1993
DOI: 10.1001/archotol.1993.01880220075010
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p53, Retinoblastoma, and Human Papillomavirus in Squamous Cell Carcinoma and Adjacent Normal Mucosa of the Upper Aerodigestive Tract

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Cited by 32 publications
(16 citation statements)
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“…Mutation of the p53 tumor suppressor gene on chromosome 17p, which is the most common genetic change in human cancers to date, is also the most frequent genetic alteration in HNSCC (Lee et al, 1993); MDM2 amplication, an alternative mechanism of p53 inactivation does not occur . Furthermore, allelic loss at 3p in HNSCC is not associated with alteration of the VHL tumor suppressor gene (Waber et al, 1996).…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Mutation of the p53 tumor suppressor gene on chromosome 17p, which is the most common genetic change in human cancers to date, is also the most frequent genetic alteration in HNSCC (Lee et al, 1993); MDM2 amplication, an alternative mechanism of p53 inactivation does not occur . Furthermore, allelic loss at 3p in HNSCC is not associated with alteration of the VHL tumor suppressor gene (Waber et al, 1996).…”
Section: Introductionmentioning
confidence: 99%
“…Nevertheless, although genetically altered, morphologically normal mucosa is polyclonal whereas adjacent tumor is clonal (Lee et al, 1994a). Although RB1 has been localized to a region of frequent allelic loss on chromosome 13 in HNSCC, speci®c genetic alterations of this gene are relatively uncommon (Lee et al, 1993(Lee et al, , 1994bLi et al, 1994); the same is true for BRCA2 which is also located near a site of LOH at 13q in HNSCC (Kirkpatrick et al, 1997).…”
Section: Introductionmentioning
confidence: 99%
“…With respect to chromosome 13, several regions have been implicated to harbor alterations in HNSCCs on the basis of LOH (Lee et al, 1993(Lee et al, , 1994. These include regions within 13q32-qter, 13q14.2-q14.3 (Maestro et al, 1996) and 13q14.1-q22 (Yoo et al, 1994).…”
Section: Introductionmentioning
confidence: 99%
“…20,21,[24][25][26][27] Immunohistochemical detection of p16 has been shown to be a reliable marker for squamous dysplasia in the uterine cervix, where the protein is frequently overexpressed as a result of infection with oncogenic strains of human papillomavirus (HPV). [28][29][30][31][32] More recently, a study showed immunohistochemical overexpression of p16 in dysplastic lesions of the oral cavity, which suggests that it may be a useful ancillary test for diagnosing dysplasia in this location.…”
mentioning
confidence: 99%