CCL

Összesen 2 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM008928
Első szerző:Klug, Stefani J.
Cím:TP53 codon 72 polymorphism and cervical cancer : a pooled analysis of individual data from 49 studies / Klug Stefani J., Ressing Meike, Koenig Jochem, Abba Martin C., Agorastos Theodoros, Brenna Sylvia M. F., Ciotti Marco, Das B. R., Del Mistro Annarosa, Dybikowska Aleksandra, Giuliano Anna R., Gudleviciene Zivile, Gyllensten Ulf, Haws Andrea L. F., Helland Aslaug, Herrington C. Simon, Hildesheim Alan, Humbey Oliver, Jee Sun H., Kim Jae Weon, Madeleine M. Margaret, Menczer Joseph, Ngan Hextan Y. S. N., Nishikawa Akira, Niwa Yosimitshu, Pegoraro Rosemary, Pillai M. R., Ranzani Gulielmina, Rezza Giovanni, Rosenthal Adam N., Roychoudhury Susanta, Saranath Dhananjaya, Schmitt Virginia M., Sengupta Sharmila, Settheetham-Ishida Wannapa, Shirasawa Hiroshi, Snijders Peter J. F., Stoler Mark H., Suárez-Rincón Angel E., Szarka Krisztina, Tachezy Ruth, Ueda Masatsugu, van der Zee Ate G. J., von Knebel Doeberitz Magnus, Wu Ming-Tsang, Yamashita Tsuyoshi, Zehbe Ingeborg, Blettner Maria
Dátum:2009
Megjegyzések:Summary Background Cervical cancer is caused primarily by human papillomaviruses (HPV). The polymorphism rs1042522 at codon 72 of the TP53 tumour-suppressor gene has been investigated as a genetic cofactor. More than 80 studies were done between 1998 and 2006, after it was initially reported that women who are homozygous for the arginine allele had a risk for cervical cancer seven times higher than women who were heterozygous for the allele. However, results have been inconsistent. Here we analyse pooled data from 49 studies to determine whether there is an association between TP53 codon 72 polymorphism and cervical cancer. Methods Individual data on 7946 cases and 7888 controls from 49 diff erent studies worldwide were reanalysed. Odds ratios (OR) were estimated using logistic regression, stratifying by study and ethnic origin. Subgroup analyses were done for infection with HPV, ethnic origin, Hardy-Weinberg equilibrium, study quality, and the material used to determine TP53 genotype. Findings The pooled estimates (OR) for invasive cervical cancer were 1.22 (95% CI 1.08-1.39) for arginine homozygotes compared with heterozygotes, and 1.13 (0.94-1.35) for arginine homozygotes versus proline homozygotes. Subgroup analyses showed signifi cant excess risks only in studies where controls were not in Hardy-Weinberg equilibrium (1.71 [1.21-2.42] for arginine homozygotes compared with heterozygotes), in non-epidemiological studies (1.35 [1.15-1.58] for arginine homozygotes compared with heterozygotes), and in studies where TP53 genotype was determined from tumour tissue (1.39 [1.13-1.73] for arginine homozygotes compared with heterozygotes). Null results were noted in studies with sound epidemiological design and conduct (1.06 [0.87-1.29] for arginine homozygotes compared with heterozygotes), and studies in which TP53 genotype was determined from white blood cells (1.06 [0.87-1.29] for arginine homozygotes compared with heterozygotes). Interpretation Subgroup analyses indicated that excess risks were most likely not due to clinical or biological factors, but to errors in study methods. No association was found between cervical cancer and TP53 codon 72 polymorphism when the analysis was restricted to methodologically sound studies. Funding German Research Foundation (DFG).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
p53
cervical cancer
Megjelenés:The Lancet Oncology. - 10 : 8 (2009), p. 772-784. -
További szerzők:Ressing, Meike Koenig, Jochem Abba, Martin C. Agorastos, Theodoros Brenna, Sylvia M. F. Ciotti, Marco Das, B. R. Del, Mistro Annaros Dybikowska, Aleksandra Giuliano, Anna R. Gudleviciene, Zivile Gyllensten, Ulf Haws, Andrea L. F. Helland, Aslaug Herrington, C. Simon Hildesheim, Alan Humbey, Oliver Jee, Sun H. Kim, Jae Weon Madeleine, M. Margaret Menczer, Joseph Ngan, Hextan Y. S. N. Nishikawa, Akira Niwa, Yosimitshu Pegoraro, Rosemary Pillai, M. R. Ranzani, Gulielmina Rezza, Giovanni Rosenthal, Adam N. Roychoudhury, Susanta Saranath, Dhananjaya Schmitt, Virginia M. Sengupta, Sharmila Settheetham-Ishida, Wannapa Shirasawa, Hiroshi Snijders, Peter J. F. Stoler, Mark H. Suárez-Rincón, Angel E. Szarka Krisztina (1971-) (molekuláris biológus, mikrobiológus) Tachezy, Ruth Ueda, Masatsugu Zee, Ate G. J., van der Knebel, Doeberitz Magnus, Von Wu, Ming-Tsang Yamashita, Tsuyoshi Zehbe, Ingeborg Blettner Maria
Internet cím:DOI
elektronikus változat
Borító:

