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Catherine A Reznikoff - One of the best experts on this subject based on the ideXlab platform.
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20q gain associates with immortalization 20q13 2 amplification correlates with genome instability in Human Papillomavirus 16 e7 transformed Human uroepithelial cells
Oncogene, 1997Co-Authors: Elena Savelieva, Cassandra D. Belair, Michael A Newton, Sandy Devries, Joe W Gray, Frederic M Waldman, Catherine A ReznikoffAbstract:Breast, bladder, colon, and ovarian carcinomas show frequent low level 20q gain and less frequently high level 20q13.2 amplification, but the significance of these 20q amplifications in transformation has not been defined. Using karyotypic and comparative genomic hybridization (CGH) analyses, chromosome losses and gains were analysed in six newly immortalized Human uroepithelial cell (HUC) lines transformed by Human Papillomavirus 16 (HPV16) E7. Results showed clonal chromosomes with 20q11->qter gain in all six lines. CGH revealed a peak of 20q13.2 amplification in two cell lines. FISH with whole chromosome 20 paint showed expanded chromosome regions (ECRs) and double minute chromosomes (DMs) that contained chromosome 20 material in cell lines with 20q13.2 amplification. FISH with probes from the center of the 20q13.2 Human breast cancer amplicon showed as many as 24 signals in cells with 20q13.2 amplification. The acquisition of genome instability in these E7-HUCs did not correlate with TP53 mutation, as all E7-HUCs contained only wildtype TP53. These results suggest that low level 20q gain is associated with overcoming cellular senescence in E7 transformed cells (P-value=2×10−7), but does not confer genome instability, while high level 20q13.2 amplification is associated with chromosome instability. Loss of 10p (P-value=3×10−5) was also important in immortalization of E7-transformed HUCs. Thus, these results have profound implications for interpreting the significance of high versus low level 20q gains in Human cancers.
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Elevated p16 at Senescence and Loss of p16 at Immortalization in Human Papillomavirus 16 E6, but not E7, Transformed Human Uroepithelial Cells
Cancer Research, 1996Co-Authors: Catherine A Reznikoff, Thomas R. Yeager, Cassandra D. Belair, Elena Savelieva, Jairaj A. Puthenveettil, Walter M StadlerAbstract:CDKN2/p16 inhibits the cyclin D/cyclin-dependent kinase complexes that phosphorylate pRb, thus blocking cell cycle progression. We previously reported that p16 levels are low to undetectable in normal Human uroepithelial cells (HUCs) and in immortalized uroepithelial cells with functional pRb, whereas p16 levels are markedly elevated in immortal HUCs with altered pRb (T. Yeager et al., Cancer Res., 55: 493-497, 1995). We now report that elevation of p16 levels occurs at senescence in HUCs, including HUCs transformed by Human Papillomavirus 16 E7 or E6, whose oncoprotein products lead to functional loss of pRb and p53, respectively. We also report that six of six independently immortalized E7 HUCs show high levels of p16 similar to those observed at HUC senescence, whereas p16 is undetectable in five of five immortal E6 HUCs. Four of the five independent E6 HUCs that lost p16 at immortalization showed hemizygous deletion of the 9p21 region. However, no homozygous CDKN2 deletions were detected, and only one CDKN2 mutation was identified. For the first time, these data associate elevated p16 with senescence in Human epithelial cells. These data also suggest that a component of immortalization may be abrogation, either by pRb inactivation (as in the E7-transformed HUCs) or by p16 inactivation (as in the E6-transformed HUCs), of a p16-mediated senescence cell cycle block.
Elena Savelieva - One of the best experts on this subject based on the ideXlab platform.
