Allelic loss on chromosome 9 in bladder cancer tissues and urine samples detected by blunt-end single-strand DNA conformation polymorphism

Shigyo, Masanori; Sugano, Kokichi; Fukayama, Noriko; Taniguchi, Takahiro; Tobisu, Ken‐ichi; Fujimoto, Hiroyuki; Doi, Naoto; Niwakawa, Masashi; Shimamura, Kayako; Tsukamoto, Taiji; Sekiya, Takao; Kakizoe, Tadao

doi:10.1002/(sici)1097-0215(19981109)78:4<425::aid-ijc6>3.0.co;2-w

Cited by 21 publications

(17 citation statements)

References 8 publications

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“…4 Frequencies of LOH of the ABO locus examined in this study seems higher than those reported previously. 17,18 In previous studies, allelic status of the ABO gene was examined by PCR/RFLP; however, LOH is barely detectable by PCR/RFLP if the proportion of tumor cells in the sample is below 60%, due to the formation of heteroduplex dimers that are resistant to the restriction enzyme digestion.…”

Section: Discussioncontrasting

confidence: 71%

“…values of the normal heterozygous DNA were used as a cutoff value for tumor cellularity, and tumor samples showing tumor cellularities above the cutoff level were considered to have LOHs. 4 A104 allele was indistinguishable from B allele in this analysis, while the observed frequency of the A104 allele in the Japanese is reported to be as low as 1.3%. In fact, in all samples tested, the genotypes coincided with the patient's ABO isotypes.…”

Section: Expression Of Blood-group a Antigen By Immunohistochemical Scontrasting

confidence: 62%

“…LOH was determined by measuring the signal ratio between the opposing alleles and defined as tumor cellularity according to the equation that we previously reported. 4,26,27 Supposing that the A1 allele is lost in a heterozygote carrying A1 and A2 alleles, T is the peak height of the signal from the tumor samples and N is the peak height of the signal from normal control. The tumor cellularity in the sample is thus given as follows:…”

Section: Expression Of Blood-group a Antigen By Immunohistochemical Smentioning

confidence: 99%

“…Allelic loss on chromosome 9 is the most frequent genetic event in transitional cell carcinomas of the bladder, [1][2][3][4] that is observed in 70% of invasive bladder cancers and even in 50% of superficial bladder cancers at Stage G1. 4 Whether or not loss on chromosome 9 arises in urothelial lesions such as dysplasia is crucial to the understanding of early genetic events in bladder carcinogenesis. Some authors have reported on the allelic loss of chromosome 9 that occurs in the small urothelial lesions and normal bladder urothelium in their attempts to trace genetic alterations using microsatellite markers.…”

mentioning

confidence: 99%

“…This phenomenon drew our attention, due to the fact that the determinant of the ABO blood-group antigen is synthesized by the action of the ABO gene encoding ABO glycosyltransferase assigned to chromosome 9q34.1, where loss of heterozygosity (LOH) was frequently reported in bladder cancer. [1][2][3][4] The ABO gene is composed of seven exons and six introns and encodes ABO glycosyltransferase, of which substrate specificity is determined by genetic polymorphisms in exons 6 and 7 ( Figure 1). 13,14 Blood-group A antigen is synthesized by a-N-acetylgalactosaminyltransferase (A-GalNAc transferase), which catalyzes the transfer of N-acetylgalactosamine to the subterminal b-galactosyl residue of the blood-group H carbohydrate chain.…”

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confidence: 99%

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Loss of blood group A antigen expression in bladder cancer caused by allelic loss and/or methylation of the ABO gene

Chihara

Sugano

Kobayashi

et al. 2005

Laboratory Investigation

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Loss of ABO blood group antigen expression has been reported in transitional cell carcinoma (TCC) of the bladder. Synthesis of the ABO blood group antigen was genetically determined by allelic variants of the ABO gene assigned on 9q34.1. We analyzed loss of heterozygosity (LOH) and promoter hypermethylation of the ABO gene in TCC and compared them with alterations of A antigen expression in TCC, dysplasia and normal urothelium. A total of 81 samples of TCC of the bladder obtained from transurethral resection (TUR) (n ¼ 44) and radical cystectomy (n ¼ 37) were examined. Expression of the A antigen was evaluated by immunohistochemical staining (IHC) using anti-A antigen monoclonal antibody. LOH of the ABO gene locus was examined by blunt-end single-strand DNA conformational polymorphism (SSCP) analysis using flouresence-based auto sequencer. Promoter hypermethylation of the ABO gene were examined by bisulfite PCR-SSCP (BiPS) analysis and/or methylation-specific PCR (MSP). Loss of A allele and/or hypermethylation were significantly associated with abnormal expression of the A antigen in cases undergoing TUR (P ¼ 0.02) and radical cystectomy (P ¼ 0.0005). For the analysis of the concomitant dysplasia in 23 cases with TCC of the bladder, the expression of the A antigen was maintained, regardless of the A allelic loss or methylation status in the tumor. In conclusion, A allelic loss and hypermethylation in the promoter region of the ABO gene showed significant correlation with reduction of A antigen expression in TCC, while the expression of the A antigen is maintained in concomitant dysplasia or normal urothelium, suggesting that loss of the ABO gene and/or its promoter hypermethylation is a specific marker for TCC. Laboratory Investigation (2005) 85, 895-907.

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Section: Discussioncontrasting

confidence: 71%

Section: Expression Of Blood-group a Antigen By Immunohistochemical Scontrasting

confidence: 62%

Section: Expression Of Blood-group a Antigen By Immunohistochemical Smentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Loss of blood group A antigen expression in bladder cancer caused by allelic loss and/or methylation of the ABO gene

Chihara

Sugano

Kobayashi

et al. 2005

Laboratory Investigation

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Ancillary methods for the detection of recurrent urothelial neoplasia

Ross

Cohen

2000

Cancer

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Cytogenetics and molecular genetics of bladder cancer: A personal view

Sandberg

2002

Am. J. Med. Genet.

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The cytogenetic and molecular genetic aspects that may be involved in the pathogenesis of bladder cancer are presented. Although anomalies of chromosome 9 may play an initial causative role in this cancer, the subsequent events, involving a succession of genetic changes, are less established or understood. This presentation is a distillation of what generally are considered to be the cytogenetic and molecular genetic events that constitute the array of changes underlying bladder cancer. ß

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Allelic loss on chromosome 9 in bladder cancer tissues and urine samples detected by blunt-end single-strand DNA conformation polymorphism

Cited by 21 publications

References 8 publications

Loss of blood group A antigen expression in bladder cancer caused by allelic loss and/or methylation of the ABO gene

Loss of blood group A antigen expression in bladder cancer caused by allelic loss and/or methylation of the ABO gene

Ancillary methods for the detection of recurrent urothelial neoplasia

Cytogenetics and molecular genetics of bladder cancer: A personal view

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