Human papillomavirus DNA in squamous cell carcinoma of the lung.

Hirayasu, Tsuneo; Iwamasa, Teruo; Kamada, Yoshihiko; Koyanagi, Yoshio; Usuda, Hiroyuki; Genka, Keiichiro

doi:10.1136/jcp.49.10.810

Cited by 74 publications

(89 citation statements)

References 22 publications

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“…Moreover, female lung cancer cases were more prone to HPV 16 infection than males and the prevalence in adenocarcinoma was higher than that of squamous carcinomas. For this difference in tumor type, although a previous study had detected HPV in up to 79% of squamous carcinoma of the lung, 11 Miyagi et al 12 had revealed a decreasing trend in the prevalence of HPV in lung squamous carcinoma from 79% in 1993 to 24% in 1998. Furthermore, HPV DNA was detected in a high proportion (78%) of lung adenocarcinoma in a previous study.…”

Section: Discussionmentioning

confidence: 98%

The presence of human papillomavirus type 16/18 DNA in blood circulation may act as a risk marker of lung cancer in Taiwan

Chiou¹,

Wu²,

Liaw³

et al. 2003

Cancer

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BACKGROUNDLung cancer is the leading cause of cancer death in Taiwan, and the paucity of dependable risk markers has impeded the early management of lung cancer. An association of human papillomavirus (HPV) 16/18 infection with lung cancer among nonsmoking Taiwanese women was revealed in our previous study.METHODSNested PCR was employed to detect HPV 16/18 DNA in the blood circulation of 149 lung cancer patients and 174 noncancer controls. In addition, correlation of prevalence of HPV DNA between the blood circulation and lung tumor tissue was compared from 70 sets of paired tumor tissues and peripheral blood samples available.RESULTSThe results showed that the prevalence rate of HPV 16/18 in the blood circulation of lung cancer cases was significantly higher than that of noncancer controls (47.7% vs. 12.6% for HPV 16, P < 0.0001; 30.9% vs. 5.2% for HPV 18, P < 0.0001). A significantly higher HPV 16 prevalence was detected in female lung cancer patients than that of male (57.6% vs. 41.1%, P = 0.048), as well as in cases with tumor Stages III/IV than those with tumor Stages I/II (54.6% vs. 29.3%, P = 0.006). After adjusting the effects of age, gender, and smoking status, a 6.5‐fold greater risk of lung cancer was demonstrated for those subjects with HPV Type 16 positive (95% CI 3.7–11.3, P < 0.0001), a 9.2‐fold for HPV Type 18 positive (95% CI 4.2–20.2, P < 0.0001), and a 75.7‐fold greatest risk for those with both HPV Type 16 and 18 positive (95% CI 9.8–582.1, P < 0.0001).CONCLUSIONSThese results suggested that the presence of HPV DNA in the blood circulation may serve as a feasible risk marker of lung cancer. Cancer 2003;97:1558–63. © 2003 American Cancer Society.DOI 10.1002/cncr.11191

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Section: Discussionmentioning

confidence: 98%

The presence of human papillomavirus type 16/18 DNA in blood circulation may act as a risk marker of lung cancer in Taiwan

Chiou¹,

Wu²,

Liaw³

et al. 2003

Cancer

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“…3), familial tumor history (4), or diet (5,6), may also be associated with the development of lung cancer (7). In Western countries, 70% to 90% of lung cancers are attributable to cigarette smoking, whereas in Taiwan, only 7% of female lung cancer cases are associated with smoking (8,9). Many genes [e.g., TP53 (10,11), EGFR (12, 13), KRAS (14), PIK3CA (15), and EML4-ALK (16)] have been reported in association with lung cancer in never smokers, although the molecular mechanisms of NSCLC in nonsmoking women still remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Identification of a Novel Biomarker, SEMA5A, for Non–Small Cell Lung Carcinoma in Nonsmoking Women