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20q gain associates with immortalization 20q13 2 amplification correlates with genome instability in Human Papillomavirus 16 e7 transformed Human uroepithelial cells
Oncogene, 1997Co-Authors: Elena Savelieva, Cassandra D. Belair, Michael A Newton, Sandy Devries, Joe W Gray, Frederic M Waldman, Catherine A ReznikoffAbstract:Breast, bladder, colon, and ovarian carcinomas show frequent low level 20q gain and less frequently high level 20q13.2 amplification, but the significance of these 20q amplifications in transformation has not been defined. Using karyotypic and comparative genomic hybridization (CGH) analyses, chromosome losses and gains were analysed in six newly immortalized Human uroepithelial cell (HUC) lines transformed by Human Papillomavirus 16 (HPV16) E7. Results showed clonal chromosomes with 20q11->qter gain in all six lines. CGH revealed a peak of 20q13.2 amplification in two cell lines. FISH with whole chromosome 20 paint showed expanded chromosome regions (ECRs) and double minute chromosomes (DMs) that contained chromosome 20 material in cell lines with 20q13.2 amplification. FISH with probes from the center of the 20q13.2 Human breast cancer amplicon showed as many as 24 signals in cells with 20q13.2 amplification. The acquisition of genome instability in these E7-HUCs did not correlate with TP53 mutation, as all E7-HUCs contained only wildtype TP53. These results suggest that low level 20q gain is associated with overcoming cellular senescence in E7 transformed cells (P-value=2×10−7), but does not confer genome instability, while high level 20q13.2 amplification is associated with chromosome instability. Loss of 10p (P-value=3×10−5) was also important in immortalization of E7-transformed HUCs. Thus, these results have profound implications for interpreting the significance of high versus low level 20q gains in Human cancers.
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Elevated p16 at Senescence and Loss of p16 at Immortalization in Human Papillomavirus 16 E6, but not E7, Transformed Human Uroepithelial Cells
Cancer Research, 1996Co-Authors: Catherine A Reznikoff, Thomas R. Yeager, Cassandra D. Belair, Elena Savelieva, Jairaj A. Puthenveettil, Walter M StadlerAbstract:CDKN2/p16 inhibits the cyclin D/cyclin-dependent kinase complexes that phosphorylate pRb, thus blocking cell cycle progression. We previously reported that p16 levels are low to undetectable in normal Human uroepithelial cells (HUCs) and in immortalized uroepithelial cells with functional pRb, whereas p16 levels are markedly elevated in immortal HUCs with altered pRb (T. Yeager et al., Cancer Res., 55: 493-497, 1995). We now report that elevation of p16 levels occurs at senescence in HUCs, including HUCs transformed by Human Papillomavirus 16 E7 or E6, whose oncoprotein products lead to functional loss of pRb and p53, respectively. We also report that six of six independently immortalized E7 HUCs show high levels of p16 similar to those observed at HUC senescence, whereas p16 is undetectable in five of five immortal E6 HUCs. Four of the five independent E6 HUCs that lost p16 at immortalization showed hemizygous deletion of the 9p21 region. However, no homozygous CDKN2 deletions were detected, and only one CDKN2 mutation was identified. For the first time, these data associate elevated p16 with senescence in Human epithelial cells. These data also suggest that a component of immortalization may be abrogation, either by pRb inactivation (as in the E7-transformed HUCs) or by p16 inactivation (as in the E6-transformed HUCs), of a p16-mediated senescence cell cycle block.
S. Gerber - One of the best experts on this subject based on the ideXlab platform.
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Clinical follow-up of women infected with Human Papillomavirus-16, either alone or with other Human Papillomavirus types: identification of different risk groups.
