Corrections:

Marta Mellai^1,*, Monica Cattaneo^2,*, Alessandra Maria Storaci², Laura Annovazzi¹, Paola Cassoni³, Antonio Melcarne⁴, Pasquale De Blasio⁶, Davide Schiffer¹ and Ida Biunno^2,5

¹ Neuro-Bio-Oncology Center/Policlinico di Monza Foundation, Vercelli 13100, Italy
² Institute for Genetic and Biomedical Research, National Research Council, Milan 20138, Italy
³ Department of Medical Sciences, University of Turin/Città della Salute e della Scienza, Turin 10126, Italy
⁴ Department of Neurosurgery, CTO Hospital/Città della Salute e della Scienza, Turin 10126, Italy
⁵ IRCCS-Multimedica, Milan 20138, Italy
⁶ ISENET Stem Cell Bank, Milan 20138, Italy
^* These authors have contributed equally to this work

Published: August 24, 2018

This article has been corrected: In the paragraph titled "Single nucleotide genetic variant selection" on page 12463, the term “somatic mutation” was incorrectly substituted for “genetic mutation”. The correct term has been included below:

The SEL1L gene spans more than 62.24 kb pairs within a “gene desert region” and displays only weak linkage disequilibrium pattern according to the HapMap CEU population data. A total of five single nucleotide genetic variants in the SEL1L gene (GenBank Reference sequence NM_005065) were selected (Table 6). Two of them (c.–366T > C and c.–354T > C) were first identified in the minimal promoter region of the SEL1L gene in lung carcinoma patients [47]. The c.341–88T > C genetic variant is a common SNP (rs12435998) within intron 3, containing potential binding sites for transcription factors involved in ER-induced stress, and it is a predicted splice site [23]. The c.485A > G (p.Asp162Gly) variant corresponds to the SNP rs11499034, maps in exon 4 encoding for the fibronectin type II domain (FN2), and affects a highly conserved amino acid residue [24]. The amino acid change from Asp to Gly may have a disruptive role in the collagen binding. The c.1972T > C (p.Ser658Pro) variant in exon 19 has been described as genetic mutation responsible for the progressive early-onset cerebellar ataxia in canine species [49]. Of note, the SEL1L gene is highly conserved between dog and human, with 98% identity at protein level (HomoloGene). The Ser658 residue located in the eleventh SEL1L-like repeat is completely conserved in all aligned vertebrates and maps within a functionally relevant domain for tumor growth inhibition [50].

Original article: Oncotarget. 2015; 6:12452-12467. DOI: https://doi.org/10.18632/oncotarget.3611.