SomaticINK4a-ARF locus mutations: A significant mechanism of gene inactivation in squamous cell carcinomas of the head and neck

Co-Expression of p16INK4A and Laminin 5 γ2 by Microinvasive and Superficial Squamous Cell Carcinomas in Vivo and by Migrating Wound and Senescent Keratinocytes in Culture

“…Consistent with previous p16 allelic analyses of headand-neck SCCs, 8,13,14 we found a complete absence of, or at most very rare, p16-positive cells in deeply invasive SCCs, even at the epithelial-stromal interface. In contrast, we found p16 expression in many cells at the superficial circumferential margins of advanced SCCs.…”

Co-Expression of p16INK4A and Laminin 5 γ2 by Microinvasive and Superficial Squamous Cell Carcinomas in Vivo and by Migrating Wound and Senescent Keratinocytes in Culture

“…Consistent with previous p16 allelic analyses of headand-neck SCCs, 8,13,14 we found a complete absence of, or at most very rare, p16-positive cells in deeply invasive SCCs, even at the epithelial-stromal interface. In contrast, we found p16 expression in many cells at the superficial circumferential margins of advanced SCCs.…”

Proliferative Verrucous Leukoplakia (PVL)

“…In earlier studies, loss of heterozygosity at chromosome 9p loci were frequently reported using a combination of limited microsatellite markers. 38 Interestingly, these findings are similar to those reported for dysplastic premalignant lesions of the oral cavity. 39,40 Other specific gene targets have also been investigated in PVL; the most commonly reported being the p16, p14, and p53 tumor-suppressor genes.…”

Abrogation of the p16-retinoblastoma-cyclin D1 pathway in head and neck squamous cell carcinomas

“…This mutation could result in the truncation of the p16 protein, which may not be detected by Western blotting. The same mutation was reported by Poi et al (27) and by Tripathi et al (28) in HNSCC and cervical carcinoma, respectively. The missense mutation at codon 9 (Amc-HN-1), the single base deletion at codon 38 (Amc-HN-2), and the silent mutation at codon 106 (Amc-HN-7), have not been previously reported.…”

Co-Expression of p16INK4A and Laminin 5 γ2 by Microinvasive and Superficial Squamous Cell Carcinomas in Vivo and by Migrating Wound and Senescent Keratinocytes in Culture

“…Consistent with previous p16 allelic analyses of headand-neck SCCs, 8,13,14 we found a complete absence of, or at most very rare, p16-positive cells in deeply invasive SCCs, even at the epithelial-stromal interface. In contrast, we found p16 expression in many cells at the superficial circumferential margins of advanced SCCs.…”

Proliferative Verrucous Leukoplakia (PVL)

“…In earlier studies, loss of heterozygosity at chromosome 9p loci were frequently reported using a combination of limited microsatellite markers. 38 Interestingly, these findings are similar to those reported for dysplastic premalignant lesions of the oral cavity. 39,40 Other specific gene targets have also been investigated in PVL; the most commonly reported being the p16, p14, and p53 tumor-suppressor genes.…”

Abrogation of the p16-retinoblastoma-cyclin D1 pathway in head and neck squamous cell carcinomas

“…This mutation could result in the truncation of the p16 protein, which may not be detected by Western blotting. The same mutation was reported by Poi et al (27) and by Tripathi et al (28) in HNSCC and cervical carcinoma, respectively. The missense mutation at codon 9 (Amc-HN-1), the single base deletion at codon 38 (Amc-HN-2), and the silent mutation at codon 106 (Amc-HN-7), have not been previously reported.…”

Co-Expression of p16INK4A and Laminin 5 γ2 by Microinvasive and Superficial Squamous Cell Carcinomas in Vivo and by Migrating Wound and Senescent Keratinocytes in Culture

“…Consistent with previous p16 allelic analyses of headand-neck SCCs, 8,13,14 we found a complete absence of, or at most very rare, p16-positive cells in deeply invasive SCCs, even at the epithelial-stromal interface. In contrast, we found p16 expression in many cells at the superficial circumferential margins of advanced SCCs.…”

Proliferative Verrucous Leukoplakia (PVL)

“…In earlier studies, loss of heterozygosity at chromosome 9p loci were frequently reported using a combination of limited microsatellite markers. 38 Interestingly, these findings are similar to those reported for dysplastic premalignant lesions of the oral cavity. 39,40 Other specific gene targets have also been investigated in PVL; the most commonly reported being the p16, p14, and p53 tumor-suppressor genes.…”

Abrogation of the p16-retinoblastoma-cyclin D1 pathway in head and neck squamous cell carcinomas

“…This mutation could result in the truncation of the p16 protein, which may not be detected by Western blotting. The same mutation was reported by Poi et al (27) and by Tripathi et al (28) in HNSCC and cervical carcinoma, respectively. The missense mutation at codon 9 (Amc-HN-1), the single base deletion at codon 38 (Amc-HN-2), and the silent mutation at codon 106 (Amc-HN-7), have not been previously reported.…”