Allelotype analysis of adenocarcinoma of the gastric cardia

Gleeson, C. M.; Sloan, James M.; McGuigan, James A.; Ritchie, Andrew J.; Weber, J. L.; Russell, S. E. H.

doi:10.1038/bjc.1997.578

Cited by 35 publications

(38 citation statements)

References 45 publications

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“…Loss of 4q was associated with an elevated serum α-fetoprotein in HCCs patients from Taiwan (Yeh et al, 1996). Loss of chromosome 4q has also been reported in head and neck squamous cell carcinoma (Perhouse et al, 1997), cervical carcinoma (Mitra et al, 1994;Hampton et al, 1996), bladder carcinoma (Polascik et al, 1995), oesophageal and gastric cardia adenocarcinomas (Hammoud et al, 1996;Gleeson et al, 1997) and Hodgkin's disease (Dohner et al, 1992).…”

Section: Microsatellite Instability and Loh Of Chromosomes 1p 4q 13mentioning

confidence: 89%

Genetic alterations in hepatocellular carcinomas: association between loss of chromosome 4q and p53 gene mutations

et al. 1999

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The major risk factors for hepatocellular carcinomas (HCC) in high incidence areas include infection with hepatitis B and C viruses (HBV, HCV) and exposure to aflatoxin. Genetic alterations in 24 liver resection specimens from Shanghai and Qidong were studied. Hepatitis B virus was integrated in all patient samples, and a null phenotype for the GSTM1 enzyme was present in 63% of patients. Alteration of p53 was present in 95% (23/24) of cases: mutations of the p53 gene in 12 HCC, p53 overexpression in 13 and loss of heterozygosity (LOH) of chromosome 17p in 17. All seven HCCs with a p53 mutation from Qidong and three of five from Shanghai had the aflatoxin-associated point mutation with a G to T transversion at codon 249, position 3. No HCC had microsatellite instability. LOH of chromosome 4q, 1p, 16q and 13q was present in 50%, 46%, 42% and 38%, respectively, and 4q was preferentially lost in HCCs containing a p53 mutation: LOH of 4q was present in 75% (9/12) of HCC with, but only 25% (3/12) of HCC without, a p53 gene mutation ( P = 0.01). These data indicate a possible interaction between p53 gene mutation and 4q loss in the pathogenesis of HCC. © 1999 Cancer Research Campaign

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Section: Microsatellite Instability and Loh Of Chromosomes 1p 4q 13mentioning

confidence: 89%

Genetic alterations in hepatocellular carcinomas: association between loss of chromosome 4q and p53 gene mutations

et al. 1999

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“…Our identi®cation of this region at the p53 locus is consistent with the established importance of p53 in BOA. In other studies on Barrett's tumours the concurrent ®nding of a high frequency of LOH at the p53 locus and a high frequency of p53 mutation has led to the implicit assumption that p53 is the sole target of loss on 17p (Gleeson et al, 1995;Galipeau et al, 1996;Blount et al, 1994). We have also found a very high frequency of LOH at the p53 locus (82%).…”

Section: Discussionmentioning

confidence: 99%

“…Genetic alterations involving the p53 TSG are amongst the most commonly found abnormality, present in many di erent tumours (Harris and Hollstein, 1993;Greenwald et al, 1992;Wang and Wang, 1996). In Barrett's oesophagus loss of heterozygosity (LOH), mutation and overexpression of the p53 TSG occurs frequently and in most cases precedes the development of invasive cancer (Gleeson et al, 1995;Krishnadath et al, 1995;Flejou et al, 1994;Casson et al, 1994;Blount et al, 1994;Galipeau et al, 1996;Audrezet et al, 1996;Campomenosi et al, 1996;Neshat et al, 1994;Gonzalez et al, 1997). Other genetic abnormalities found in BOA include LOH, homozygous deletion and mutation within the MTS1/p16 TSG at 9p21 (Gonzalez et al, 1997;Barrett et al, 1996a), LOH on 5q, 13q and 18q Blount et al, 1993), aneuploidy (Barrett et al, 1996b;Blount et al, 1994;Galipeau et al, 1996), and the ampli®cation and overexpression of certain oncogenes, notably c-erbB-2 and EGF-R. (Filipe and Jankowski, 1993;AlKasspooles et al, 1993;Nakamura et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Multiple target sites of allelic imbalance on chromosome 17 in Barrett's oesophageal cancer

