Corrigendum: Discovery of Novel and Clinically Relevant Markers in Formalin-Fixed Paraffin-Embedded Esophageal Cancer Specimen

摘要

In the original article, there was a mistake in Figure 2 and Figure 3 as published. The tissue sample N's were reported as (Normal = 20, Barrett's = 10, Tumor = 20), the actual N's analyzed were (Normal = 20, Barrett's = 7, Tumor = 18). The units for the mass spec quantification data in the Figure 2 and Figure 3 were listed as femtomol per microgram (fmol/μg), however, it should have been classified as “Relative Expression.” The corrected Figure 2 and Figure 3 appears below. Figure 2 Upregulated proliferation markers. These six markers are associated with more advanced progression in various cancers and were found to be upregulated or overexpressed in our cohort's esophageal adenocarcinoma tumor tissue compared to normal squamous esophageal epithelium, possibly contributing to enhanced invasiveness and shorter overall survival. **** P & 0.0001, *** P & 0.001, ** P & 0.01, * P & 0.1. Figure 3 Downregulated tumor suppressors. These six markers are associated with inducing programmed cell death in various cancers and were found to be downregulated in our cohort's esophageal adenocarcinoma tumor tissue compared to normal squamous esophageal epithelium, possibly contributing to enhanced invasiveness and shorter overall survival. **** P & 0.0001, *** P & 0.001, ** P & 0.01, * P & 0.1. Additionally, in the introduction it was reported that 50 tissues were analyzed via mass spectrometry. Forty-five tissue samples were used for the mass spectrometry quantification. In the results section, T-scores were reported rather than the magnitude of expression differences between the normal and esophageal adenocarcinoma tissue in all 12 reported markers of interest. A correction has been made to the Materials and Methods , subsection Patient Selection : “For the mass spectrometry arm of our study we utilized 18 esophageal adenocarcinoma, 7 Barrett's esophagus, and 20 normal squamous mucosa samples, all randomly selected. 15 of the 45 specimens (33%) were from female patients, which reflects the national percentages of gender manifestations for this disease. Ten of the 20 normal esophagus specimen and 9 of the 18 adenocarcinoma specimen were from patients with no visible Barrett's esophagus (50%).” Furthermore, corrections have been made to the Results , subsection Proliferation Markers (Prognostic) : HMGB1 “HMGB1, or high mobility group box 1, is located in the nucleus and is one of the major chromatin-associated non-histone proteins, acting as a DNA chaperone involved in replication, transcription, chromatin remodeling, and DNA repair (35) (for expression patterns of all six proteins, see Figure 2 ). Treatment with HMGB1 inhibitors prolonged the survival of malignant mesothelioma xenograft mice (14). HMGB1 overexpression is associated with poorer prognosis in colorectal cancer patients (15). HMGB1 was expressed 2.33x more in EAC tumors compared to the adjacent normal esophagus epithelium according to our findings ( P & 0.0001).” KRT7 “KRT7, or keratin 7, stimulates DNA synthesis in several cell types. Aberrant expression of KRT7 in budding cancer cells represents a modification of the epithelial phenotype (epithelial–epithelial transition) which may be linked to gains in motility and invasive potential (18). KRT7 expression is associated with a higher morbidity and a higher progression in colorectal cancer (18). KRT7 is overexpressed 11.67x more in EAC tumors compared to normal esophageal tissue according to our findings ( P & 0.0001).” LGALS3BP “LGALS3BP, or Galectin-3-binding protein, promotes integrin-mediated cell adhesion associated with cancer. This protein has a high affinity for beta-galactoside and has been found to be expressed in many tumor cells associated with aggressive carcinogenesis (19). Breast and lung cancer cells overexpressing LGALS3BP demonstrated resistance to apoptosis in response to cisplatin (20). We found that LGALS3BP is overexpressed at a 3.50x greater level in EAC tumor cells compared to normal esophageal cells ( P & 0.0001).” LTF “LTF, or lactotransferrin, stimulates the TLR4-signaling pathway, leading to NFkβ activation and subsequent pro-inflammatory cytokine production while also interfering with the lipopolysaccharide-stimulated TLR4 signaling and also stimulates VEGF-mediated endothelial cell migration and proliferation (21). Malignant transformation of endometrial tissue is associated with overexpressed LTF (22). LTF is expressed at a 9.56x greater level in EAC tumors compared to normal esophageal tissue according to our findings ( P & 0.0001).” PRMT1 “PRMT1 is the main enzyme that mediates the methylation of histone H4, a specific tag for epigenetic transcriptional activation. PRMT1 has also been identified as a key regulator of the epithelial–mesenchymal transition in breast cancer (36). PRMT1 expression is associated with poor prognosis in gastric cancer patients and has been observed to be significant