Tsai

Lee

et al. 2010

Cancer Epidemiology, Biomarkers &Amp; Prevention

261

230

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Background: Although cigarette smoking is the major risk factor for lung cancer, only 7% of female lung cancer patients in Taiwan have a history of smoking. The genetic mechanisms of carcinogenesis in nonsmokers are unclear, but semaphorins have been suggested to play a role as lung tumor suppressors. This report is a comprehensive analysis of the molecular signature of nonsmoking female lung cancer patients in Taiwan, with a particular focus on the semaphorin gene family.Methods: Sixty pairs of tumor and adjacent normal lung tissue specimens were analyzed by using Affymetrix U133plus2.0 expression arrays. Differentially expressed genes in tumor tissues were identified by a paired t test and validated by reverse transcriptase-PCR and immunohistochemistry. Functional analysis was conducted by using Ingenuity Pathway Analysis as well as gene set enrichment analysis and sigPathway algorithms. Kaplan-Meier survival analyses were used to evaluate the association of SEMA5A expression and clinical outcome.Results: We identified 687 differentially expressed genes in non-small cell lung carcinoma (NSCLC). Many of these genes, most notably the semaphorin family, were participants in the axon guidance signaling pathway. The downregulation of SEMA5A in tumor tissue, both at the transcriptional and translational levels, was associated with poor survival among nonsmoking women with NSCLC.Conclusions: In summary, several semaphorin gene family members were identified as potential therapeutic targets, and SEMA5A may be useful as a prognostic biomarker for NSCLC, which may also be gender specific in Taiwanese patients.Impact: A novel biomarker for NSCLC is identified. Cancer Epidemiol Biomarkers Prev; 19(10); 2590-7. ©2010 AACR.

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“…Etiological involvement of HPV in development of lung cancer was originally postulated (8)(9)(10). Inconsistency in prevalence of human papillomavirus (HPV) infection in lung cancer was found among recent studies from different countries with racial and geographic variations.…”

Section: Introductionmentioning

confidence: 99%

Correlation of HPV-16/18 infection of human papillomavirus with lung squamous cell carcinomas in Western China

Yan

2009

Oncol Rep

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Abstract. Prevalent inconsistency of human papillomavirus (HPV) infection in lung cancer was found among recent studies from different countries with racial and geographic variations. Even in Chinese populations, the prevalent discrepancy of HPV infection in lung cancer patients was also found with the geographic variations and tumor types. To study the difference of HPV-16/18 infection in lung squamous cell carcinomas and non-cancer controls, we conducted this study to verify whether there was a similar HPV infection prevalence pattern in lung squamous cell carcinoma patients from the Western part of China. Paraffinembedded samples (180), of 72 lung squamous cell carcinomas, 37 lung adenocarcinomas and 71 non-cancer controls, were analyzed by INNO-LIPA Genotype polymerase chain reaction (PCR) and real-time PCR analysis. The data showed that 51.4% (37/72) of lung squamous cell carcinoma samples, 16.2% (6/37) of adenocarcinoma, and 22.5% (16/71) of non-cancer controls were HPV DNA positive. The risk of lung squamous cell carcinomas was 3.5 times higher among people HPV-positive (odds ratio 3.5, 95% CI 1.6-7.3, p<0.001) compared with the HPV-negative population. Adjusted by smoking status, the risk of lung squamous cell carcinomas was 3.5 times higher among people HPVpositive (odds ratio 3.5, 95% CI 1.7-7.5, p=0.001) compared with the HPV-negative population. The risk of lung squamous cell carcinomas was 16.9 times higher for patients with positive HPV-16 (odds ratio 16.9, 95% CI 3.8-75.3, p<0.0001) than negative HPV-16. Adjusted by smoking status, the risk of lung squamous cell carcinomas was 17.4 times higher among people HPV-16 positive (odds ratio 17.4, 95% CI 3.9-77.5, p<0.0001) compared with HPV-16 negative people. INNO-LIPA Genotype analysis revealed that the frequency of high risk HPV-16 and 18 genotype in lung squamous cell carcinoma cases appeared to be significant higher than that in the non-cancer controls (P<0.001), and the most frequent genotype was HPV-16 (21 cases), followed by HPV-18 (6 cases), HPV-16/18 (4 cases) in lung squamous cell carcinomas, respectively, and the majority genotype was HPV-6 (9 cases) in controls. The HPV-16 E 2 /E 6 ratio was significantly lower than the unity, suggested that the main presence of integrated form of HPV-16 genome (16/27) may contribute more to lung squamous cell carcinomas, despite its viral load estimated to be only <1 to 2 copies per cell.

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Human papillomavirus DNA in squamous cell carcinoma of the lung.

Cited by 74 publications

References 22 publications

The presence of human papillomavirus type 16/18 DNA in blood circulation may act as a risk marker of lung cancer in Taiwan

The presence of human papillomavirus type 16/18 DNA in blood circulation may act as a risk marker of lung cancer in Taiwan

Identification of a Novel Biomarker, SEMA5A, for Non–Small Cell Lung Carcinoma in Nonsmoking Women

Correlation of HPV-16/18 infection of human papillomavirus with lung squamous cell carcinomas in Western China

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