상세 정보

underline
Metadata Downloads : dc(xml) or Excel
Cited 0 time in scopus ci

Title 

DMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin

Authors 

M O KimS H KimM J ShinD H YuB S KimKyu Tae ChangS LeeY B ParkT H LeeZ Y Ryoo

Publisher 

Cognizant Communication

Issue Date 

2007

Citation 

Oncology Research, vol. 16, no. 7, pp. 325-332

Keywords 

DMBA/TPAhK14 promoterHPV16 E6/E7keratinocytesskin cancertransgenic miceprotein E6protein E7E6 protein, human papillomavirus type 16oncogene protein E7, human papillomavirus type 16

Abstract 

Human papillomavirus type 16 (HPV16) is a major causative factor in the development of uterine cervical carcinomas. We investigated the role of E6/E7 in tumor formation. Skin-specific E6/E7 transgenic mice showed approximately twice as many tumors compared with nontransgenic mice in dimethylbenz[a]anthracene (DMBA)-initiated and a 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted two-stage skin carcinogenesis. This model showed a significant increase of epidermal cell proliferation in the transgenic mice. The 8-hydroxy- 2'deoxyguanosine (8OH-dG) detection assay showed that oxidative DNA damage was significantly higher in the transgenic mice after TPA treatments. The overexpression of E6/E7 in the skin in the DMBA/TPA two-stage-induced carcinogenesis model aggravated the incidence of tumor formation. HPV16 E6/E7 appears to act as an enhancer of carcinogenesis that requires initiation by DMBA and promotion by TPA.

URI 

https://doi.org/10.3727/000000006783980964

ISSN 

0965-0407

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


Files in This Item: SizeFormat
7071.pdf2611KbAdobe PDF
qrcode

FusionCharts.
DSpace Software Coptright(c) 2010 MIT and Hewleft-Packard  /  KRIBB-REPOSITORY ( Email:jakim@kribb.re.kr)