‘Hit and run’ oncogenesis by human papillomavirus type 18 DNA

Iwasaka, Tsuyoshi; Hayashi, Yoshinobu; Yokoyama, Masatoshi; Hara, Kunihiko; Matsuo, Noritaka; Sugimori, Hajime

doi:10.3109/00016349209009922

Cited by 36 publications

(29 citation statements)

References 18 publications

(8 reference statements)

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“…Regarding the role of HPV in LCs, Kinjo et al (2003) has argued that HPV is not aetiologically involved in LC development but that HPV induces squamous metaplasia in ACs. Another possible explanation for such a low viral load may suggest a 'hit-and-run' mechanism, where the virus DNA may be lost after transformation, as shown in studies on a bovine model, and as suggested in HPV-18 oncogenesis and in non-melanoma skin cancer developments mediated by HPV (Iwasaka et al, 1992;Aubin et al, 2003).…”

Section: Discussionmentioning

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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Section: Discussionmentioning

confidence: 99%

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

et al. 2007

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“…The region 3 0 of the L1 amplicon was extended at least as far as 7244 bp. This suggests that the HPV is fragmented and/or incomplete and may indicate 'hit-and-run' oncogenesis as described for HPV in Syrian hamster embryo cells (Iwasaka et al, 1992) and for human mesothelial cells (De Silva et al, 1994). We are continuing our analysis of the HPV sequence in MBA-MB-175VII and SK-Br-3 cell lines, as well as in two other HPV-containing breast cancer cell lines that are yet to be described and characterised.…”

Section: Sirmentioning

confidence: 98%

Reply to Letter to the Editor : Is HPV-18 present in human breast cancer cell lines

et al. 2010

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“…Subsequently, many examples of hit and run' have been reported, involving notably the herpes viruses, herpes simplex (HSV) McDougall, 1980, 1990;Bauer et al, 1992) and EpsteinBarr (EBV) viruses (Gri n and Karran, 1984;Karran et al, 1990;Yao et al, 1990;Lin et al, 1993;Delecluse et al, 1997;Wolf et al, 1995;Jox et al, 1997;Srinivas et al, 1998, reviewed, Ambinder, 2000, or on occasion cytomegalo (CMV) (Gelb and Dohner, 1984) or varicella zoster (VZV) (Iwasaka et al, 1992) viruses. Shen et al (1997) proposed that`hit and run' transformation by human papilloma (HPV) viruses might be a consequence of mutations induced in cellular genes.…”

Section: Introductioǹmentioning

confidence: 99%