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author:("Feng, xinghua")
1.  Epidemiology of Human Papillomavirus (HPV) Detected in the Oral Cavity and Fingernails of Mid-Adult Women 
Sexually transmitted diseases  2015;42(12):677-685.
Background
Oral and fingernail human papillomavirus (HPV) detection may be associated with HPV-related carcinoma risk at these non-genital sites and foster transmission to the genitals. We describe the epidemiology of oral and fingernail HPV among mid-adult women.
Methods
Between 2011–2012, 409 women aged 30–50 years were followed for 6 months. Women completed health and behavior surveys and provided self-collected oral, fingernail, and vaginal specimens at enrollment and exit for type-specific HPV DNA testing. Concordance of type-specific HPV detection across anatomic sites was described with kappa statistics. Using generalized estimating equations or exact logistic regression, we measured the univariate associations of various risk factors with type-specific oral and fingernail HPV detection.
Results
Prevalence of detecting HPV in the oral cavity (2.4%) and fingernails (3.8%) was low compared to the vagina (33.1%). Concordance across anatomic sites was poor (kappa<.20 for all comparisons). However, concurrent vaginal infection with the same HPV type (OR=101.0;95%CI: 31.4–748.6) and vaginal HPV viral load (OR per one log10 viral load increase=2.2;95%CI:1.5–5.5) were each associated with fingernail HPV detection. Abnormal Pap history (OR=11.1;95%CI:2.8-infinity), lifetime number of male vaginal sex partners ≥10 (OR vs. 0–3 partners=5.0;95%CI:1.2-infinity), and lifetime number of open-mouth kissing partners ≥16 (OR vs. 0–15 partners=infinity;95%CI:2.6-infinity, by exact logistic regression) were each associated with oral HPV detection.
Conclusions
While our findings support HPV DNA deposition or autoinoculation between anatomic sites in mid-adult women, the rarity of HPV in the oral cavity and fingernails suggests that oral/fingernail HPV does not account for a significant fraction of HPV in genital sites.
doi:10.1097/OLQ.0000000000000362
PMCID: PMC4646722  PMID: 26562696
human papillomavirus; women; oral; fingernail
2.  ONCOGENIC HUMAN PAPILLOMAVIRUS (HPV) INFECTIONS IN 18 TO 24 YEAR OLD FEMALE ONLINE DATERS 
Sexually transmitted diseases  2015;42(9):492-497.
Background
While risk factors for HPV infections in young women are well-defined, the risk associated with meeting male sex partners via the internet is unclear.
Methods
We analyzed cross-sectional data from 282 18-24-year old women who reported using Internet dating websites in the past year. Women were mailed vaginal self-sampling kits for PCR-based HPV genotyping (including 19 oncogenic types) and sexual behavior and health history questionnaires. Generalized linear models were used to evaluate risk factors for prevalent oncogenic HPV infections.
Results
35% of women reported having met a male sex partner via the Internet in the past 6 months, and 42% reported a history of HPV vaccination. The prevalence of oncogenic HPV infection was 37%, and 9% of women tested positive for HPV-16 or HPV-18. Having met a male sex partner via the Internet in the past 6 months was not significantly associated with oncogenic HPV infection. In multivariate analyses, variables associated with an increased likelihood of oncogenic HPV infection included male partners in the past 6 months who were reported to have ≥1 concurrent partnership (adjusted prevalence ratio [aPR]=1.51,95%CI:1.11-2.06) and not always using condoms with male partners in the past 6 months (aPR=1.86,95%CI:1.05-3.30). Self-reporting a history of receiving ≥1 dose of HPV vaccine was inversely associated with testing positive for HPV-16 or HPV-18 (aPR=0.39,95%CI:0.16–0.97).
