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Human papillomavirus and oral cancer.

Liu, Xuan.

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Human papillomavirus and oral cancer.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Human papillomavirus and oral cancer./
Author:	Liu, Xuan.
Description:	171 p.
Notes:	Source: Dissertation Abstracts International, Volume: 59-09, Section: B, page: 4708.
Contained By:	Dissertation Abstracts International59-09B.
Subject:	Health Sciences, Dentistry. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9906156
ISBN:	0599037873

Human papillomavirus and oral cancer.
Liu, Xuan.

Human papillomavirus and oral cancer. - 171 p.

Source: Dissertation Abstracts International, Volume: 59-09, Section: B, page: 4708.

Thesis (Ph.D.)--University of California, Los Angeles, 1998.

The goal of this research project is to elucidate the role of human papillomavirus in oral carcinogenesis.

ISBN: 0599037873Subjects--Topical Terms:

1019378
Health Sciences, Dentistry.

Human papillomavirus and oral cancer.
LDR:03594nmm 2200325 4500 001 1839478
005 20050624104408.5
008 130614s1998 eng d
020 $a 0599037873
035 $a (UnM)AAI9906156
035 $a AAI9906156
040 $a UnM $c UnM
100 1 $a Liu, Xuan. $3 1253013
245 1 0 $a Human papillomavirus and oral cancer.
300 $a 171 p.
500 $a Source: Dissertation Abstracts International, Volume: 59-09, Section: B, page: 4708.
500 $a Chair: No-Hee Park.
502 $a Thesis (Ph.D.)--University of California, Los Angeles, 1998.
520 $a The goal of this research project is to elucidate the role of human papillomavirus in oral carcinogenesis.
520 $a Normal human oral keratinocytes (NHOK), like other somatic cells, undergo a limited number of population doubling levels (PDL) in culture and enter an irreversible replicative senescence in G1 and G2/M phases of cell cycle. In order to proliferate indefinitely, these cells have to overcome cell cycle control checkpoints resulting in many genetic changes termed "genetic instability". Recent work suggests that p53 is responsible for this integrator function in mammalian cells.
520 $a To test whether the wild-type p53 is necessary for the growth arrest of cells at the end of their proliferative lifespan, we have examined PDLs in NHOK expressing a dominant negative p53 mutant (ala $\ sp{143}) $ and human papillomavirus (HPV) proteins. The HPV proteins consisted of high-risk (HPV 16) E6, E7 or E6/E7 or low-risk (HPV6b) E6 or E7. These proteins in addition to the mutant p53 were compared in the normal parental NHOK cells. Our studies indicated that, HPV 16 E6 extended the lifespan to 75 PDLs, HPV 16 E7 to 101 PDLs, and p53 mutant up to 129 PDLs. Cells expressing HPV 16 E6/E7 were able to overcome M1 and M2 crisis and entered the process towards immortalization. Abrogation of either p53 or its down stream gene, pRb, permits temporary escape from senescence. Inhibition of both p53 and pRb functions results in continued proliferation.
520 $a To study the pathways associated with genomic instability in oral cancer, we examined the frequency rates of both spontaneous and MNNG-induced mutations of the shuttle vector pS189 in the above cells at early passages. Mutant p53 (ala $\ sp{143}), $ and high-risk E6 and E7 proteins disrupted the normal cell cycle progression in response to DNA damage, while low-risk E6 and E7 proteins failed to disrupt the cell cycle checkpoints. Also, we have found that an increase or decrease in the expression levels of p21WAF1/CIP1 and GADD45 is dependent on the functionality of the p53 protein. Cells expressing mutant p53, HPV16 E6, E7 and E6/E7 rapidly increased the rate of mutation in the pS189 shuttle vector when treated with N-methyl-N $\ sp\prime $- nitro-N-nitrosoguanidine (MNNG) compared with normal cell. An increased levels of spontaneous mutation occurred in cells expressing the mutant p53, HPV16 E6, E7 and E6/E7 genes. Fluctuation analysis revealed a 3-fold elevation in mutation rates of cells expressing mutant p53, a 5-fold increase in HPV 16 E6-infected cells and a 4-fold increase in HPV 16E7 infected cells. However, HPV 6b E6 or E7 had no effect on the rate of mutation of the these cells. (Abstract shortened by UMI.)
590 $a School code: 0031.
650 4 $a Health Sciences, Dentistry. $3 1019378
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Health Sciences, Pathology. $3 1017854
690 $a 0567
690 $a 0307
690 $a 0571
710 2 0 $a University of California, Los Angeles. $3 626622
773 0 $t Dissertation Abstracts International $g 59-09B.
790 1 0 $a Park, No-Hee, $e advisor
790 $a 0031
791 $a Ph.D.
792 $a 1998
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9906156