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B lymphocyte expression of cyclooxyg...

Ryan, Elizabeth Pansy.

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B lymphocyte expression of cyclooxygenase-2: Implications for humoral immunity and cancer.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	B lymphocyte expression of cyclooxygenase-2: Implications for humoral immunity and cancer./
作者:	Ryan, Elizabeth Pansy.
面頁冊數:	203 p.
附註:	Source: Dissertation Abstracts International, Volume: 67-06, Section: B, page: 3101.
Contained By:	Dissertation Abstracts International67-06B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3222109
ISBN:	9780542726231

B lymphocyte expression of cyclooxygenase-2: Implications for humoral immunity and cancer.
Ryan, Elizabeth Pansy.

B lymphocyte expression of cyclooxygenase-2: Implications for humoral immunity and cancer. - 203 p.

Source: Dissertation Abstracts International, Volume: 67-06, Section: B, page: 3101.

Thesis (Ph.D.)--University of Rochester, 2006.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for the treatment of inflammatory diseases and target cyclooxygenases 1 and 2 (Cox-1, Cox-2) that are responsible for prostaglandin (PG) production. Newer Cox-2-selective drugs are heavily prescribed to quench inflammation. Little is known about whether or not these drugs influence B lineage cells. Initial studies in this thesis first characterized Cox-2 expression and PG production by both normal and malignant human B lineage cells. The role of Cox-2 in promoting humoral immune responses was investigated using both nonselective and selective Cox-2 inhibitors, as well as a genetic mouse model of Cox-2 deficiency. Activated human B lymphocytes not only highly express Cox-2 and produce PGs, but the NSAID Indomethacin and Cox-2 selective drugs profoundly inhibit the ability of human B cells to produce IgG and IgM in vitro . In support that Cox-2 plays a seminal role in B lymphocyte antibody production, Cox-2 knock out mice produced significantly less serum IgG in response to human papillomavirus type 16 virus-like-particles compared to wildtype mice. Taken together, these findings support that NSAIDs and the new Cox-2 selective drugs have an unsuspected target, the B cell, and may attenuate antibody production in humans.

ISBN: 9780542726231Subjects--Topical Terms:

1017686
Biology, Cell.

B lymphocyte expression of cyclooxygenase-2: Implications for humoral immunity and cancer.
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502 $a Thesis (Ph.D.)--University of Rochester, 2006.
520 $a Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for the treatment of inflammatory diseases and target cyclooxygenases 1 and 2 (Cox-1, Cox-2) that are responsible for prostaglandin (PG) production. Newer Cox-2-selective drugs are heavily prescribed to quench inflammation. Little is known about whether or not these drugs influence B lineage cells. Initial studies in this thesis first characterized Cox-2 expression and PG production by both normal and malignant human B lineage cells. The role of Cox-2 in promoting humoral immune responses was investigated using both nonselective and selective Cox-2 inhibitors, as well as a genetic mouse model of Cox-2 deficiency. Activated human B lymphocytes not only highly express Cox-2 and produce PGs, but the NSAID Indomethacin and Cox-2 selective drugs profoundly inhibit the ability of human B cells to produce IgG and IgM in vitro . In support that Cox-2 plays a seminal role in B lymphocyte antibody production, Cox-2 knock out mice produced significantly less serum IgG in response to human papillomavirus type 16 virus-like-particles compared to wildtype mice. Taken together, these findings support that NSAIDs and the new Cox-2 selective drugs have an unsuspected target, the B cell, and may attenuate antibody production in humans.
520 $a It was also established that certain B lymphomas and chronic lymphocytic leukemia B cells (B-CLL) constitutively express Cox-2. Constitutive and activation-inducible Cox-2 expression has prognostic value as a subgroup of B-CLL samples with biomarkers of poor prognosis, namely variable heavy chain mutational status and elevated CD38 expression demonstrated elevated levels of Cox-2. Furthermore, modulation of intracellular thiol redox status was evaluated as the mechanism by which SC-58125, a close structural analog of Celebrex, and a highly Cox-2 selective inhibitor, reduced malignant B cell proliferation and viability. Our findings confirm that Cox-2 promotes lymphoma/leukemic cell survival and support that Cox-2 selective inhibitors are potential therapeutic agents to control malignant human B cell proliferation and possibly metastasis in vivo.
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