| Literature DB >> 29859122 |
Duarte Mendes Oliveira1, Katia Grillone1, Chiara Mignogna2, Valentina De Falco3, Carmelo Laudanna1, Flavia Biamonte1, Rosa Locane4, Francesco Corcione5, Massimiliano Fabozzi5, Rosario Sacco4, Giuseppe Viglietto6, Donatella Malanga7, Antonia Rizzuto4.
Abstract
In the publication of this article [1], there is an error in Fig. 7. The minus and plus signals are inverted which impairs understanding of the results described.Entities:
Year: 2018 PMID: 29859122 PMCID: PMC5984746 DOI: 10.1186/s13046-018-0776-5
Source DB: PubMed Journal: J Exp Clin Cancer Res ISSN: 0392-9078
Fig. 7From: Next-generation sequencing analysis of receptor-type tyrosine kinase genes in surgically resected colon cancer: identification of gain-of-function mutations in the RET proto-oncogene. The RET-G533C mutant is inhibited by vandetanib. a. MTT assay was performed in the presence of two different concentrations of vandetanib. HEK293 cells expressing pBabe were used as negative control and HEK293 cells expressing RET-C634R mutant were used as positive control. Values are shown as bar graphs and all results are the average of experiments performed in triplicate. Statistical significance compared with vehicle was evaluated by Two-Way ANOVA (with multiple comparison Dunnet’s test) (n = 3; **p < 0.01; ***p < 0.001). b. Immunoblot analysis of RET/MAPK pathway (with anti-phosphoY1062 RET, anti-RET, anti phospho-Y202T204 ERK1/2, anti-ERK1/2 antibodies) of HEK293 cells transfected with RET-G533C mutant treated with vehicle or vandetanib (500 nM) for 2 h. HEK293 cells transfected with RET-634 mutant were used as control