American Journal of Obstetrics and Gynecology, 2009Co-Authors: Olivier Cottier, Roland Sahli, Anca Mihaescu, Pierre De Grandi, Michel Boulvain, S. GerberAbstract:Objectives Evaluation of the clinical impact of multiple infections of the cervix by Human Papillomavirus, including Human Papillomavirus-16, compared with single Human Papillomavirus-16 infection. Study Design One hundred sixty-nine women were classified in 3 categories depending on their Human Papillomavirus profile: Human Papillomavirus-16 only, Human Papillomavirus-16 and low-risk type(s), and Human Papillomavirus-16 and other high-risk type(s). Cervical brush samples were analyzed for Human Papillomavirus DNA by polymerase chain reaction and reverse line blot hybridization. All women were evaluated with colposcopy during 24 months or more. Management was according to the Bethesda recommendations. Results Women infected with Human Papillomavirus-16 and other high-risk Human Papillomavirus type(s) presented more progression or no change in the grade of dysplasia, compared with women of the other groups (relative risk [RR], 1.39; 95% confidence interval [CI], 1.07-1.82; P = .02 at 6 months; RR, 2.10; 95% CI, 1.46-3.02; P P = .004 at 24 months). Conclusion Coinfection of women with Human Papillomavirus-16 and other high-risk Human Papillomavirus type(s) increases the risk of unfavorable evolution.
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Clinical follow-up of women infected with Human Papillomavirus-16, either alone or with other Human Papillomavirus types: identification of different risk groups.
American journal of obstetrics and gynecology, 2009Co-Authors: Olivier Cottier, Roland Sahli, Anca Mihaescu, Pierre De Grandi, Michel Boulvain, S. GerberAbstract:Evaluation of the clinical impact of multiple infections of the cervix by Human Papillomavirus, including Human Papillomavirus-16, compared with single Human Papillomavirus-16 infection. One hundred sixty-nine women were classified in 3 categories depending on their Human Papillomavirus profile: Human Papillomavirus-16 only, Human Papillomavirus-16 and low-risk type(s), and Human Papillomavirus-16 and other high-risk type(s). Cervical brush samples were analyzed for Human Papillomavirus DNA by polymerase chain reaction and reverse line blot hybridization. All women were evaluated with colposcopy during 24 months or more. Management was according to the Bethesda recommendations. Women infected with Human Papillomavirus-16 and other high-risk Human Papillomavirus type(s) presented more progression or no change in the grade of dysplasia, compared with women of the other groups (relative risk [RR], 1.39; 95% confidence interval [CI], 1.07-1.82; P = .02 at 6 months; RR, 2.10; 95% CI, 1.46-3.02; P < .001 at 12 months; RR, 1.82; 95% CI, 1.21-2.72; P = .004 at 24 months). Coinfection of women with Human Papillomavirus-16 and other high-risk Human Papillomavirus type(s) increases the risk of unfavorable evolution.
Walter M Stadler - One of the best experts on this subject based on the ideXlab platform.
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Elevated p16 at Senescence and Loss of p16 at Immortalization in Human Papillomavirus 16 E6, but not E7, Transformed Human Uroepithelial Cells
Cancer Research, 1996Co-Authors: Catherine A Reznikoff, Thomas R. Yeager, Cassandra D. Belair, Elena Savelieva, Jairaj A. Puthenveettil, Walter M StadlerAbstract:CDKN2/p16 inhibits the cyclin D/cyclin-dependent kinase complexes that phosphorylate pRb, thus blocking cell cycle progression. We previously reported that p16 levels are low to undetectable in normal Human uroepithelial cells (HUCs) and in immortalized uroepithelial cells with functional pRb, whereas p16 levels are markedly elevated in immortal HUCs with altered pRb (T. Yeager et al., Cancer Res., 55: 493-497, 1995). We now report that elevation of p16 levels occurs at senescence in HUCs, including HUCs transformed by Human Papillomavirus 16 E7 or E6, whose oncoprotein products lead to functional loss of pRb and p53, respectively. We also report that six of six independently immortalized E7 HUCs show high levels of p16 similar to those observed at HUC senescence, whereas p16 is undetectable in five of five immortal E6 HUCs. Four of the five independent E6 HUCs that lost p16 at immortalization showed hemizygous deletion of the 9p21 region. However, no homozygous CDKN2 deletions were detected, and only one CDKN2 mutation was identified. For the first time, these data associate elevated p16 with senescence in Human epithelial cells. These data also suggest that a component of immortalization may be abrogation, either by pRb inactivation (as in the E7-transformed HUCs) or by p16 inactivation (as in the E6-transformed HUCs), of a p16-mediated senescence cell cycle block.