et al. 1999

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Twelve Barrett's adenocarcinomas have been analysed for the occurrence of allelic imbalance (LOH) on chromosome 17 using 41 microsatellite markers. This study provides evidence for 13 minimal regions of LOH, six on 17p and seven on 17q. Four of these centre in the vicinity of the known tumour suppressor genes (TSGs) TP 53 (17p13.1), NF1 (17q11.2), BRCA1 (17q21.1), and a putative TSG (17p13.3). The tumours all displayed relatively small regions of LOH (1 ± 10 cM), and in several tumours extensive regions of LOH were detected. One tumour displayed only two very small regions of LOH; 17p11.2 and 17p13.1. The frequency of allelic imbalance has been calculated based on the LOH encompassing only one minimal region, and based on all the LOH observations. By both evaluations the highest LOH frequencies were found for regions II (p53), III (17p13.1 centromeric to p53), IV (17p12), V (17p11.2) and VII (NF1, 17q11.2). Our data supports the existence of multiple TSGs on chromosome 17 and challenges the view that p53 is the sole target of LOH on 17p in Barrett's adenocarcinoma.

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“…This variation may, in part, be due to differences in the microsatellites studied. Mao et al (1994) and Gleeson et al (1996) reported that higher frequencies of instability are seen at tetranucleotide than mono-and dinucleotide repeats in lung, head and neck and bladder, and oesophageal tumours, respectively, and when MSI-H tumours are excluded a subset of tumours with instability at selected tetranucleotides remains. This form of instability appears unrelated to the MSI typical of HNPCC and has been termed EMAST (elevated microsatellite alterations at select tetranucleotides) (Boland et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Distinct patterns of microsatellite instability are seen in tumours of the urinary tract

Catto

Azzouzi

Amira³

et al. 2003

Oncogene

123

109

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To date, two forms of microsatellite instability (MSI) have been described in human cancer. MSI typical of hereditary nonpolyposis colon cancer (HNPCC), is due to deficient DNA mismatch repair (MMR) and is defined with mono-and dinucleotide repeat microsatellites. A second variety of instability is best seen at selective tetranucleotide repeats (EMAST; elevated microsatellite alterations at select tetranucleotides). While MSI occurs infrequently in bladder cancers, EMAST is common. Sporadic tumours with the largest proportion showing MSI are those found most frequently in HNPCC kindreds. While bladder cancer is not frequently seen in HNPCC, upper urinary tract tumours (UTTs) are. Having previously found a low frequency of MSI in bladder cancer, we sought to determine the relative levels of MSI and EMAST in transitional cell carcinoma (TCC) of the upper and lower urinary tracts. Microsatellite analysis was performed at 10 mono-and dinucleotide and eight tetranucleotide loci, in 89 bladder and 71 UTT TCC. Contrasting patterns of instability were seen in urinary tumours. In bladder cancer, MSI was rare and EMAST was common. The presence of EMAST was not related to tumour grade, stage, subsequent outcome or immunohistochemical expression of the MMR proteins. In UTT, while MSI occurred frequently, EMAST was seen less frequently than in bladder cancer. When TCC of the upper and lower urinary tracts are compared, MSI-H is more frequent in UTT and EMAST more frequent in bladder cancer. Our findings show that, as for colorectal cancer, the pattern of MSI varies with location in the urinary tract. In addition, we have confirmed that MSI and EMAST are discrete forms of MSI, and that the presence of EMAST does not affect tumour phenotype.

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Allelotype analysis of adenocarcinoma of the gastric cardia

Cited by 35 publications

References 45 publications

Genetic alterations in hepatocellular carcinomas: association between loss of chromosome 4q and p53 gene mutations

Genetic alterations in hepatocellular carcinomas: association between loss of chromosome 4q and p53 gene mutations

Multiple target sites of allelic imbalance on chromosome 17 in Barrett's oesophageal cancer

Distinct patterns of microsatellite instability are seen in tumours of the urinary tract

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