E. Buck

发表

EGFR Oncogenes Expressed In Glioblastoma Are Activated As Covalent Dimers And Paradoxically Stimulated By Erlotinib

A. Flohr, A. Mayweg, N. Ishiyama, 2019, bioRxiv.

Retrospective biochemical screening of fatty acid oxidation disorders in postmortem livers of 418 cases of sudden death in the first year of life.

T. Cowan, R. Boles, M. Blitzer, 1998, The Journal of pediatrics.

Compensatory Insulin Receptor (IR) Activation on Inhibition of Insulin-Like Growth Factor-1 Receptor (IGF-1R): Rationale for Cotargeting IGF-1R and IR in Cancer

S. Koujak, P. Gokhale, E. Brown, 2010, Molecular Cancer Therapeutics.

The effect of the flavonoid quercetin on phase 1 and phase 2 enzyme activities in the SW-480 human colon carcinoma cell line

E. Buck, 2003 .

Old dog, new tricks: extracellular domain arginine methylation regulates EGFR function.

D. Epstein, E. Buck, 2015, The Journal of clinical investigation.

Small molecule inhibitors of the IGF-1R/IR axis for the treatment of cancer

E. Buck, M. Mulvihill, 2011, Expert opinion on investigational drugs.

Cloning, expression, and chromosomal assignment of the human mitochondrial intermediate peptidase gene (MIPEP).

G. Sirugo, P. Rinaldo, G. Isaya, 1997, Genomics.

Discovery of an Orally Efficacious Imidazo[5,1-f][1,2,4]triazine Dual Inhibitor of IGF-1R and IR.

D. Werner, P. Gokhale, E. May, 2010, ACS medicinal chemistry letters.

Feedback mechanisms promote cooperativity for small molecule inhibitors of epidermal and insulin-like growth factor receptors.

S. Thomson, D. Epstein, J. Haley, 2008, Cancer research.

A novel, potent, and selective insulin-like growth factor-I receptor kinase inhibitor blocks insulin-like growth factor-I receptor signaling in vitro and inhibits insulin-like growth factor-I receptor–dependent tumor growth in vivo

N. Gibson, L. Arnold, J. Pachter, 2007, Molecular Cancer Therapeutics.

Abstract 1632: Co-targeting mTOR and IGF-1R/IR results in synergistic activity against a broad array of tumor cell lines, independent ofKRASmutation status

D. Epstein, M. Miglarese, S. Russo, 2010 .

Rapamycin synergizes with the epidermal growth factor receptor inhibitor erlotinib in non–small-cell lung, pancreatic, colon, and breast tumors

Siobhan McCormack, E. Brown, F. Petti, 2006, Molecular Cancer Therapeutics.

Discovery of OSI-906: a selective and orally efficacious dual inhibitor of the IGF-1 receptor and insulin receptor.

N. Gibson, L. Arnold, K. Foreman, 2009, Future medicinal chemistry.

Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions

S. Thomson, F. Petti, Izabela Sujka-Kwok, 2008, Clinical & Experimental Metastasis.

Epithelial to mesenchymal transition is a determinant of sensitivity of non-small-cell lung carcinoma cell lines and xenografts to epidermal growth factor receptor inhibition.

E. Brown, S. Thomson, F. Petti, 2005, Cancer research.

Utilizing combinations of molecular targeted agents to sensitize tumor cells to EGFR inhibitors

E. Buck, A. Eyzaguirre, K. Iwata, 2008 .

Mechanisms of resistance to EGFR tyrosine kinase inhibitors: implications for patient selection and drug combination strategies

J. Haley, M. Miglarese, E. Buck, 2008, Targeted Oncology.

Epithelial–Mesenchymal Transition Predicts Sensitivity to the Dual IGF-1R/IR Inhibitor OSI-906 in Hepatocellular Carcinoma Cell Lines

Hui Zhao, D. Epstein, M. Miglarese, 2011, Molecular Cancer Therapeutics.

Small-molecule ATP-competitive dual IGF-1R and insulin receptor inhibitors: structural insights, chemical diversity and molecular evolution.

Jing Wang, E. Buck, M. Mulvihill, 2012, Future medicinal chemistry.

A kinome-wide screen identifies the insulin/IGF-I receptor pathway as a mechanism of escape from hormone dependence in breast cancer.

G. Mills, J. Balko, Y. Shyr, 2011, Cancer research.

Molecular Medicine in Practice Epithelial – Mesenchymal Transition Predicts Sensitivity to the Dual IGF-1 R / IR Inhibitor OSI-906 in Hepatocellular Carcinoma Cell Lines

Hui Zhao, D. Epstein, M. Miglarese, 2012 .

Pursuit of personalized anticancer therapy: leveraging collaboration between academia and the biotech/pharmaceutical industry.

E. Buck, M. Mulvihill, K. Iwata, 2010, The Mount Sinai journal of medicine, New York.

Modulation of Insulin-Like Growth Factor-1 Receptor and its Signaling Network for the Treatment of Cancer: Current Status and Future Perspectives

E. Buck, M. Mulvihill, Meizhong Jin, 2013, Oncology reviews.

Loss of homotypic cell adhesion by epithelial-mesenchymal transition or mutation limits sensitivity to epidermal growth factor receptor inhibition

J. Haley, N. Gibson, E. Buck, 2007, Molecular Cancer Therapeutics.

Inactivation of Akt by the epidermal growth factor receptor inhibitor erlotinib is mediated by HER-3 in pancreatic and colorectal tumor cell lines and contributes to erlotinib sensitivity

J. Haley, N. Gibson, E. Buck, 2006, Molecular Cancer Therapeutics.

Organization and Functions of Interacting Domains for Signaling by Protein-Protein Interactions

Ravi Iyengar, Elizabeth Buck, R. Iyengar, 2003, Science's STKE.

In vivo evaluation of OSI-906, a novel small molecule kinase inhibitor of the insulin-like growth factor-1 receptor (IGF-1R)

R. Wild, J. Pachter, E. Buck, 2007 .

The Discovery of Dual IGF‐1R and IR Inhibitor FQIT for the Treatment of Cancer

E. Buck, M. Mulvihill, Meizhong Jin, 2012 .

Disulfide trapping to localize small-molecule agonists and antagonists for a G protein-coupled receptor.

Elizabeth Buck, James A Wells, E. Buck, 2005, Proceedings of the National Academy of Sciences of the United States of America.

Site-specific Disulfide Capture of Agonist and Antagonist Peptides on the C5a Receptor*

Elizabeth Buck, H. Bourne, James A Wells, 2005, Journal of Biological Chemistry.

Computational and Functional Analyses of HER2 Mutations Reveal Allosteric Activation Mechanisms and Altered Pharmacologic Effects

G. Frampton, J. Hopkins, N. Ishiyama, 2022, Cancer research.