Area of research
Molecular Biology · Immunology
Research interest
Research interests include Glycosylation and Glycoproteins Research, Immunotherapy and Immune Responses, Monoclonal and Polyclonal Antibodies Research, and RNA modifications and cancer.
M1C mediates LINE-1 transcription in PARP inhibitor-treated prostate cancer cells
MUC1-C dependency in drug resistant HR+/HER2- breast cancer identifies a new target for antibody-drug conjugate treatment.
MUC1-C auto-regulatory complex with EBNA1 is responsible for latent Epstein-Barr virus-associated gastric cancer progression.
Activation of APOBEC3 cytidine deaminases and endogenous retroviruses is integrated by MUC1-C in NSCLC cells.
MUCIN 1 confers inflammatory memory of tyrosine kinase inhibitor resistance in non-small cell lung cancer.
Targeting KRAS Inhibitor-Resistant Pancreatic Cancer with an MUC1-C Antibody-Drug Conjugate.
Figure S6 from Targeting KRAS Inhibitor–Resistant Pancreatic Cancer with an MUC1-C Antibody–Drug Conjugate
Figure S2 from Targeting KRAS Inhibitor–Resistant Pancreatic Cancer with an MUC1-C Antibody–Drug Conjugate
Figure 1 from Dependence on the MUC1-C Oncoprotein in Classic, Variant, and Non–neuroendocrine Small Cell Lung Cancer
Figure S7 from Targeting KRAS Inhibitor–Resistant Pancreatic Cancer with an MUC1-C Antibody–Drug Conjugate
Figure 6 from MUC1-C Dictates JUN and BAF-Mediated Chromatin Remodeling at Enhancer Signatures in Cancer Stem Cells
Figure 5 from MUC1-C Dictates JUN and BAF-Mediated Chromatin Remodeling at Enhancer Signatures in Cancer Stem Cells
Figure 2 from MUC1-C Dictates JUN and BAF-Mediated Chromatin Remodeling at Enhancer Signatures in Cancer Stem Cells
Figure 4 from Dependence on the MUC1-C Oncoprotein in Classic, Variant, and Non–neuroendocrine Small Cell Lung Cancer
Figure 4 from MUC1-C Dictates PBRM1-Mediated Chronic Induction of Interferon Signaling, DNA Damage Resistance, and Immunosuppression in Triple-Negative Breast Cancer
Figure 1 from MUC1-C Dictates PBRM1-Mediated Chronic Induction of Interferon Signaling, DNA Damage Resistance, and Immunosuppression in Triple-Negative Breast Cancer
Figure 4 from MUC1-C Dictates JUN and BAF-Mediated Chromatin Remodeling at Enhancer Signatures in Cancer Stem Cells
Figure 2 from MUC1-C Dictates PBRM1-Mediated Chronic Induction of Interferon Signaling, DNA Damage Resistance, and Immunosuppression in Triple-Negative Breast Cancer
M1C is a druggable target for NSCLC KRAS G12C mutant tumors resistant to KRAS inhibitors
Figure 5 from Dependence on the MUC1-C Oncoprotein in Classic, Variant, and Non–neuroendocrine Small Cell Lung Cancer
Figure 6 from Dependence on the MUC1-C Oncoprotein in Classic, Variant, and Non–neuroendocrine Small Cell Lung Cancer
Supplementary Data1 from Targeting KRAS Inhibitor–Resistant Pancreatic Cancer with an MUC1-C Antibody–Drug Conjugate
Supplemental Table S1 from Targeting KRAS Inhibitor–Resistant Pancreatic Cancer with an MUC1-C Antibody–Drug Conjugate
Figure 2 from Dependence on the MUC1-C Oncoprotein in Classic, Variant, and Non–neuroendocrine Small Cell Lung Cancer
Data from MUC1-C Dictates PBRM1-Mediated Chronic Induction of Interferon Signaling, DNA Damage Resistance, and Immunosuppression in Triple-Negative Breast Cancer
Figure S8 from Targeting KRAS Inhibitor–Resistant Pancreatic Cancer with an MUC1-C Antibody–Drug Conjugate
Figure S5 from Targeting KRAS Inhibitor–Resistant Pancreatic Cancer with an MUC1-C Antibody–Drug Conjugate
Figure 7 from MUC1-C Dictates PBRM1-Mediated Chronic Induction of Interferon Signaling, DNA Damage Resistance, and Immunosuppression in Triple-Negative Breast Cancer
Figure 3 from MUC1-C Dictates PBRM1-Mediated Chronic Induction of Interferon Signaling, DNA Damage Resistance, and Immunosuppression in Triple-Negative Breast Cancer
Figure 3 from MUC1-C Dictates JUN and BAF-Mediated Chromatin Remodeling at Enhancer Signatures in Cancer Stem Cells