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Experimental and molecular pathology (1)
Journal of Clinical Microbiology (1)
PLoS ONE (1)
Feng, Qinghua (3)
Kiviat, Nancy B. (2)
Argenyi, Zsolt B. (1)
Asgari, Maryam M. (1)
Baseman, Janet G. (1)
Hawes, Stephen (1)
Hawes, Stephen E. (1)
Kiviat, Nancy (1)
Koutsky, Laura A. (1)
Loeb, Keith R. (1)
Lu, Hiep (1)
Mao, Constance (1)
Stern, Joshua (1)
Stern, Joshua E. (1)
Toland, Amanda Ewart (1)
Xi, Long Fu (1)
de Villiers, Ethel-Michele (1)
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Analysis of Tp53 Codon 72 Polymorphisms, Tp53 Mutations, and HPV Infection in Cutaneous Squamous Cell Carcinomas
Loeb, Keith R.
Asgari, Maryam M.
Hawes, Stephen E.
Stern, Joshua E.
Argenyi, Zsolt B.
de Villiers, Ethel-Michele
Kiviat, Nancy B.
Toland, Amanda Ewart
Non-melanoma skin cancers are one of the most common human malignancies accounting for 2–3% of tumors in the US and represent a significant health burden. Epidemiology studies have implicated Tp53 mutations triggered by UV exposure, and human papilloma virus (HPV) infection to be significant causes of non-melanoma skin cancer. However, the relationship between Tp53 and cutaneous HPV infection is not well understood in skin cancers. In this study we assessed the association of HPV infection and Tp53 polymorphisms and mutations in lesional specimens with squamous cell carcinomas.
We studied 55 cases of histologically confirmed cutaneous squamous cell carcinoma and 41 controls for the presence of HPV infection and Tp53 genotype (mutations and polymorphism).
We found an increased number of Tp53 mutations in the squamous cell carcinoma samples compared with perilesional or control samples. There was increased frequency of homozygous Tp53-72R polymorphism in cases with squamous cell carcinomas, while the Tp53-72P allele (Tp53-72R/P and Tp53-72P/P) was more frequent in normal control samples. Carcinoma samples positive for HPV showed a decreased frequency of Tp53 mutations compared to those without HPV infection. In addition, carcinoma samples with a Tp53-72P allele showed an increased incidence of Tp53 mutations in comparison carcinomas samples homozygous for Tp53-72R.
These studies suggest there are two separate pathways (HPV infection and Tp53 mutation) leading to cutaneous squamous cell carcinomas stratified by the Tp53 codon-72 polymorphism. The presence of a Tp53-72P allele is protective against cutaneous squamous cell carcinoma, and carcinoma specimens with Tp53-72P are more likely to have Tp53 mutations. In contrast Tp53-72R is a significant risk factor for cutaneous squamous cell carcinoma and is frequently associated with HPV infection instead of Tp53 mutations. Heterozygosity for Tp53-72R/P is protective against squamous cell carcinomas, possibly reflecting a requirement for both HPV infection and Tp53 mutations.
DNA methylation changes in normal liver tissues and hepatocellular carcinoma with different viral infection
Experimental and molecular pathology
Hepatocellular carcinoma (HCC) is known to be associated with both HBV and HCV and HVC. While epigenetic changes have been previously reported to be associated with hepatocellular carcinoma (HCC), whether the epigenetic profile of HBC associated HCC differs from that of HCV associated HCC is unclear. We analyzed DNA methylation of ten genes (APC, CCND2, CDKN2A, GSTP1, HOXA9, RARB, RASSF1, RUNX, SFRP1, and TWIST1) using MethyLight assays on 65 archived liver tissue blocks. Three genes (APC, CCND2, and GSTP1) were frequently methylated in normal liver tissues. Five genes (APC, CDKN2A, HOXA9, RASSF1, and RUNX) were significantly more frequently methylated in malignant liver tissues than normal liver tissues. Among HCC cases, HOXA9, RASSF1 and SFRP1 were methylated more frequently in HBV positive HCC cases, while CDKN2A were significantly more frequently methylated in HCV positive HCC cases. Our data support the hypothesis that HCC resulting from different viral etiologies are associated with different epigenetic changes.
hypermethylation; HBV; HCV; hepatocellular carcinoma
Sequence Variation of Human Papillomavirus Type 16 and Measurement of Viral Integration by Quantitative PCR▿
Baseman, Janet G.
Koutsky, Laura A.
Kiviat, Nancy B.
Xi, Long Fu
Journal of Clinical Microbiology
Given that the integration of human papillomavirus type 16 (HPV16) into the host genome occurs preferentially with the disruption of the E2 gene, a ratio of E2 to E7 gene copies is often used as a marker for integration. It is largely undetermined, however, whether ratio estimates are affected by HPV intratypic variations. We assembled four plasmid constructs, each containing a DNA fragment from an HPV16 European, Asian-American, African-1, or African-2 variant. These constructs and nine cervical swab samples were assayed by real-time PCR with two primer-probe sets for each gene: a specific set, fully complementary to the HPV16 prototype, and a degenerate set, incorporating degenerate bases at positions where nucleotides differed among the variants. The ratio of E2 to E7 gene copies for the European variant construct was close to 1, no matter which sets of primers and probes were used. While the ratios for the African-1 and Asian-American variant constructs remained close to 1 with the degenerate sets of primers and probes, the ratios were 0.36 and 2.57, respectively, with the specific sets of primers and probes. In addition, a nucleotide alteration at the position immediately following the 3′ end of the E2 forward primer binding site was found to be responsible for an underestimation of E2 gene copies for the African-2 variant construct. Similar patterns were found in nine cervical samples. In conclusion, mismatches between the primers and probes and their targets due to HPV16 intratypic variations would introduce errors in testing for integration; this situation can be sufficiently ameliorated by incorporating degenerate bases into the primers and probes.
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