作者
João Vinagre, Joana Nabais, Jorge Pinheiro, Rui Batista, Rui Caetano Oliveira, António Pedro Gonçalves, Ana Pestana, Marta Reis, Bárbara Mesquita, Vasco Pinto, Joana Lyra, Maria Augusta Cipriano, Miguel Godinho Ferreira, José Manuel Lopes, Manuel Sobrinho-Simões, Paula Soares
发表日期
2016/7/14
期刊
Scientific reports
卷号
6
期号
1
页码范围
29714
出版商
Nature Publishing Group UK
简介
One of the hallmarks of cancer is its unlimited replicative potential that needs a compensatory mechanism for the consequential telomere erosion. Telomerase promoter (TERTp) mutations were recently reported as a novel mechanism for telomerase re-activation/expression in order to maintain telomere length. Pancreatic endocrine tumors (PETs) were so far recognized to rely mainly on the alternative lengthening of telomeres (ALT) mechanism. It was our objective to study if TERTp mutations were present in pancreatic endocrine tumors (PET) and could represent an alternative mechanism to ALT. TERTp mutations were detected in 7% of the cases studied and were mainly associated to patients harbouring hereditary syndromes. In vitro, using PET-derived cell lines and by luciferase reporter assay, these mutations confer a 2 to 4-fold increase in telomerase transcription activity. These novel alterations are able to …
引用总数
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