It has been suggested that Id-1 has a critical role in the tumour progression and aggressiveness of several human cancers. However, the clinicopathological and biological significance of Id-1 overexpression remains unclear in human primary cancer. To investigate the association between Id-1 expression and cell proliferation or tumour angiogenesis, we examined the cell cycle kinetic indices (the proliferation and apoptotic indices, PI and AI) and intratumoral microvessel density (MVD) in 65 human pancreatic cancers. We also investigated the relationship between its expression and various clinicopathological factors to determine the clinical significance of Id-1 overexpression. Out of a total 65 cases, 32 (49.3%) showed overexpression of Id-1 vs normal tissues. Id-1 expression was found to be significantly associated with MVD (P ¼ 0.002). In further analysis of subgroups with higher and lower Id-1 expression, tumours with higher Id-1 expression (scores 4 and 5) showed significantly higher MVD than tumours with lower expression of Id-1 (scores 2 and 3) (111.18757.14 vs 64.13728.19, Po0.001). However, no significant association was found between Id-1 overexpression and patient survival rate. No significant association was also found between Id-1 expression and cell cycle kinetic indices (PI or AI) in pancreatic cancer. Moreover, the overexpression of Id-1 protein was not correlated with any significant clinicopathologic factors. These findings indicate that Id-1 overexpression is closely related with tumour angiogenesis and a higher density of intratumoral vessel, but that it is not associated with a poorer prognosis of survival or a higher cell proliferative potential in human pancreatic cancer.

It has been brought to our attention that there is a possible error in Figure 5 of the above paper whereby the western blot panel for beta-catenin representing the two cell lines MKN45 and MKN7 cells is identical. On inspection we agree with this observation, which is clearly an error on our part and which was also missed during the peer review process. Unfortunately we are unable to access the original gels and it is therefore not possible to offer the journal a full corrigendum, but nevertheless we feel it is important to acknowledge the error and formally put it on the record. Figure 5 in this paper represents our study of the linkage between E-cadherin and beta-catenin in these cell lines. Previous (Shibamoto et al, 1994) and subsequent publications (Ono et al, 2004;Atsumi et al, 2007) looking at the E-cadherin-catenin complex in these cell lines have shown concordant results with the conclusions of our paper, where we show that despite the similar expression and interaction of the E-cadherin and betacatenin in both cell lines, cell to cell adhesion characteristics are different. Other authors have proposed this to be due to other factors influencing cellcell adhesion, such as differences in tyrosine phosphorylation levels of these proteins. Our paper is purely descriptive and our findings are supported by other publications in the field. We therefore conclude that this error in Figure 5 does not alter interpretation of the findings of our paper.We have scrutinised the other data and images in the paper and can confidently confirm that there are no further errors or inaccuracies.This note has been approved by all the authors below: Current addresses: Aida U Jawhari, Queens Medical Centre, Nottingham, UK Michael JG Farthing, Vice-Chancellor, Sussex House, University of Sussex, Brighton, UK Massimo Pignatelli, Nazarbayev University Astana, Kazakhstan Estimating the asbestos-related lung cancer burden from mesothelioma mortality Following the publication of this paper, an omission was recognised. It is corrected below. REFERENCES CONFLICT OF INTERESTPB has acted as an expert witness in a trial involving asbestos exposure in the manufacture of synthetic polymers and risk of mesothelioma. VMcC, JP, GB and KS declare no conflicts of interest.