Coll. Antropol. 34 (2010) 1: 159–162 Original scientific paper Detection of Human Papillomaviruses Type 16, 18 and 33 in Bronchial Aspirates of Lung Carcinoma Patients by Polymerase Chain Reaction: A Study of 84 Cases in Croatia Bo`ica Vrabec Branica 1 , Silvana Smojver-Je`ek 1 , Zrinka Juro{ 1 , Sandra Grgi} 2 , Nives Srpak 2 , Dinko Mitre~i} 2 and Sre}ko Gajovi} 2 1 Department of Cytology, University Hospital for Lung Diseases »Jordanovac«, Zagreb, Croatia 2 Croatian Institute for Brain Research, School of Medicine, University of Zagreb, Zagreb, Croatia ABSTRACT Besides its well-known role in cervical carcinoma, HPV is also suggested to be involved in lung cancer development. A number of authors have been investigating the presence of HPV in histological materials. We used routine bronchial as- pirates from 84 patients with lung carcinoma for DNA extraction and then performed polymerase chain reaction for high-risk HPV types 16, 18 and 33. The results were compared to those obtained from buccal and eyelid mucosa. Only three patients were positive for HPV in bronchial aspirates: one for HPV 16 type, one for HPV 18 type, and one for HPV 33. Our data indicated the low prevalence of HPV in patients with lung carcinomas in Croatia, therefore it seems un- likely that HPV contributes to the development of lung carcinomas in this region. Key words: lung carcinoma, human papilloma virus, polymerase chain reaction Introduction The etiology of lung carcinoma is only partially re- solved. The majority of tobacco users do not develop such tumors and at least 10–15% of lung carcinomas occur in non smokers 1 . Some studies suggested that HPV may play an aetiologic role in bronchial carcinogenesis and possibility of a latent HPV infection as a cocarcinogen cannot be excluded 2 . High-risk genotypes, including HPV 16, 18 and 33 are associated with the cancer of the uter- ine cervix 3 but they can be also detected in cancers of the upper aerodigestive tract, including cancers of the oral cavity, larynx and oesophagus tract 4–6 . A study in Fin- land 7 reported HPV integration in cancers of the hypo- pharynx, larynx, tongue and oral cavity and review of Syrjanen showed that HPV was detected in 22% of bron- chial carcinomas with wide racial and geographic varia- tion from 0–100% 2 . Recent article of Klein and al. re- viewed 53 publications and 4508 cases showing the mean incidence of HPV in lung carcinoma was 24.5% and sug- gested that HPV is the second most important cause of lung cancer after cigarette smoking 8 . Those HPVs, which are considered as high risk for the cancer development, express the early oncoproteins E7 and E6. E7 inactivates the cellular tumor suppressor protein Rb, while E6 pro- tein binds to the host cellular tumor suppressor protein p53 and triggers its degradation through the ubiquitin pathway 9 . The inactivation of p53 by HPV-E6 is consid- ered to play a crucial role in human carcinogenesis 10 . Some studies showed that tracheal epithelial cells could be immortalised by HPV18 E6 and E7 oncogenes. Simi- lar experiments were carried out with bronchial epithe- lial cells, which were immortalised by the HPV 16 E6 and E7 oncogenes and showed terminal differentiation of the keratinocytes but were not-tumorigenic in nude mice 2 . The aim of our work was to study the prevalence of high-risk HPV types 16, 18 and 33 in 84 bronchial aspi- rates of lung carcinoma patients by PCR and to elucidate whether the HPV infection is associated with lung cancer development in Croatia. The incidence of bronchial carci- noma in Croatia for the year 2005 was 2996 per 100000 11 . 159 Received for publication June 19, 2009