Cassandra D. Belair - One of the best experts on this subject based on the ideXlab platform.
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20q gain associates with immortalization 20q13 2 amplification correlates with genome instability in Human Papillomavirus 16 e7 transformed Human uroepithelial cells
Oncogene, 1997Co-Authors: Elena Savelieva, Cassandra D. Belair, Michael A Newton, Sandy Devries, Joe W Gray, Frederic M Waldman, Catherine A ReznikoffAbstract:Breast, bladder, colon, and ovarian carcinomas show frequent low level 20q gain and less frequently high level 20q13.2 amplification, but the significance of these 20q amplifications in transformation has not been defined. Using karyotypic and comparative genomic hybridization (CGH) analyses, chromosome losses and gains were analysed in six newly immortalized Human uroepithelial cell (HUC) lines transformed by Human Papillomavirus 16 (HPV16) E7. Results showed clonal chromosomes with 20q11->qter gain in all six lines. CGH revealed a peak of 20q13.2 amplification in two cell lines. FISH with whole chromosome 20 paint showed expanded chromosome regions (ECRs) and double minute chromosomes (DMs) that contained chromosome 20 material in cell lines with 20q13.2 amplification. FISH with probes from the center of the 20q13.2 Human breast cancer amplicon showed as many as 24 signals in cells with 20q13.2 amplification. The acquisition of genome instability in these E7-HUCs did not correlate with TP53 mutation, as all E7-HUCs contained only wildtype TP53. These results suggest that low level 20q gain is associated with overcoming cellular senescence in E7 transformed cells (P-value=2×10−7), but does not confer genome instability, while high level 20q13.2 amplification is associated with chromosome instability. Loss of 10p (P-value=3×10−5) was also important in immortalization of E7-transformed HUCs. Thus, these results have profound implications for interpreting the significance of high versus low level 20q gains in Human cancers.
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Elevated p16 at Senescence and Loss of p16 at Immortalization in Human Papillomavirus 16 E6, but not E7, Transformed Human Uroepithelial Cells
Cancer Research, 1996Co-Authors: Catherine A Reznikoff, Thomas R. Yeager, Cassandra D. Belair, Elena Savelieva, Jairaj A. Puthenveettil, Walter M StadlerAbstract:CDKN2/p16 inhibits the cyclin D/cyclin-dependent kinase complexes that phosphorylate pRb, thus blocking cell cycle progression. We previously reported that p16 levels are low to undetectable in normal Human uroepithelial cells (HUCs) and in immortalized uroepithelial cells with functional pRb, whereas p16 levels are markedly elevated in immortal HUCs with altered pRb (T. Yeager et al., Cancer Res., 55: 493-497, 1995). We now report that elevation of p16 levels occurs at senescence in HUCs, including HUCs transformed by Human Papillomavirus 16 E7 or E6, whose oncoprotein products lead to functional loss of pRb and p53, respectively. We also report that six of six independently immortalized E7 HUCs show high levels of p16 similar to those observed at HUC senescence, whereas p16 is undetectable in five of five immortal E6 HUCs. Four of the five independent E6 HUCs that lost p16 at immortalization showed hemizygous deletion of the 9p21 region. However, no homozygous CDKN2 deletions were detected, and only one CDKN2 mutation was identified. For the first time, these data associate elevated p16 with senescence in Human epithelial cells. These data also suggest that a component of immortalization may be abrogation, either by pRb inactivation (as in the E7-transformed HUCs) or by p16 inactivation (as in the E6-transformed HUCs), of a p16-mediated senescence cell cycle block.