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• W2896914319 abstract "Background: The PTEN tumour suppressor gene and PIK3CA proto-oncogene encode proteins which contribute to regulation and propagation of signal transduction through the PI3K/AKT signalling pathway. This study investigates the prevalence of loss of PTEN expression and mutations in both PTEN and PIK3CA in colorectal cancers (CRC) and their associations with tumour clinicopathological features, lifestyle factors and dietary consumptions. Methods: 186 adenocarcinomas and 16 adenomas from the EPIC Norfolk study were tested for PTEN and PIK3CA mutations by DNA sequencing and PTEN expression changes by immunohistochemistry. Dietary and lifestyle data were collected prospectively using seven day food diaries and lifestyle questionnaires. Results: Mutations in exons 7 and 8 of PTEN were observed in 2.2% of CRC and PTEN loss of expression was identified in 34.9% CRC. Negative PTEN expression was associated with lower blood low-density lipoprotein concentrations (p = 0.05). PIK3CA mutations were observed in 7% of cancers and were more frequent in CRCs in females (p = 0.04). Analysis of dietary intakes demonstrated no link between PTEN expression status and any specific dietary factor. PTEN expression negative, proximal CRC were of more advanced Dukes’ stage (p = 0.02) and poor differentiation (p < 0.01). Testing of the prevalence of PIK3CA mutations and loss of PTEN expression demonstrated that these two events were independent (p = 0.55). Conclusion: These data demonstrated the frequent occurrence (34.9%) of PTEN loss of expression in colorectal cancers, for which gene mutations do not appear to be the main cause. Furthermore, dietary factors are not associated with loss of PTEN expression. PTEN expression negative CRC were not homogenous, as proximal cancers were associated with a more advanced Dukes’ stage and poor differentiation, whereas distal cancers were associated with earlier Dukes’ stage. Background The PI3K/AKT signalling pathway affects many cellular processes including cell proliferation, apoptosis and invasion [1]. Signal transduction through this pathway is mediated through conversion of phosphatidylinositol bisphosphate (PIP2) to phosphatidylinositol triphosphate (PIP3) by phosphatidylinositol 3 kinases (PI3K) following their activation, and this reaction is antagonised by phosphatase and tensin homolog, deleted on chromosome ten (PTEN) activity. Of the genes which encode the enzymatic subunit of PI3K heterodimers, the PIK3CA gene, encoding the p110∝ protein, has been found to be most frequently, in not exclusively, mutationally activated in some human cancers [1,2]. In colorectal cancer (CRC), PIK3CA activating mutations have been described at frequencies of 10-20% [3-6], with two distinct regions, the helical and kinase domains, harbouring up to 80% of mutations [7]. The prevalence of PTEN mutations in CRC has been reported to vary between 1% and 29% [8-13]. This variability in observed PTEN mutation frequencies relates to tumour genomic instability, with PTEN mutations * Correspondence: mja40@cam.ac.uk Department of Pathology, University of Cambridge, Addenbrooke’s Hospital, Cambridge CB2 0QQ, UK Full list of author information is available at the end of the article Naguib et al. BMC Cancer 2011, 11:123 http://www.biomedcentral.com/1471-2407/11/123 © 2011 Naguib et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. having been described in 14-30% of CRC with microsatellite instability (MSI-H) [9,14,15], but at very low frequencies (<5%) in unselected CRC [13]. Exons 7 and 8 of PTEN have been described to acquire more mutations than other regions of the gene in CRC, with insertions and deletions of adenine bases in poly-A tracts present in these exons being the predominant genetic change, consistent with frequent changes in repetitive sequences in MSI-H CRC [15]. Loss of PTEN expression has been reported at higher frequencies than mutation [12,15] with approximately 20-40% of CRC exhibiting loss of PTEN expression [16,17]. Incidence rates of colorectal cancer can vary up to 25fold between countries [18] and it has been postulated that approximately 80% of observed national differences in incidence between can be attributed to dietary factors [19]. Although analysis of dietary components has been performed in relation to general colorectal cancer incidence, their exact relation to specific tumour suppressor gene losses and signalling pathway alterations remains to be fully investigated. To date, analysis of dietary factors in relation to PI3K/AKT pathway component changes in CRC has not been undertaken and little data exists describing the type of CRC in which PIK3CA oncogenic activations and PTEN inactivation occurs. The present study aimed to investigate the relationship between PTEN and PIK3CA mutations and loss of PTEN expression in 186 colorectal adenocarcinomas from the EPIC Norfolk cohort and clinicopathological features, lifestyle traits and dietary factors, as well as analysing PTEN expression negative CRC stratified by stage and tumour location." @default.
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• W2896914319 date "2016-01-01" @default.
• W2896914319 modified "2023-09-27" @default.
• W2896914319 title "Alterations in PTEN and PIK3CA in colorectal cancers in the EPIC Norfolk study" @default.
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