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Background  The molecular mechanisms driving the papillary thyroid carcinoma (PTC) are still poorly understood. The most frequent genetic alteration in PTC is the  BRAF V600E mutation–its impact may extend even beyond PTC genomic profile and influence the tumor characteristics and even clinical behavior.    Methods  In order to identify  BRAF -dependent signature of early carcinogenesis in PTC, a transgenic mouse model with  BRAF V600E-induced PTC was developed. Mice thyroid samples were used in microarray analysis and the data were referred to a human thyroid dataset.    Results  Most of  BRAF (+) mice developed malignant lesions. Nevertheless, 16% of  BRAF (+) mice displayed only benign hyperplastic lesions or apparently asymptomatic thyroids. After comparison of non-malignant  BRAF (+) thyroids to  BRAF (−) ones, we selected 862 significantly deregulated genes. When the mouse  BRAF -dependent signature was transposed to the human HG-U133A microarray, we identified 532 genes, potentially indicating the  BRAF  signature (representing early changes, not related to developed malignant tumor). Comparing  BRAF (+) PTCs to healthy human thyroids, PTCs without  BRAF  and  RET  alterations and  RET (+),  RAS (+) PTCs, 18 of these 532 genes displayed significantly deregulated expression in all subgroups. All 18 genes, among them 7 novel and previously not reported, were validated as  BRAF V600E-specific in the dataset of independent PTC samples, made available by The Cancer Genome Atlas Project.    Conclusion  The study identified 7  BRAF -induced genes that are specific for  BRAF V600E -driven PTC and not previously reported as related to  BRAF  mutation or thyroid carcinoma:  MMD ,  ITPR3 ,  AACS ,  LAD1 ,  PVRL3 ,  ALDH3B1 , and  RASA1 . The full signature of  BRAF -related 532 genes may encompass other  BRAF -related important transcripts and require further study.

BRAFV600E-Associated Gene Expression Profile: Early Changes in the Transcriptome, Based on a Transgenic Mouse Model of Papillary Thyroid Carcinoma