Conclusions
While measures of recent sexual behavior were associated with prevalent oncogenic HPV infection, male partners met online were not associated with an increased likelihood of infection in this cohort of young women.
doi:10.1097/OLQ.0000000000000331
PMCID: PMC4596246  PMID: 26267875
HPV; human papilloma virus; women; prevalence; risk factors
3.  VIRAL LOAD AND SHORT-TERM NATURAL HISTORY OF TYPE-SPECIFIC ONCOGENIC HUMAN PAPILLOMAVIRUS INFECTIONS IN A HIGH-RISK COHORT OF MID-ADULT WOMEN 
Oncogenic human papillomavirus (HPV) viral load may inform the origin of newly detected infections and characterize oncogenic HPV natural history in mid-adult women. From 2007–2011, we enrolled 521 25–65 year old female online daters and followed them triannually with mailed health and sexual behavior questionnaires and kits for self-sampling for PCR-based HPV DNA testing. Samples from oncogenic HPV positive women were selected for type-specific DNA load testing by real-time PCR with adjustment for cellularity. Linear or logistic regression models were used to evaluate relationships between viral levels, health and sexual behavior, and longitudinal oncogenic HPV detection. Type-specific viral levels were borderline significantly higher in oncogenic HPV infections that were prevalent versus newly detected (p=0.092), but levels in newly detected infections were higher than in infections re-detected after intercurrent negativity (p<.001). Recent sex partners were not significantly associated with viral levels. Compared to prevalent infections detected intermittently, the likelihood of persistent (OR=4.31,95%CI:2.20–8.45) or single-time (OR=1.32,95%CI:1.03–1.71) detection increased per 1-unit increase in baseline log10 viral load. Viral load differences between re-detected and newly detected infections suggest a portion of new detections were due to new acquisition, although report of recent new sex partners (a potential marker of new infection) was not predictive of viral load; oncogenic HPV infections in mid-adult women with new partners likely represent a mix of new acquisition and reactivation or intermittent detection of previous infection. Intermittent detection was characterized by low viral levels, suggesting that intermittent detection of persisting oncogenic HPV infection may be of limited clinical significance
doi:10.1002/ijc.28509
PMCID: PMC3947429  PMID: 24136492
human papillomavirus; viral load; persistence; women; epidemiology
4.  Analysis of Tp53 Codon 72 Polymorphisms, Tp53 Mutations, and HPV Infection in Cutaneous Squamous Cell Carcinomas 
PLoS ONE  2012;7(4):e34422.
Background
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.
Methods
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).
Results
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.
Conclusions
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.
doi:10.1371/journal.pone.0034422
PMCID: PMC3335843  PMID: 22545084
5.  DNA hypermethylation of tumors from non-small cell lung cancer (NSCLC) patients is associated with gender and histologic type 
Background
We previously identified a number of genes which were methylated significantly more frequently in the tumor compared to the non-cancerous lung tissues from non-small cell lung cancer (NSCLC) patients. Detection of methylation profiles of genes in NSCLC could provide insight into differential pathways to malignancy and lead to strategies for better treatment of individuals with NSCLC.
Methods
We determined the DNA methylation status of 27 genes using quantitative MethyLight assays in lung tumor samples from 117 clinically well-characterized NSCLC patients.
Results
Hypermethylation was detected in one of more of the genes in 106 (91%) of 117 cases and was detected at high levels (Percentage of Methylation Reference (PMR)≥4%) in 79% of NSCLC cases. Methylation of APC, CCND2, KCNH5 and, RUNX was significantly more frequent in adenocarcinomas compared to squamous cell carcinomas (SCC), while methylation of CDKN2A was more common in SCC. Hypermethylation of KCNH5, KCNH8, and RARB was more frequent in females compared to males. Hypermethylation of APC and CCND2 was inversely associated with proliferation score assessed by Ki-67 level.
Conclusions
Our findings of differential gene hypermethylation frequencies in tumor tissues from patients with adenocarcinoma or squamous cell cancers and in females compared to males suggests that further investigation is warranted in order to more fully understand the potential disparate pathways and/or risk factors for NSCLC associated with histologic type and gender.
doi:10.1016/j.lungcan.2009.11.002
PMCID: PMC2888601  PMID: 19945765
hypermethylation; lung cancer; gender; histology
6.  Hypermethylation of CCND2 May Reflect a Smoking-Induced Precancerous Change in the Lung 
Journal of Oncology  2011;2011:950140.
