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The role of tumor necrosis factor in...

Jones, Yava L.

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The role of tumor necrosis factor in acute and chronic colitis and colitis associated colon cancer.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	The role of tumor necrosis factor in acute and chronic colitis and colitis associated colon cancer./
Author:	Jones, Yava L.
Description:	229 p.
Notes:	Source: Dissertation Abstracts International, Volume: 72-06, Section: B, page: .
Contained By:	Dissertation Abstracts International72-06B.
Subject:	Health Sciences, Pathology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3450381
ISBN:	9781124590042

The role of tumor necrosis factor in acute and chronic colitis and colitis associated colon cancer.
Jones, Yava L.

The role of tumor necrosis factor in acute and chronic colitis and colitis associated colon cancer. - 229 p.

Source: Dissertation Abstracts International, Volume: 72-06, Section: B, page: .

Thesis (Ph.D.)--Michigan State University, 2011.

Inflammatory bowel disease (IBD) consists of two disease entities, Crohn's Disease (CD) and Ulcerative Colitis (UC). Both diseases manifest as chronic, relapsing and remitting bouts of gastrointestinal inflammation. The etiology of these disease, although not completely understood, consists of a complex interplay between genetic alterations rendering increased susceptibility, the gastrointestinal flora, and hyper-responsiveness of the immune system. Tumor necrosis factor (TNF) is a multifunctional cytokine that has been shown to be upregulated in the colon of and systemically in patients with inflammatory bowel disease. Additionally, anti-TNF therapy has proven effective for the treatment of CD. However, TNF has been shown to have divergent roles in the pathogenesis of disease, depending upon the cellular source of secretion, the length of time of production, the local and systemic concentration of the cytokine and the receptor signaling pathway activated. Here we demonstrate that TNF required for protection against acute colitis and enterocytes derived TNF is the determinant for conferring this protection. In addition, the increased inflammation seen in mice with complete Tnf deficiency and enterocyte derived Tnf deficient mice is accompanied by changes in the microbioal flora which could be contributory components of the disease. In contrast, as colitis progresses from acute to chronic, the protective role of TNF is lost and with chronicity, TNF promotes atypical glandular hyperplasia, inflammation, and cancer. Evaluation of the role of TNF from specific cellular sources in the context of colitis associated colon cancer (CAC) revealed disparate roles for TNF in cancer development depending on the cell type secreting the cytokine. Here we show that enterocyte derived TNF promotes CAC, whereas TNF from T cells protects against CAC. These findings highlight the potentially beneficial versus pathogenic effects of TNF in colitis and CAC and underscore the need more evaluation of the current therapeutic practices for IBD patients.

ISBN: 9781124590042Subjects--Topical Terms:

1017854
Health Sciences, Pathology.

The role of tumor necrosis factor in acute and chronic colitis and colitis associated colon cancer.
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245 1 4 $a The role of tumor necrosis factor in acute and chronic colitis and colitis associated colon cancer.
300 $a 229 p.
500 $a Source: Dissertation Abstracts International, Volume: 72-06, Section: B, page: .
500 $a Adviser: Matti Kiupel.
502 $a Thesis (Ph.D.)--Michigan State University, 2011.
520 $a Inflammatory bowel disease (IBD) consists of two disease entities, Crohn's Disease (CD) and Ulcerative Colitis (UC). Both diseases manifest as chronic, relapsing and remitting bouts of gastrointestinal inflammation. The etiology of these disease, although not completely understood, consists of a complex interplay between genetic alterations rendering increased susceptibility, the gastrointestinal flora, and hyper-responsiveness of the immune system. Tumor necrosis factor (TNF) is a multifunctional cytokine that has been shown to be upregulated in the colon of and systemically in patients with inflammatory bowel disease. Additionally, anti-TNF therapy has proven effective for the treatment of CD. However, TNF has been shown to have divergent roles in the pathogenesis of disease, depending upon the cellular source of secretion, the length of time of production, the local and systemic concentration of the cytokine and the receptor signaling pathway activated. Here we demonstrate that TNF required for protection against acute colitis and enterocytes derived TNF is the determinant for conferring this protection. In addition, the increased inflammation seen in mice with complete Tnf deficiency and enterocyte derived Tnf deficient mice is accompanied by changes in the microbioal flora which could be contributory components of the disease. In contrast, as colitis progresses from acute to chronic, the protective role of TNF is lost and with chronicity, TNF promotes atypical glandular hyperplasia, inflammation, and cancer. Evaluation of the role of TNF from specific cellular sources in the context of colitis associated colon cancer (CAC) revealed disparate roles for TNF in cancer development depending on the cell type secreting the cytokine. Here we show that enterocyte derived TNF promotes CAC, whereas TNF from T cells protects against CAC. These findings highlight the potentially beneficial versus pathogenic effects of TNF in colitis and CAC and underscore the need more evaluation of the current therapeutic practices for IBD patients.
590 $a School code: 0128.
650 4 $a Health Sciences, Pathology. $3 1017854
650 4 $a Biology, Veterinary Science. $3 1021733
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710 2 $a Michigan State University. $b Pathology. $3 1684900
773 0 $t Dissertation Abstracts International $g 72-06B.
790 1 0 $a Kiupel, Matti, $e advisor
790 1 0 $a Trinchieri, Giorgio $e committee member
790 1 0 $a Bauer, Alison $e committee member
790 1 0 $a Yuzbasiyan-Gurkan, Vilma $e committee member
790 1 0 $a Simpson, Mark $e committee member
790 $a 0128
791 $a Ph.D.
792 $a 2011
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3450381