| Literature DB >> 31572061 |
Matteo Fassan1, Luca Vianello1, Diana Sacchi1, Giuseppe N Fanelli1, Giada Munari1, Marco Scarpa2, Rocco Cappellesso1, Fotios Loupakis3, Cristiano Lanza1, Roberta Salmaso1, Claudia Mescoli1, Nicola Valeri4,5, Marco Agostini2,6,7, Edoardo D'Angelo2, Sara Lonardi3, Salvatore Pucciarelli4, Nicola Veronese8,9, Claudio Luchini10, Massimo Rugge1,11.
Abstract
[This corrects the article DOI: 10.1186/s12935-018-0634-8.].Entities:
Year: 2019 PMID: 31572061 PMCID: PMC6757372 DOI: 10.1186/s12935-019-0966-z
Source DB: PubMed Journal: Cancer Cell Int ISSN: 1475-2867 Impact factor: 5.722
Fig. 2a Mutational profiling of the 15 cases profiled through a hotspot multigene mutational custom panel, including 164 hotspot regions of AKT1, APC, BRAF, CTNNB1, KIT, KRAS, NRAS, PDGFRA, PIK3CA, PTEN and TP53 genes. In red are the samples showing a different mutational landscape in comparison to the other matched samples (scale bars = 100 µm). b Representative Sequenom MassArray output profiles for KRAS c.436G> A (p.A146T), PIK3CA c.1634A>C (p.E545A), BRAF c1799T>A (p.V600E) and NRAS c.35G>A (p.G12D) mutations. On the right the correspondent Sanger chromatogram