V. Pirazzoli

发表

Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5

F. Orsenigo, F. Breviario, E. Dejana, 2008, Nature Cell Biology.

ROLE OF VITRONECTIN INTERACTION IN THE BIOLOGY OF THE UROKINASE RECEPTOR

V. Pirazzoli, 2011 .

Direct evidence of the importance of vitronectin and its interaction with the urokinase receptor in tumor growth.

V. Pirazzoli, N. Sidenius, G. S. Ferraris, 2013, Blood.

De novo selection of oncogenes

K. Politi, D. DiMaio, V. Pirazzoli, 2013, Proceedings of the National Academy of Sciences.

Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells.

D. Rimm, S. Kobayashi, K. Politi, 2016, Cell reports.

HER2 amplification: a potential mechanism of acquired resistance to EGFR inhibition in EGFR-mutant lung cancers that lack the second-site EGFRT790M mutation.

M. Ladanyi, M. Kris, W. Pao, 2012, Cancer discovery.

Next-generation sequencing of paired tyrosine kinase inhibitor-sensitive and -resistant EGFR mutant lung cancer cell lines identifies spectrum of DNA changes associated with drug resistance

Junfeng Xia, Peilin Jia, William Pao, 2013, Genome research.

resistance lines identifies spectrum of DNA changes associated with drug inhibitor-sensitive and-resistant EGFR mutant lung cancer cell Next-generation sequencing of paired tyrosine kinase Material Supplemental

Zhongming Zhao, P. Jia, W. Pao, 2013 .

Noncovalent wild-type-sparing inhibitors of EGFR T790M.

J. Settleman, K. Politi, S. Sideris, 2013, Cancer discovery.

Abstract B10: Acquired resistance to afatinib plus cetuximab in EGFR-mutant lung adenocarcinoma may be mediated by EGFR overexpression and overcome by the mutant-specific EGFR inhibitor, AZD9291.

X. Chen, M. Ladanyi, E. Stanchina, 2014 .

Acquired resistance of EGFR-mutant lung adenocarcinomas to afatinib plus cetuximab is associated with activation of mTORC1.

Peilin Jia, William Pao, Zhongming Zhao, 2014, Cell reports.

Afatinib plus Cetuximab Delays Resistance Compared to Single-Agent Erlotinib or Afatinib in Mouse Models of TKI-Naïve EGFR L858R-Induced Lung Adenocarcinoma

F. Hyder, W. Pao, K. Politi, 2015, Clinical Cancer Research.

HER2 Amplifi cation: A Potential Mechanism of Acquired Resistance to EGFR Inhibition in EGFR -Mutant Lung Cancers That Lack the Second-Site EGFR

M. Ladanyi, M. Kris, E. Stanchina, 2012 .

HER 2 Amplifi cation : A Potential Mechanism of Acquired Resistance to EGFR Inhibition in EGFR-Mutant Lung Cancers That Lack the Second-Site EGFR T 790 M Mutation

M. Ladanyi, M. Kris, E. Stanchina, 2012 .

Optimizing the Sequence of Anti-EGFR–Targeted Therapy in EGFR-Mutant Lung Cancer

X. Chen, Zhongming Zhao, M. Ladanyi, 2014, Molecular Cancer Therapeutics.

Whole-exome sequencing of cervical carcinomas identifies activating ERBB2 and PIK3CA mutations as targets for combination therapy

Gloria S. Huang, L. Alexandrov, T. Boggon, 2019, Proceedings of the National Academy of Sciences.

Generation of drug-resistant tumors using intermittent dosing of tyrosine kinase inhibitors in mouse.

K. Politi, V. Pirazzoli, 2014, Cold Spring Harbor Protocols.

HER2 amplification: a potential mechanism of acquired resistance to EGFR inhibition in EGFR-mutant lung cancers that lack the second-site EGFRT790M mutation.

M. Ladanyi, M. Kris, W. Pao, 2012, Cancer discovery.