東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁 到查詢結果 [ subject:"Oncology." ]

切換: 標籤 | MARC模式 | ISBD

The interaction between Bcl-6 and ST...

Bunce, Kimberly Diane.

FindBook

Google Book

Amazon

博客來

The interaction between Bcl-6 and STAT6 pathway in non -Hodgkin lymphoma.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The interaction between Bcl-6 and STAT6 pathway in non -Hodgkin lymphoma./
作者:	Bunce, Kimberly Diane.
面頁冊數:	189 p.
附註:	Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2460.
Contained By:	Dissertation Abstracts International67-05B.
標題:	Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3218711
ISBN:	9780542702938

The interaction between Bcl-6 and STAT6 pathway in non -Hodgkin lymphoma.
Bunce, Kimberly Diane.

The interaction between Bcl-6 and STAT6 pathway in non -Hodgkin lymphoma. - 189 p.

Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2460.

Thesis (Ph.D.)--The University of Texas Graduate School of Biomedical Sciences at Houston, 2006.

Non-Hodgkin lymphoma is a heterogeneous group of malignancies that has continued to increase in both frequency and death rate since the 1950's. The Bcl-6 proto-oncogene was first identified by its involvement in chromosomal translocations in non-Hodgkin lymphoma, particularly diffuse large cell lymphoma and follicular lymphoma. One of the most well described functions of Bcl-6 is as a competitive inhibitor of IL-4 induced STAT6-mediated gene expression. In this study, we examined the interaction of Bcl-6 and the STAT6 pathway in non-Hodgkin lymphoma and normal B cells, and how this interaction was changed in response to stimulation with various B cell activating agents. Our results showed that Bcl-6 could be up-regulated in normal B cells and follicular lymphoma patient cells in response to activation with various combinations of CD40L, anti-IgM, PMA and ionomycin. Diffuse large cell lymphoma cell lines that did not express Bcl-6 could not up-regulate it in response to these stimuli, while diffuse large cell lymphoma cell lines that were Bcl-6 positive down-regulated its expression following stimulation with these agents. In addition, normal B cells and follicular lymphoma grade II patient cells could up-regulate P-STAT6 upon stimulation with these agents, while the diffuse large cell lymphoma cell lines could not. The STAT6 pathway was present and functional in the diffuse large cell lymphoma cell lines as shown by the presence of P-STAT6 following stimulation with exogenous IL-4. Two diffuse large cell lymphoma cell lines, one Bcl-6 protein negative and one Bcl-6 protein positive, could up-regulate Bcl-6 protein expression in response to prolonged IL-4 stimulation. This up-regulation corresponded to increases in P-STAT6 expression and cellular proliferation. Therefore, we concluded that Bcl-6 and STAT6 do not act as competitive inhibitors in diffuse large cell lymphoma cell lines. This lack of competitive inhibition would allow the B cell to proliferate without normal cell cycle controls, and could be one of the transforming events leading from normal B cells and indolent lymphomas to aggressive B cell lymphomas.

ISBN: 9780542702938Subjects--Topical Terms:

611031
Immunology.

The interaction between Bcl-6 and STAT6 pathway in non -Hodgkin lymphoma.
LDR:03076nmm a2200277 4500 001 2064022
005 20151109121400.5
008 170521s2006 ||||||||||||||||| ||eng d
020 $a 9780542702938
035 $a (MiAaPQ)AAI3218711
035 $a AAI3218711
040 $a MiAaPQ $c MiAaPQ
100 1 $a Bunce, Kimberly Diane. $3 3178581
245 1 4 $a The interaction between Bcl-6 and STAT6 pathway in non -Hodgkin lymphoma.
300 $a 189 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2460.
500 $a Adviser: Richard Ford.
502 $a Thesis (Ph.D.)--The University of Texas Graduate School of Biomedical Sciences at Houston, 2006.
520 $a Non-Hodgkin lymphoma is a heterogeneous group of malignancies that has continued to increase in both frequency and death rate since the 1950's. The Bcl-6 proto-oncogene was first identified by its involvement in chromosomal translocations in non-Hodgkin lymphoma, particularly diffuse large cell lymphoma and follicular lymphoma. One of the most well described functions of Bcl-6 is as a competitive inhibitor of IL-4 induced STAT6-mediated gene expression. In this study, we examined the interaction of Bcl-6 and the STAT6 pathway in non-Hodgkin lymphoma and normal B cells, and how this interaction was changed in response to stimulation with various B cell activating agents. Our results showed that Bcl-6 could be up-regulated in normal B cells and follicular lymphoma patient cells in response to activation with various combinations of CD40L, anti-IgM, PMA and ionomycin. Diffuse large cell lymphoma cell lines that did not express Bcl-6 could not up-regulate it in response to these stimuli, while diffuse large cell lymphoma cell lines that were Bcl-6 positive down-regulated its expression following stimulation with these agents. In addition, normal B cells and follicular lymphoma grade II patient cells could up-regulate P-STAT6 upon stimulation with these agents, while the diffuse large cell lymphoma cell lines could not. The STAT6 pathway was present and functional in the diffuse large cell lymphoma cell lines as shown by the presence of P-STAT6 following stimulation with exogenous IL-4. Two diffuse large cell lymphoma cell lines, one Bcl-6 protein negative and one Bcl-6 protein positive, could up-regulate Bcl-6 protein expression in response to prolonged IL-4 stimulation. This up-regulation corresponded to increases in P-STAT6 expression and cellular proliferation. Therefore, we concluded that Bcl-6 and STAT6 do not act as competitive inhibitors in diffuse large cell lymphoma cell lines. This lack of competitive inhibition would allow the B cell to proliferate without normal cell cycle controls, and could be one of the transforming events leading from normal B cells and indolent lymphomas to aggressive B cell lymphomas.
590 $a School code: 2034.
650 4 $a Immunology. $3 611031
650 4 $a Oncology. $3 751006
690 $a 0982
690 $a 0992
710 2 $a The University of Texas Graduate School of Biomedical Sciences at Houston. $3 1019338
773 0 $t Dissertation Abstracts International $g 67-05B.
790 $a 2034
791 $a Ph.D.
792 $a 2006
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3218711