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Carcinogenesis. 2014 Jun;35(6):1267-75. doi: 10.1093/carcin/bgu038. Epub 2014 Feb 12.

HPV-associated lung cancers: an international pooled analysis.

Author information

1
Cancer Prevention and Control Program, Fox Chase Cancer Center, Philadelphia, PA, USA, camille.ragin@fccc.edu.
2
Cancer Prevention and Control Program, Fox Chase Cancer Center, Philadelphia, PA, USA.
3
Biostatistics & Bioinformatics, Winship Cancer Institute, Emory University, Atlanta, GA, USA.
4
Department of Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, NY, USA.
5
Department of Epidemiology and Preventative Medicine, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima, Japan.
6
Virology Program, Instituto de Ciencias Biomédicas (ICBM), Faculty of Medicine, University of Chile, Santiago, Chile.
7
Infections and Immunoepidemiology Branch and.
8
Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
9
Department of Medical and Surgical Sciences, Faculty of Medicine, University of Foggia, Foggia, Italy.
10
Laboratory of Molecular Virology, Foundation Polyclinic Tor Vergata, Rome, Italy.
11
Department of Medical Oncology, Hokkaido University, Graduate School of Medicine, North 15, West 7, Kita-ku, Sapporo 060-8638, Japan.
12
Department and Cellular and Organ Pathology, Graduate School of Medicine, Akita University, 1-1-1 Hondo, Akita 010-8543, Japan.
13
Faculty of Medicine, Laboratory of Clinical Virology, 5D10, University of Crete, Vassilika Voutes, 71110 Heraklion, Crete, Greece.
14
Laboratory of Histology & Embryology, School of Medicine, University of Athens, Athens, Greece.
15
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands.
16
Department of Pathology, Tokyo Women's Medical University Yachiyo Medical Center, 477-96 Owada-Shinden, Yachiyo-shi, Chiba 276-8524, Japan.
17
Division of Multistep Carcinogenesis, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo 104-0045, Japan.
18
Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
19
Department of Medical Oncology and Developmental Therapeutics Program, Fox Chase Cancer Center, Philadelphia, PA, USA.
20
Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA, USA.
21
Department of Medical Oncology, National Cancer Center Singapore, 11 Hospital Drive, Singapore 169610, Republic of Singapore.
22
Department of Oncology & Radiotherapy, Turku University Hospital, Turku, Finland, Fundação Pio XII- Hospital de Câncer de Barretos, Barretos, Brazil.
23
Department of Pathology and.
24
Department of Biostatistics, University Health Network, Princess Margaret Cancer Centre, Toronto, Ontario M5G2M9, Canada.
25
Division of Health Sciences, Warwick Medical School, The University of Warwick, Coventry, UK and.
26
Department of Population Health, North Shore Long Island Jewish Health System, Hofstra Medical School, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, USA.

Abstract

Human papillomavirus (HPV) is the etiologic risk factor for cervical cancer. Some studies have suggested an association with a subset of lung tumors, but the etiologic link has not been firmly established. We performed an international pooled analysis of cross-sectional studies (27 datasets, n = 3249 patients) to evaluate HPV DNA prevalence in lung cancer and to investigate viral presence according to clinical and demographic characteristics. HPV16/18 were the most commonly detected, but with substantial variation in viral prevalence between geographic regions. The highest prevalence of HPV16/18 was observed in South and Central America, followed by Asia, North America and Europe (adjusted prevalence rates = 22, 5, 4 and 3%, respectively). Higher HPV16 prevalence was noted in each geographic region compared with HPV18, except in North America. HPV16/18-positive lung cancer was less likely observed among White race (adjusted odds ratio [OR] = 0.33, 95% confidence interval [CI] = 0.12-0.90), whereas no associations were observed with gender, smoking history, age, histology or stage. Comparisons between tumor and normal lung tissue show that HPV was more likely to be present in lung cancer rather than normal lung tissues (OR = 3.86, 95% CI = 2.87-5.19). Among a subset of patients with HPV16-positive tumors, integration was primarily among female patients (93%, 13/14), while the physical status in male cases (N = 14) was inconsistent. Our findings confirm that HPV DNA is present in a small fraction of lung tumors, with large geographic variations. Further comprehensive analysis is needed to assess whether this association reflects a causal relationship.

PMID:
24523449
PMCID:
PMC4043241
DOI:
10.1093/carcin/bgu038
[Indexed for MEDLINE]
Free PMC Article
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