Human papillomavirus in lung carcinomas among three Latin American countries

Castillo, Andres; Aguayo, Francisco; Koriyama, Chihaya; Shuyama, K; Akiba, Suminori; Herrera‐Goepfert, Roberto; Carrascal, Edwin; Klinge, German; Sánchez, Juvenal; Eizuru, Yoshito

doi:10.3892/or.15.4.883

Cited by 23 publications

(25 citation statements)

References 12 publications

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“…Among HPV genotypes detected, 85% were high-risk HPV. The most frequently detected genotype in the present study was HPV-16, which accounted for 55% of HPV-positive cases, as was also the case in our previous study conducted in other Latin-American countries, including Mexico, Colombia, and Chile (Castillo et al, 2006). Our findings are also in accordance with those shown in a review published by Syrjänen (2002), where HPV was positive in 25% of SQCs, 19% of SCCs, and 8% of ACs.…”

Section: Discussionsupporting

confidence: 93%

“…In the case of the lung, the association of HPV-18 with ACs was shown by a study of nonsmoking Taiwanese women (Cheng et al, 2001). A Latin-American study also detected HPV-18 only in lung ACs (Castillo et al, 2006). A recent meta-analysis by Chen et al (2004) showed that 9 -42% of pulmonary ACs among Asians were HPV positive.…”

Section: Discussionmentioning

confidence: 96%

“…On the other hand, studies in Latin-American and Asian LCs reported relatively high prevalence of HPV, including HPV16 (Miyagi et al, 2000, Castillo et al, 2006 even though they used formalin-fixed paraffin-embedded carcinoma specimens.…”

Section: Discussionmentioning

confidence: 99%

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Human papillomavirus-16 is integrated in lung carcinomas: a study in Chile

et al. 2007

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The human papillomavirus (HPV) was detected in 20 (29%) out of 69 lung carcinomas (LCs) in Chile, by PCR and Southern blot, and was more frequently detected in squamous cell carcinoma (SQC) than in adenocarcinomas (46 vs 9%, P ¼ 0.001). HPV-16, positive in 11 cases, was the most frequently detected HPV genotype determined by DNA sequencing. HPV-16 E2/E6 ratio, estimated from real-time PCR analysis, was much lower than the unity, suggesting that at least a partial HPV-16 genome was integrated in all but one HPV-16-positive SQCs. The remaining one case was suspected to have only episomal HPV-16. Although the viral load was low in most of the LCs, a case showed the HPV-16 copy number as high as 8479 per nanogram DNA, which was even a few times higher than the minimum viral load of seven cervical carcinomas (observed viral load: 3356 -609 392 per nanogram DNA). The expression of the HPV-16/18 E6 protein was found in only two HPV-16-positive SQCs (13%) but not in the case with the highest viral load. Although the viral load was in general very low and HPV E6 expression is none or weak, further studies seem warranted to examine aetiological involvement of high-risk HPV in lung carcinogenesis.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 96%

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Human papillomavirus-16 is integrated in lung carcinomas: a study in Chile

et al. 2007

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“…A large sample investigation reported that HPV DNA infection rate was 21.7% in 2468 lung carcinomas (11). HPV infection is considered a cocarcinogen of lung cancer and its contribution to pathogenesis has been evaluated (12)(13)(14)(15)(16)(17)(18). However, even in Asian populations, the prevalence discrepancy of HPV infection in lung cancer patients was also found with the geographic variations and tumor types.…”

Section: Introductionmentioning

confidence: 87%

“…In the majority of carcinomas associated with high-risk HPV and some advanced HPV-associated precancerous lesions, the whole viral genome or its fragment is integrated into the chromosomal DNA of the host cell whereas the HPV genome was retained as episomal molecules in early dysplastic low-grade lesions (17). Although the mechanism involved in switching from episomal state to viral integration was yet unclear, it was suspected that methylation pattern on HPV genome was different in episomal and integrated states.…”

Section: Discussionmentioning

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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