ECE2014 Poster Presentations Thyroid Cancer (70 abstracts)
Gene expression signature associated with BRAFV600E mutation in human papillary thyroid carcinoma based on transgenic mouse model
Dagmara Rusinek 1 , Michal Swierniak 1, , Ewa Chmielik 3 , Monika Kowal 1 , Malgorzata Kowalska 1 , Agnieszka Czarniecka 4 , Cezary Przeorek 5 , Renata Cyplinska 1 , Michal Jarzab 6 , Wieslawa Widlak 7 & Barbara Jarzab 1
1Department of Nuclear Medicine and Endocrine Oncology, Institute of Oncology, MSC Memorial Cancer Center, Gliwice Branch, Gliwice, Poland; 2Genomic Medicine, Department of General, Transplant and Liver Surgery, Medical University of Warsaw, Warsaw, Poland; 3Department of Tumor Pathology, MSC Memorial Cancer Center, Institute of Oncology, Gliwice Branch, Gliwice, Poland; 4Oncologic Surgery Clinic, MSC Memorial Cancer Center, Institute of Oncology, Gliwice Branch, Gliwice, Poland; 5PET Diagnostics Department, MSC Memorial Cancer Center, Institute of Oncology, Gliwice Branch, Gliwice, Poland; 6III Radiotherapy Clinic, MSC Memorial Cancer Center, Institute of Oncology, Gliwice Branch, Gliwice, Poland; 7Center for Translational Research and Molecular Biology of Cancer, MSC Memorial Cancer Center, Institute of Oncology, Gliwice Branch, Gliwice, Poland.
Objectives: Recent studies on BRAFV600E mutation, known as initiating event in papillary thyroid carcinoma (PTC) and related to more aggressive clinical course of the disease, revealed its significant influence on gene expression profile suggesting that BRAF(+)PTCs represent a molecular subtype of PTC. However, the human material disables distinction of possible molecular causes of cancer from its effects, unlike the mouse model. The main goal of our project was to find genes deregulated in a BRAFV600E-dependent manner in human PTCs using the transgenic mouse model of BRAF-induced PTC.
Material and methods: The mice material included ten BRAF(+)PTCs, ten BRAF(+)borderline lesions, four BRAF(+) and four BRAF(−) colloid goiters (CG), five BRAF(+) and five BRAF(−) healthy thyroids (HT). The human material consisted on Polish cohort of patients (31 PTCs, 18 healthy thyroids) and data made available by Giordano et al. (41 PTCs). The microarray data were obtained with the Affymetrix platform. The bioinformatical analysis was oriented on finding BRAF-specific genes from CG and HT mice samples and verifying them on the human dataset. The potential differences between gene signatures of human PTCs with distinct molecular events have been analyzed as well. The microarray data were validated with the QPCR.
Results and conclusions: Over 800 genes were deregulated between BRAF(+) and BRAF(−) CG and HT mice samples. The analysis of distinct molecular PTC subtypes in human samples revealed that expression profile of obtained signatures for BRAF(+)PTCs and PTCs with RET rearrangements are more similar to each other than to RAS(+)PTCs. The last ones are much closer in their gene expression profile to WT-PTCs and healthy thyroids. Finally, 18 genes were selected as deregulated in BRAF(+)PTCs in comparison to each of the analyzed group. Next, 57 genes, differentially expressed between BRAF(+)PTCs and other groups except of RET(+)PTCs, are described.
Volume 35
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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