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Mechanisms of cellular immortalizati...

University of California, Los Angeles.

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Mechanisms of cellular immortalization in normal human oral keratinocytes.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Mechanisms of cellular immortalization in normal human oral keratinocytes./
作者:	Kim, Reuben Han-Kyu.
面頁冊數:	170 p.
附註:	Adviser: No-Hee Park.
Contained By:	Dissertation Abstracts International69-07B.
標題:	Health Sciences, Dentistry. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3322034
ISBN:	9780549721673

Mechanisms of cellular immortalization in normal human oral keratinocytes.
Kim, Reuben Han-Kyu.

Mechanisms of cellular immortalization in normal human oral keratinocytes. - 170 p.

Adviser: No-Hee Park.

Thesis (Ph.D.)--University of California, Los Angeles, 2008.

Together, our findings suggest that NHOK might convert to immortal cells when the cells lose several defensive mechanisms including TGF-beta-mediated growth arrest and the loss of telomerase activity, but not p 16INK4A , p53, or p21WAF1.

ISBN: 9780549721673Subjects--Topical Terms:

1019378
Health Sciences, Dentistry.

Mechanisms of cellular immortalization in normal human oral keratinocytes.
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100 1 $a Kim, Reuben Han-Kyu. $3 1025271
245 1 0 $a Mechanisms of cellular immortalization in normal human oral keratinocytes.
300 $a 170 p.
500 $a Adviser: No-Hee Park.
500 $a Source: Dissertation Abstracts International, Volume: 69-07, Section: B, page: 4058.
502 $a Thesis (Ph.D.)--University of California, Los Angeles, 2008.
520 $a Together, our findings suggest that NHOK might convert to immortal cells when the cells lose several defensive mechanisms including TGF-beta-mediated growth arrest and the loss of telomerase activity, but not p 16INK4A , p53, or p21WAF1.
520 $a The development of cancer is a multi-step process that occurs via accumulation of a series of discrete, irreversible, and complementary events. Among these events, the escape of cells from senescence is a critical step, since it could lead to immortalization and tumorigenic transformation of cells. To understand the in-depth mechanisms of cellular senescence and immortalization we investigated the role of Bmi-1, a polycomb group protein identified as c-myc cooperating oncogene in murine lymphomagenesis, in oral carcinogenesis and on the phenotypic changes of normal human oral keratinocytes (NHOK).
520 $a First, we determined the status of in situ Bmi-1 expression in human squamous cell carcinomas and human oral preneoplastic tissues using immunohistochemical staining. The level of Bmi-1 was almost negligible in normal tissues, but it was notably increased in preneoplastic oral lesions and cancer tissue, indicating that enhanced Bmi-1 expression is likely associated with oral carcinogenesis and the phenotypic changes of NHOK. Second, we found that an ectopic expression of Bmi-1 extended the lifespan of NHOK in vitro. Extension of life span by Bmi-1 was not associated with enhanced expression of hTERT (human telomerase reverse transcriptase) or repression of p53 and p16INK4A. We found that Bmi-1 interfered with the TGF-beta-mediated growth arrest response in NHOK by inhibiting phosphorylation of Smad2 and led to reduced expression of TGF-beta-specific cyclin-dependent kinase inhibitors such asp15INK4B and p57KIP2. However, Bmi-1 alone did not result in cellular immortalization of NHOK, which required additional factors, such as human papillomavirus type 16 (HPV-16) E6. HPV-16 E6 expression in NHOK overexpressing Bmi-1 led to immortalization by allowing enhanced expression of hTERT and activation of telomerase. hTERT activation during immortalization occurred by physical interaction of hsp90 protein onto hTERT promoter region, which was necessary for the enhanced hTERT expression in cells.
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650 4 $a Health Sciences, Oncology. $3 1018566
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710 2 $a University of California, Los Angeles. $3 626622
773 0 $t Dissertation Abstracts International $g 69-07B.
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791 $a Ph.D.
792 $a 2008
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