Detection of gene amplification is a process that is recognised as a means of identifying oncogenes. This presentation discusses a study in which the gene copy number of a putative oncogene (ZNF217) was assessed in 80 colon carcinomas by multiplex quantitative real-time PCR. The study found that ZNF217 amplification is a frequent event in colon cancer and that the extent of its amplification can vary greatly between tumours

Boonsong, A.

Cassidy, J.

McFadyen, M.

McLeod, H.L.

Murray, G.I.

Rooney, P.H.

English

Open Access Institutional Repository at Robert Gordon University

ROONEY, P.H., BOONSONG, A., MCFADYEN, M., MCLEOD, H.L., CASSIDY, J. and MURRAY, G.I. 2002. Assessment of a putative oncogene ZNF217 in colorectal cancer by multiplex quantitative real-time PCR. Presented at the 184th Meeting of the Pathological Society of Great Britain and Ireland, 2-5 July 2002, Dublin, Ireland.     The extended abstract in this file is taken from the book of abstracts (page 64, abstract number 135), which is also available on the Internet Archive: https://bit.ly/3ZNA25H. The extended abstract has also been published with the following citation: ROONEY, P.H., BOONSONG, A., MCFADYEN, M., MCLEOD, H.L., CASSIDY, J. and MURRAY, G.I. 2002. Assessment of a putative oncogene ZNF217 in colorectal cancer by multiplex quantitative real-time PCR. Journal of pathology [online], 198(1): synopses of papers from the 184th Meeting of the Pathological Society of Great Britain and Ireland, 2-5 July 2002, Dublin, Ireland, page A33. Available from: https://doi.org/10.1002/path.1711980102 This document was downloaded from https://openair.rgu.ac.uk Assessment of a putative oncogene ZNF217 in colorectal cancer by multiplex quantitative real-time PCR. ROONEY, P., BOONSONG, A., MCFADYEN, M., MCLEOD, H.L., CASSIDY, J. and MURRAY, G.I. 2002 64135Loss of WEEl Kinase Expression in Gastric Cancer M Shah, B Choudry, S Gray, D Greenwood1, I G Martin2, MF Dixon, P Quirke, H Grabsch. Dept ofHistopathology, The Leeds Teaching Hospitals NHS Trust, UK. 1 Academic Unit of Epidemiology & HSR, University of Leeds, UK. 2Dept of Surgery, Middlemore Hospital, Auckland, New Zealand. The G2/M cell cycle checkpoint protects cells from premature mitotic entry after DNA damage. Deregulation of the cell cycle is known to underlie the molecular mechanisms involved in the pathogenesis of many cancers. Recent evidence has demonstrated that WEE 1 kinase plays a crucial role in negatively regulating entry into mitosis at the G2/M phase transition, opposing the activity of the mitotic inducer CDC25. To date, no studies of WEE! protein expression in human tissue have been published. We investigated the expression of WEE! in 60 gastric cancer (GC) cases and adjacent non-neoplastic gastric mucosa using immuno-histochemistry. WEEl expression was recorded semi-quantitatively(% of tumour positive cells), staining intensity was not considered. Results were correlated with proliferation (Ki67 expression) and histopathological data (pT, pN, grading, tumour type according to Lauren classification). Strong nuclear WEE! expression was observed predominantly within the proliferation zone of non-neoplastic gastric mucosa. WEEl expression was localised mainly in the nucleus, however combined cyto-plasmic and nuclear staining was seen in some cases. Positive staining ranged from Oto 65% in cancer cells. In 50% ofGC cases, less than 10% of tumour cells expressed WEEl. Comparing consecutive tissue sections, only a subset of WEEl positive tumour cells were Ki67 positive. No correlation with histopathological data was evident. This is the first study that has investigated WEE 1 protein expression in GC tissue. The results strongly indicate that downregulation of WEEl, a key mitotic inhibitor, could be important in promoting uncontrolled cell proliferation in GC. Further molecular analyses are needed to understand the regulation of WEE 1 expression in gastric carcinogenesis. Furthermore, this may provide essential insights into the development of novel therapeutic targets. Assessment Of A Putative Oncogene ZNF217 In Colorectal Cancer By Multiplex Quantitative Real-Time PCR. PH Rooney 1• A Boonsong2, M McFadyen1, HL McLeod2, J Cassidy2 and GI Murray 1 Departments of Pathology1 and Medicine & Therapeutics2, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD UK. Detection of gene amplification is a recognised