Detection of oncogenic viruses (SV40, BKV, JCV, HCMV, HPV) and p53 codon 72 polymorphism in lung carcinoma

Giuliani, Laura; Jaxmar, Terese; Casadio, Caterina; Gariglio, Marisa; Manna, Assunta; D’Antonio, Domenico; Syrjänen, Kari; Favalli, Cartesio; Ciotti, Marco

doi:10.1016/j.lungcan.2007.02.019

Cited by 74 publications

(62 citation statements)

References 48 publications

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“…The human polyomaviruses BKV and JCV have been detected in several human tumors [White and Khalili, 2004;Giuliani et al, 2008] including the respiratory tract [Giuliani et al, 2007;Zheng et al, 2007], and induce tumors in animal models [Sariyer et al, 2004]. This prompted us to investigate the presence of KIV in normal and malignant respiratory tissue.…”

Section: Discussionmentioning

confidence: 99%

“…These specimens were already tested for the presence of HPV, SV40, BKV, JCV, and CMV [Giuliani et al, 2007]. The patients included 13 men and 7 women and the age ranged from 40 to 85 years, mean age 68.…”

Section: Study Groupmentioning

confidence: 99%

“…Polyomaviruses BKV, JCV, and SV40 have been detected in human tumors [Sariyer et al, 2004;Giuliani et al, 2007Giuliani et al, , 2008 and induce numerous tumors in experimental animals [Sariyer et al, 2004]. The mechanism by which the oncogenic transformation is achieved is through the action of the early proteins large T antigen (T-Ag) and small t antigen (t-Ag).…”

Section: Introductionmentioning

confidence: 99%

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Identification of the novel KI Polyomavirus in paranasal and lung tissues

Babakir‐Mina¹,

Ciccozzi

Campitelli

et al. 2009

Journal of Medical Virology

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KI is a novel polyomavirus identified in the respiratory secretions of children with acute respiratory symptoms. Whether this reflects a causal role of the virus in the human respiratory disease remains to be established. To investigate the presence of KIV in the respiratory tissue, we examined 20 fresh lung cancer specimens and surrounding normal tissue along with one paranasal and one lung biopsy from two transplanted children. KIV‐VP1 gene was detected in 9/20 lung cancer patients and 2/2 transplanted patients. However, amplification of the sequence coding for the C‐terminal part of the early region of KIV performed on the 11 positive cases was successful only in two malignant lung tissues, one surrounding normal tissue, and 1/2 biopsies tested. Phylogenetic analysis performed on the early region of KIV (including the four Italian isolates), BKV and JCV revealed the presence of three distinct clades. Within the KIV clade two sub‐clades were observed. A sub‐clade A containing the four Italian strains, and a sub‐clade B comprising the Swedish and Australian isolates. Interestingly, the two Italian strains identified in normal tissue clustered together, whereas those detected in malignant tissue fell outside this cluster. In vitro studies are needed to investigate the transforming potential of KIV strains. J. Med. Virol. 81:558–561, 2009. © 2009 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Section: Study Groupmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Identification of the novel KI Polyomavirus in paranasal and lung tissues

Babakir‐Mina¹,

Ciccozzi

Campitelli

et al. 2009

Journal of Medical Virology

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“…Many papers have been published on the subject, with conflicting results as we recently reviewed [23]. However, the finding of E6 and E7 transcripts in a series of non-small lung cancer cases prompted us to further investigate the role of oncogenic HPVs in lung cancer development [7, 8]. We used the lung cancer cell line A549 stably infected with HPV16E6 and E7 constructs to identify proteins modulated by the expression of these two oncogenes.Although experiments performed on nonimmortalized or malignantly transformed cells would be more informative, this cell line is commonly used in proteomic and mRNA studies [24, 25] instead of primary cultures because of technical problems in isolating, characterizing, growing and transfecting primary cultures.…”

Section: Discussionmentioning

confidence: 99%

“…HPV is the etiological agent of cervical cancer, but it has been estimated that about 15–20% of all human malignancies could be related to oncogenic HPVs [4,5,6]. In two recent studies, we have revealed the presence of oncogenic HPVs (HPV16, 18, 31 and 53) and their transcripts in a series of non-small cell lung cancers [7, 8], reinforcing the relationship between HPV and lung cancer and supporting the hypothesis that oncogenic HPVs might play a role in lung carcinogenesis. The oncogenic action of the virus is exerted through the oncoproteins E6 and E7 by binding to p53 and pRb, respectively, interfering with cell cycle control [9,10,11].…”

Section: Introductionmentioning

confidence: 99%

Proteomic Investigation in A549 Lung Cell Line Stably Infected by HPV16E6/E7 Oncogenes

et al. 2008

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Background: Data have accumulated implicating the involvement of oncogenic human papillomaviruses (HPVs) in bronchial carcinogenesis. We recently described the presence of oncogenic HPV transcripts in non-small cell lung cancers. Objective: To investigate the role of oncogenic HPVs in lung carcinogenesis. Material and Methods: The lung cell line A549 stably infected with HPV16E6, HPV16E7 and HPVE6/E7 constructs was used to investigate the protein profile changes associated with the expression of these oncogenes. Replicated two-dimensional gel electrophoresis gels from uninfected and stably HPV16E6-, E7-, and E6/E7-infected A549 cells were compared for changes in protein profile. Protein identification was achieved by peptide mass fingerprinting by MALDI-TOF-MS and nLC-ESI-Q-TOF-MS/MS peptide ladder sequencing. Results: We identified 17 different polypeptides whose average normalized spot intensity was statistically significant (p < 0.05) and differed by 2-fold. Relationships between differentially expressed proteins and the HPV-induced infection mechanism have been clustered by knowledge-base database functional association network analysis. Conclusion: The impact of Hsp27, annexin III, annexin IV, Gp96 and TPT1 on the cellular response mechanism to HPV infection is presented and discussed.

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Lung Cancer Prevention

Shojaee

Dragnev

2012

Cancer and Aging Handbook

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Detection of oncogenic viruses (SV40, BKV, JCV, HCMV, HPV) and p53 codon 72 polymorphism in lung carcinoma

Cited by 74 publications

References 48 publications

Identification of the novel KI Polyomavirus in paranasal and lung tissues

Identification of the novel KI Polyomavirus in paranasal and lung tissues

Proteomic Investigation in A549 Lung Cell Line Stably Infected by HPV16E6/E7 Oncogenes

Lung Cancer Prevention

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