2.

001-es BibID:BIBFORM069211
Első szerző:Ragin, Camille
Cím:Prevalence of HPV Infection in Racial-Ethnic Subgroups of Head and Neck Cancer Patients / Ragin Camille, Liu Jeffrey C., Jones Gieira, Shoyele Olubunmi, Sowunmi Bukola, Kennett Rachel, Groen Harry J. M., Gibbs Denise, Blackman Elizabeth, Esan Michael, Brandwein Margaret S., Devarajan Karthik, Bussu Francesco, Chernock Rebecca, Chien Chih-Yen, Cohen Marc A., Samir El-Mofty, Mikio Suzuki, D'Souza Gypsyamber, Funchain Pauline, Eng Charis, Gollin Susanne M., Hong Angela, Jung Yuh-S., Krüger Maximilian, Lewis James, Morbini Patrizia, Landolfo Santo, Rittà Massimo, Straetmans Jos, Szarka Krisztina, Tachezy Ruth, Worden Francis P., Nelson Deborah, Gathere Samuel, Taioli Emanuela
Dátum:2017
ISSN:0143-3334
Megjegyzések:The landscape of HPV infection in racial/ethnic subgroups of head and neck cancer (HNC) patients has not been evaluated carefully. In this study, a meta-analysis examined the prevalence of HPV in HNC patients of African ancestry. Additionally, a pooled analysis of subject-level data was also performed to investigate HPV prevalence and patterns of p16 (CDNK2A) expression amongst different racial groups. Eighteen publications (N = 798 Black HNC patients) were examined in the meta-analysis, and the pooled analysis included 29 datasets comprised of 3,129 HNC patients of diverse racial/ethnic background. The meta-analysis revealed that the prevalence of HPV16 was higher among Blacks with oropharyngeal cancer than Blacks with non-oropharyngeal cancer. However, there was great heterogeneity observed among studies (Q test P<0.0001). In the pooled analysis, after adjusting for each study, year of diagnosis, age, gender and smoking status, the prevalence of HPV16/18 in oropharyngeal cancer patients was highest in Whites (61.1%), followed by 58.0% in Blacks and 25.2% in Asians (P<0.0001). There was no statistically significant difference in HPV16/18 prevalence in non-oropharyngeal cancer by race (P=0.682). With regard to the pattern of HPV16/18 status and p16 expression, White patients had the highest proportion of HPV16/18+/p16+ oropharyngeal cancer (52.3%), while Asians and Blacks had significantly lower proportions (23.0% and 22.6%, respectively) [P <0.0001]. Our findings suggest that the pattern of HPV16/18 status and p16 expression in oropharyngeal cancer appears to differ by race and this may contribute to survival disparities.
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Carcinogenesis 38 : 2 (2017), p. 218-229. -
További szerzők:Liu, Jeffrey C. Jones, Gieira Shoyele, Olubunmi Sowunmi, Bukola Kennett, Rachel Groen, Harry J. M. Gibbs, Denise Blackman, Elizabeth Esan, Michael Brandwein, Margaret S. Devarajan, Karthik Bussu, Francesco Chernock, Rebecca Chien, Chih-Yen Cohen, Marc A. Samir, El-Mofty Mikio, Suzuki D'Souza, Gypsyamber Funchain, Pauline Eng, Charis Gollin, Susanne M. Hong, Angela Jung, Yuh-S. Krüger, Maximilian Lewis, James Morbini, Patrizia Landolfo, Santo Rittà, Massimo Straetmans, Jos Szarka Krisztina (1971-) (molekuláris biológus, mikrobiológus) Tachezy, Ruth Worden, Francis P. Nelson, Deborah Gathere, Samuel Taioli, Emanuela
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1