process through which oncogenes can be identified. In this study the gene copy number of a putative oncogene, ZNF2 l 7, was assessed in 80 colon carcinomas (41 Dukes' B and 39 Dukes' C) by multiplex quantitative real-time PCR. ZNF217 is mapped to chromosome 20q and lies within 20q13.2 a region which we have previously shown to be highly amplified in colorectal cancer by comparative genomic hybridisation. For each case DNA extracted from laser microdissected tumour cells was assessed by real-time PCR at two distinct gene loci, ZNF217 and Beta globin (the internal control) on an ABI7700 sequence detection system. ZNF217 gene copy number was calculated using the threshold cycle (C1) at which PCR product was detectable for the ZNF2J7 locus less the Beta globin locus' threshold cycle. The tumour values of C1 (ZNF217 - Beta globin) were compared to those of normal colon mucosa (n=IO) and colorectal cancer cell lines (n=6) for which ZNF217 copy number had been established using fluorescent in situ hybridisation. Of the 80 tumours assessed, 18 were diploid, 15 had loss of gene copy and 47 contained some level of amplification at the ZNF217 locus. In this study we found that ZNF217 amplification is a frequent event in colon cancer ( 4 7 /80 tumours = 58.7%) and that the extent of its amplification varies markedly between tumours (range 3 - 13 copies). The Significance of Increased Intra-epithelial Lymphocytes (IELs) in Duodenal Biopsies With Normal Villous Architecture. U Kapur, N.Mukherji, DP O' Donoghue, K. Sheahan. Department of Histopathology and Gastroenterology, StVincent's University Hospital, Dublin. The aim of our study was to assess the significance of increased IELs in duodenal biopsies with normal villous architecture. Eleven patients were identified over a period of four years, in addition to eight normal controls . No patient had a previous history of coeliac disease. IELs were assessed by H&E and CLA staining was done on six of the eleven cases. Subsequent findings were correlated with EMA, antigliadin and tissue Transglutaminase (tTg) status. Three of the study patients who had increased IELs were found to have positive titres for either EMA, antigliadin or tTg. The mean counts for control cases was 17%, (range 15% - 17%). The mean count for study cases was 34%, (range 18%- 46%).In 6/11 cases where CLA was performed, IELs showed a mean increase of 17% compared with H&E evaluation. A significant number (3/11) of patients with increased IELs and normal villous architecture were found to have positive serology for coeliac disease. CLA immunostaining may assist in highlighting those cases with increased IELs who need further evaluation. Relation of mismatch repair protein status with mutational and chromosomal abnormalities in colorectal cancer D Allen, G Smith, RJC Steele, CR Wolf, FA Carey Biomedical Research Centre and Departments of Surgery and Pathology, Ninewells Hospital and University of Dundee Colorectal cancers showing microsatellite instability are a feature of hereditary non-polyposis colorectal cancer. MSI is due to a defect in mismatch repair (MMR) protein function. In sporadic colorectal cancer MSI is also seen, most commonly as a result of a methylation defect of the hMLH-1 gene. We have studied MMR protein status in 114 sporadic colorectal cancers by immunohistochemical study of hMLH-1 and hMSH-2. Seven tumours from six patients (6%) showed loss of staining in one or other protein. One tumour showed loss of both, all others lost hMLH-1 only. In five patients p53, K-ras and APC mutational status was known. Three of these five showed no evidence of oncogene or tumour suppressor gene mutation. One had only an APC mutation and one had mutations of both APC and p53. In two cases, chromosomal abnonnality was detected by CGH. The abnonnalities detected (gains of chromosome 2, 9 and 20p) were not characteristic of our series of colorectal cancers. These preliminary data provide further evidence that MMR defect may be associated with a distinctive pattern of oncogene and tumour suppressor gene abnonnality. 

Assessment of a putative oncogene ZNF217 in colorectal cancer by multiplex quantitative real-time PCR.

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Assessment of a putative oncogene ZNF217 in colorectal cancer by multiplex quantitative real-time PCR.

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