It remains unknown whether tobacco smoke induces DNA hypermethylation as an early event in carcinogenesis or as a late event, specific to overt cancer tissue. Using MethyLight assays, we analyzed 316 lung tissue samples from 151 cancer-free subjects (121 ever-smokers and 30 never-smokers) for hypermethylation of 19 genes previously observed to be hypermethylated in nonsmall cell lung cancers. Only APC (39%), CCND2 (21%), CDH1 (7%), and RARB (4%) were hypermethylated in >2% of these cancer-free subjects. CCND2 was hypermethylated more frequently in ever-smokers (26%) than in never-smokers (3%). CCND2 hypermethylation was also associated with increased age and upper lobe sample location. APC was frequently hypermethylated in both ever-smokers (41%) and never-smokers (30%). BVES, CDH13, CDKN2A (p16), CDKN2B, DAPK1, IGFBP3, IGSF4, KCNH5, KCNH8, MGMT, OPCML, PCSK6, RASSF1, RUNX, and TMS1 were rarely hypermethylated (<2%) in all subjects. Hypermethylation of CCND2 may reflect a smoking-induced precancerous change in the lung.
doi:10.1155/2011/950140
PMCID: PMC3090638  PMID: 21577262
7.  DNA Methylation in Tumor and Matched Normal Tissues from Non-Small Cell Lung Cancer Patients 
We used MethyLight assays to analyze DNA methylation status of 27 genes on 49 paired cancerous and noncancerous tissue samples from non-small cell lung cancer (NSCLC) patients who underwent surgical resection. Seven genes (RARB, BVES, CDKN2A, KCNH5, RASSF1, CDH13, and RUNX) were found to be methylated significantly more frequently in tumor tissues than in noncancerous tissues. Only methylation of CCND2 and APC was frequently detected in both cancerous and noncancerous tissues, supporting the hypothesis that the methylation of these two genes is a preneoplastic change and may be associated with tobacco smoking exposure. Methylation of any one of eight genes (RASSF1, DAPK1, BVES, CDH13, MGMT, KCNH5, RARB, or CDH1) was present in 80% of NSCLC tissues but only in 14% of noncancerous tissues. Detection of methylation of these genes in blood might have utility in monitoring and detecting tumor recurrence in early-stage NSCLC after curative surgical resection.
doi:10.1158/1055-9965.EPI-07-2518
PMCID: PMC2798850  PMID: 18349282
8.  DNA Hypermethylation, Her-2/neu Overexpression and p53 Mutations in Ovarian Carcinoma 
Gynecologic oncology  2008;111(2):320-329.
Objectives
To define patterns of aberrant DNA methylation, p53 mutation and Her-2/neu overexpression in tissues from benign (N=29), malignant (N=100), and border line malignant ovaries (N=10), as compared to normal (N=68) ovarian tissues. Further, to explore the relationship between the presence of genetic and epigenetic abnormalities in ovarian cancers, and assess the association between epigenetic changes and clinical stage of malignancy at presentation and response to therapy.
Methods
The methylation status of 23 genes that were previously reported associated with various epithelial malignancies was assessed in normal and abnormal ovarian tissues by methylation specific PCR. The presence of p53 mutation (N=82 cases) and Her-2/neu overexpression (N=51 cases) were assessed by DNA sequencing and immunohistochemistry, respectively.
Results
Methylation of four genes (MINT31, HIC1, RASSF1, and CABIN1) was significantly associated with ovarian cancer but not other ovarian pathology. Her-2/neu overexpression was associated with aberrant methylation of three genes (MINT31, RASSF1, and CDH13), although aberrant methylation was not associated with p53 mutations. Methylation of RASSF1 and HIC1 was more frequent in early compared to late stage ovarian cancer, while methylation of CABIN1 and RASSF1 was associated with response to chemotherapy.
Conclusion
DNA methylation of tumor suppressor genes is a frequent event in ovarian cancer, and in some cases is associated with Her-2/neu overexpression. Methylation of CABIN1 and RASSF1 may have the utility to predict response to therapy.
doi:10.1016/j.ygyno.2008.07.036
PMCID: PMC2642648  PMID: 18757082
hypermethylation; Her-2/neu overexpression; p53; ovarian cancer

Results 1-8 (8)