1992
DOI: 10.1016/0140-6736(92)93214-8
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Loss of heterozygosity on chromosome 17p and mutant p53 in HPV-negative cervical carcinomas

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Cited by 44 publications
(18 citation statements)
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“…Many investigators (Kaelbling et al, 1992;Mitra et al, 1994;Havre et al, 1995;Hoppe-Seyler and Butz, 1995;Mansur et al, 1995;Mullokandov et al, 1996) have studied the short arm of chromosome 17 for the p53 gene, which may be involved in cervical carcinomas through its interaction with HPV-E6 oncoproteins. p53 point mutations are infrequent (< 10%) in clinical samples of squamous cell carcinomas of the uterine cervix, whereas p53 point mutations were seen more often in adenocarcinoma (30%) (Fujita et al, 1992;Jiko et al, 1994;Schneider et al, 1994).…”
mentioning
confidence: 99%
“…Many investigators (Kaelbling et al, 1992;Mitra et al, 1994;Havre et al, 1995;Hoppe-Seyler and Butz, 1995;Mansur et al, 1995;Mullokandov et al, 1996) have studied the short arm of chromosome 17 for the p53 gene, which may be involved in cervical carcinomas through its interaction with HPV-E6 oncoproteins. p53 point mutations are infrequent (< 10%) in clinical samples of squamous cell carcinomas of the uterine cervix, whereas p53 point mutations were seen more often in adenocarcinoma (30%) (Fujita et al, 1992;Jiko et al, 1994;Schneider et al, 1994).…”
mentioning
confidence: 99%
“…Only a few studies have examined the status of p53 in cervical carcinoma, but recent data have suggested it may have an important role (Crook et al, 1991a(Crook et al, , 1992Fujita et al, 1992;Kaelbling et al, 1992). There are plausible theoretical grounds for the proposition that p53 alterations may act in combination with human papillomaviruses (HPV), which have long been associated with cervical carcinogenesis (Bosch & Munoz, 1989;zur Hausen, 1989).…”
mentioning
confidence: 99%
“…Allele deletions on chromosome 17p have been reported in up to 61% of breast carcinomas (Mackay et al., 1988a); 73.1% of osteosarcomas (Toguchida et al, 1989); 75% of colonic carcinomas (Vogelstein et al, 1988); 50-60% of epithelial ovarian carcinomas (Eccles et al, 1990;Russell et al, 1990); up to 55% of brain tumours (Fults et al, 1989) and 63% of bladder carcinomas (Tsai et al, 1990) -suggesting the presence of a tumour suppressor gene that is involved in a carcinogenetic mechanism common to all of these tumours. Our data show only 15% of informative tumours with 17p allele loss; a similar proportion to that identified in a recently published series of cervical carcinomas (Kaelbling et al, 1992), but a significantly lower proportion (P <0.05; Fisher's Exact Test) than that observed using similar probes in tumours of breast, bladder, ovary, bone, and colon. This may imply that any association between 17p allele loss and carcinogenesis does not extend to cervical carcinoma.…”
Section: Resultsmentioning
confidence: 56%
“…It has further been postulated that their importance to the development of this cancer may lie in the loss of recessive genes on chromosome 17p (Atkin & Baker, 1989). Furthermore, loss of heterozygosity in primary cervical carcinomas has been reported on chromosomes 3 (Yokota et al, 1989), 11 (Riou et al, 1988;Srivatsan et al, 1991), and 17 (Kaelbling et al, 1992 Three major cervical carcinoma types -squamous carcinoma, adenocarcinoma and adenosquamous carcinoma -of various grades and stages were represented (Table II), and patients' ages ranged from 23-70 years.…”
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confidence: 99%