Presence of human papillomavirus DNA and abnormal p53 protein accumulation in lung carcinoma.

Soini, Ylermi; Nuorva, Kyösti; Kamel, Dia; Pöllänen, Raimo; Vähäkangas, Kirsi; Lehto, Veli‐Pekka; Pääkkö, Paavo

doi:10.1136/thx.51.9.887

Cited by 47 publications

(39 citation statements)

References 25 publications

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“…Genomic DNA was prepared from tissue sections by phenolchloroform extraction, ethanol precipitation, and finally dissolved in 20 AL of sterile distilled water. HPV viral DNA was first amplified with type consensus primers MY09 and MY11, followed by a second round of amplification with type-specific primers flanking the L1 region to identify the subtype (14). Ten microliters of the final PCR products were loaded onto a 2% agarose gel, stained with ethidium bromide, and visualized under UV illumination.…”

Section: Methodsmentioning

confidence: 99%

Human Papillomavirus Type 16/18 Up-Regulates the Expression of Interleukin-6 and Antiapoptotic Mcl-1 in Non–Small Cell Lung Cancer

Cheng¹,

Lee

Shiau

et al. 2008

Clinical Cancer Research

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Purpose: Human papillomavirus (HPV) 16/18 infection is reported to be associated with nonsmoking Taiwanese female lung cancer. In this study, we attempted to further reveal the association between HPV infection with Mcl-1 and interleukin (IL)-6 expressions and to elucidate the roles of HPV infection in lung tumorigenesis. Experimental Design: IL-6 and Mcl-1expressions were investigated in 79 tumor tissues from lung cancer patients by immunohitochemistry. Secreting IL-6 levels and Mcl-1expressions were examined by ELISA and Western blot, respectively, in HPV 16/18 E6-and E7-transfected A549 human lung cancer cells, as well as in the HPV16-infected TL-1lung cancer cells established from lung cancer patients. Results: Lung tumors (70.9% and 57.0%) had positive IL-6 and Mcl-1immunostainings, respectively. Significant correlation between IL-6 and Mcl-1 expression were observed (P < 0.0001).Both IL-6 and Mcl-1 expression were significantly associated with HPV 16/18 infection (P = 0.014 and P = 0.004, respectively). IL-6 and Mcl-1protein levels were not only elevated in HPV 16/18 E6-and E7-transfected A549 cells but also in TL-1 cells. Phosphatidylinositol-3-OH kinase pathway was the major pathway contributing to the up-regulation of Mcl-1 by IL-6 in HPV-infected lung cancer cells. Conclusions: The up-regulating effects of HPV 16/18 E6 and E7 to IL-6 and Mcl-1expressions were observed in E6-and E7-transfected A549 cells and in HPV16-infected TL-1 cells, mainly through the phosphatidylinositol-3-OH kinase pathway. The involvement of HPV infection in lung tumorigenesis may be partly through a concomitant increased expression of autocrine and/or paracrine IL-6 and the downstream Mcl-1.

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Section: Methodsmentioning

confidence: 99%

Human Papillomavirus Type 16/18 Up-Regulates the Expression of Interleukin-6 and Antiapoptotic Mcl-1 in Non–Small Cell Lung Cancer

Cheng¹,

Lee

Shiau

et al. 2008

Clinical Cancer Research

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“…Furthermore, DNA were extracted from whole blood or tissue samples by protease digestion, conventional phenol-chloroform extraction, ethanol precipitation, and finally dissolved in 20 l of sterile distilled water. HPV viral DNA was first amplified with type consensus primers MY09 and MY11 7 followed by a second round of amplification with type-specific primers flanking the L1 region to identify the subtype (sequences of Type 16 primers: 5Ј-TAC TAA CTT TAA GGA GTA CC-3Ј and 5Ј-GTG TAT GTT TTT GAC AAG CAA TT-3Ј; sequences of Type 18 primers: 5Ј-CCA AAT TTA AGC AGT ATA GC-3Ј and 5Ј-TTG TAC AAA ACG ATA TGT ATC CA-3Ј. Ten microliters of the final PCR product was loaded onto a 2% agarose gel, stained with ethidium bromide, and visualized under ultraviolet illumination.…”

Section: Nested Polymerase Chain Reaction (Nested Pcr)mentioning

confidence: 99%

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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“…The E6 protein of HPV interacts with the p53 tumour suppressor protein and an E6-associated protein, a host cell ubiquitin ligase, and induces accelerated proteasomal degradation of p53 (Barbosa, 1996). Another study showed an inverse relationship between the presence of HPV DNA and abnormal p53 accumulation in LCs (Soini et al, 1996). However, the overexpression of p16 INK4a is known to be observed in cancers of the uterine cervix (Schorge et al, 2004), which are almost always associated with HPV infection (Bosch et al, 2002).…”

mentioning

confidence: 99%

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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Presence of human papillomavirus DNA and abnormal p53 protein accumulation in lung carcinoma.

Cited by 47 publications

References 25 publications

Human Papillomavirus Type 16/18 Up-Regulates the Expression of Interleukin-6 and Antiapoptotic Mcl-1 in Non–Small Cell Lung Cancer

Human Papillomavirus Type 16/18 Up-Regulates the Expression of Interleukin-6 and Antiapoptotic Mcl-1 in Non–Small Cell Lung Cancer

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

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

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