@misc{10481/101016,
year = {2016},
month = {11},
url = {https://hdl.handle.net/10481/101016},
abstract = {Erlotinib is an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that showed activity against pancreatic ductal adenocarcinoma (PDAC). The drug's most frequently reportedside effectasa result ofEGFR inhibition is skin rash (SR), a symptom which has been associated with a better therapeutic response to the drug. Gene expression profiling can be used as a tool to predict which patients will develop this important cutaneous manifestation. The aim of the present study was to identify which genes may influence the appearance of SR in PDAC patients. The study included 34 PDAC patients treated with erlotinib: 21 patients developed any grade of SR, while 13 patients did not (controls). Before administering any chemotherapy regimen and the development of SR,we collected RNA from peripheral blood samples of all patients and studied the differential gene expression pattern using the Illumina microarray platform HumanHT-12 v4 Expression BeadChip. Seven genes (FAM46C, IFITM3, GMPR, DENND6B, SELENBP1, NOL10,andSIAH2),involved in different pathways including regulatory, migratory, and signalling processes, were downregulated in PDAC patients with SR. Our results suggest the existence of a gene expression profiling significantly correlated with erlotinib-induced SR in PDAC that could be used as prognostic indicator in this patients.},
organization = {This work was supported by the Spanish Ministry of Economy and Competitiveness [grant number TIN2015-71873-R], and the Instituto de Salud Carlos III [grant number DTS15/00201]},
publisher = {Elsevier},
keywords = {Pancreatic ductal adenocarcinoma},
keywords = {Erlotinib},
keywords = {Skin},
keywords = {Microarray},
title = {Identification of gene expression profiling associated with erlotinib-related skin toxicity in pancreatic adenocarcinoma patients},
doi = {10.1016/j.taap.2016.10.003},
author = {Caba Pérez, Octavio and Irigoyen, Antonio and Jiménez Luna, Cristina and Benavides, Manuel and Ortuño, Francisco M. and Gallego, Javier and Rojas Ruiz, Ignacio and Guillen-Ponce, Carmen and Torres Perales, Carolina and Aranda, Enrique and Prados Salazar, José Carlos},
}