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Infection of Human Papillomavirus Type 18 and p53 Codon 72 Polymorphism in Lung Cancer Patients From India*

Neeraj Jain, PhD; Vikram Singh, MD; Suresh Hedau, PhD; Suresh Kumar, MD; Mradul K. Daga, MD; Richa Dewan, MD; Nandagudi S. Murthy, PhD; Syed A. Husain, PhD; Bhudev C. Das, PhD
Author and Funding Information

From the Division of Molecular Oncology (Drs. Jain, Hedau, and Das), Institute of Cytology and Preventive Oncology, Noida; Department of Medicine (Drs. Singh, Kumar, Daga, and Dewan), Maulana Azad Medical College, Bahadur Shah Zafar Marg, New Delhi; Department of Biosciences (Dr. Husain), Jamia Millia Islamia, Jamia Nagar, New Delhi; and Institute for Research in Medical Statistics (Dr. Murthy), Indian Council of Medical Research, Ansari Nagar, New Delhi, India.

Correspondence to: Bhudev C. Das, PhD, Division of Molecular Oncology, Institute of Cytology and Preventive Oncology, I-7, Sector-39, Noida, 201301, India; e-mail: bcdas48@hotmail.com



Chest. 2005;128(6):3999-4007. doi:10.1378/chest.128.6.3999
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Study objectives: Infection with specific high-risk HPV types 16 and 18 and polymorphism of p53 codon 72 has been strongly associated with the genesis of various neoplasms in humans, but such study in lung cancer is limited and the results are controversial. In India, the role of these two factors has been strongly implicated in cervical and other cancers, but the occurrence of HPV or p53 codon 72 polymorphism has not been examined in lung cancer, which is the most common cause of cancer-related death in India.

Design and patients: A total of 40 tumor biopsy specimens from advanced lung cancer patients and blood samples from 40 matching control subjects were obtained for the analysis of high-risk HPV types 16 and 18 infection and p53 codon 72 polymorphism by polymerase chain reaction.

Results: Only HPV type 18 was detected in 5% (2 of 40 lung cancer patients), but no other HPV could be detected. A significantly increased frequency of Arg/Arg homozygotes was observed in patients with advanced lung cancer when compared to that of control subjects (p = 0.004; odds ratio, 5.13; 95% confidence interval, 1.59 to 17.26). However, no significant correlation could be made between p53 polymorphism and different clinical stages, except for advanced stage IV patients, who showed a higher proportion of Arg/Pro heterozygous genotype.

Conclusions: HPV detected in a small proportion of lung cancer patients in India demonstrated an exclusive prevalence of HPV type 18, and there was a significantly higher frequency of p53 Arg/Arg genotype when compared to that of control subjects. Observation of a shorter duration of symptoms (≤ 4 months) in as many as 78% (seven of nine stage IV patients) with Arg/Pro genotype may be an indication that lung cancer patients with the heterozygous p53 genotype are more susceptible to early progression.

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