De fi nition of PKC-a , CDK 6 , and MET as Therapeutic Targets in Triple-Negative Breast Cancer

G. Mills, Jun Yao, G. Hortobagyi, 2014 .

Inhibition of ATR downregulates PD-L1 and sensitizes tumor cells to T cell-mediated killing.

M. Hung, B. Shao, Lin-lin Sun, 2018, American journal of cancer research.

Irradiation-induced dynamic changes of gene signatures reveal gain of metastatic ability in nasopharyngeal carcinoma.

M. Hung, Dung-Fang Lee, R. Zhao, 2019, American journal of cancer research.

NUCLEAR TRANSLOCATION OF MET VIA INTERNET MECHANISM

Mei-Kuang Chen, 2014 .

Proteolytic cleavage, trafficking, and functions of nuclear receptor tyrosine kinases

M. Hung, Mei-Kuang Chen, 2015, The FEBS journal.

EGFR and c-MET Cooperate to Enhance Resistance to PARP Inhibitors in Hepatocellular Carcinoma.

M. Hung, Chunxiao Liu, Yufan Qiu, 2018, Cancer research.

A tumor vessel-targeting fusion protein elicits a chemotherapeutic bystander effect in pancreatic ductal adenocarcinoma.

R. DePinho, R. Bouchard, M. Hung, 2017, American journal of cancer research.

Regulation of therapeutic resistance in cancers by receptor tyrosine kinases.

M. Hung, Mei-Kuang Chen, 2016, American journal of cancer research.

Nuclear receptor tyrosine kinase transport and functions in cancer.

M. Hung, J. Hsu, Mei-Kuang Chen, 2020, Advances in cancer research.

Blocking c-Met and EGFR reverses acquired resistance of PARP inhibitors in triple-negative breast cancer.

Jeffrey T. Chang, K. Hess, G. Hortobagyi, 2020, American journal of cancer research.

PD-L1 deficiency sensitizes tumor cells to DNA-PK inhibition and enhances cGAS-STING activation.

Jiaming Song, M. Hung, Lin-lin Sun, 2022, American journal of cancer research.

Proteolytic cleavage, trafficking, and functions of nuclear receptor tyrosine kinases

M. Hung, Mei-Kuang Chen, 2015, The FEBS journal.

Nuclear translocation of the receptor tyrosine kinase c-MET reduces the treatment efficacies of olaparib and gemcitabine in pancreatic ductal adenocarcinoma cells.

M. Hung, Dihua Yu, Ying-bin Liu, 2021, American journal of cancer research.