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

切換: 標籤 | MARC模式 | ISBD

Endogenous prolactin, prolactin sign...

Gutzman, Jennifer Hinchey.

FindBook

Google Book

Amazon

博客來

Endogenous prolactin, prolactin signaling, and prolactin and estrogen interactions in breast cancer cells.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Endogenous prolactin, prolactin signaling, and prolactin and estrogen interactions in breast cancer cells./
作者:	Gutzman, Jennifer Hinchey.
面頁冊數:	174 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1630.
Contained By:	Dissertation Abstracts International65-04B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3127971
ISBN:	0496752345

Endogenous prolactin, prolactin signaling, and prolactin and estrogen interactions in breast cancer cells.
Gutzman, Jennifer Hinchey.

Endogenous prolactin, prolactin signaling, and prolactin and estrogen interactions in breast cancer cells. - 174 p.

Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1630.

Thesis (Ph.D.)--The University of Wisconsin - Madison, 2004.

Prolactin (PRL) and 17beta-estradiol (E2) are critical for normal mammary gland growth, development, and differentiation. Based on their roles in the mammary gland, it can be hypothesized that PRL and E2 may interact in the development and progression of breast cancer. While the mitogenic actions of E2 in this disease have been well established, increased expression of PRL receptors in human mammary tumors, local PRL production within the mammary epithelium, and a correlation between circulating PRL and breast cancer, support a role for PRL as well.

ISBN: 0496752345Subjects--Topical Terms:

1017686
Biology, Cell.

Endogenous prolactin, prolactin signaling, and prolactin and estrogen interactions in breast cancer cells.
LDR:03244nmm 2200325 4500 001 1840326
005 20050721102958.5
008 130614s2004 eng d
020 $a 0496752345
035 $a (UnM)AAI3127971
035 $a AAI3127971
040 $a UnM $c UnM
100 1 $a Gutzman, Jennifer Hinchey. $3 1928666
245 1 0 $a Endogenous prolactin, prolactin signaling, and prolactin and estrogen interactions in breast cancer cells.
300 $a 174 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1630.
500 $a Supervisor: Linda A. Schuler.
502 $a Thesis (Ph.D.)--The University of Wisconsin - Madison, 2004.
520 $a Prolactin (PRL) and 17beta-estradiol (E2) are critical for normal mammary gland growth, development, and differentiation. Based on their roles in the mammary gland, it can be hypothesized that PRL and E2 may interact in the development and progression of breast cancer. While the mitogenic actions of E2 in this disease have been well established, increased expression of PRL receptors in human mammary tumors, local PRL production within the mammary epithelium, and a correlation between circulating PRL and breast cancer, support a role for PRL as well.
520 $a In specifically engineered MCF-7 cells, induced endogenous PRL, but not exogenous PRL, increased the expression of the long PRLR isoform and ER&agr;. The elevated ER&agr; levels were associated with increased estrogen responsiveness. These results suggest that endogenous PRL can amplify estrogenic effects on breast cancer development and progression by cross-regulation of ER&agr; levels.
520 $a In another MCF-7 cell line derived to no longer express endogenous PRL, we investigated activation of the AP-1 transcription factor by PRL and E2. AP-1 has been implicated in the control of cell cycle regulators and is commonly elevated in breast cancer, making AP-1 a possible target for PRL, and PRL and E2 crosstalk. PRL activated AP-1 detectable as early as 4 h and sustained activity for at least 24 h. Activation of AP-1 by PRL involved Jak2, c-Src, and multiple MAP kinases, particularly ERK1/2. PRL increased levels of c-Jun, c-Fos and JunB protein, as well as phosphorylation of both c-Jun and c-Fos.
520 $a PRL and E2 together further enhanced AP-1 activity at 24 h involving a complex web of signaling pathways. PRL maintained AP-1 activity through Jak2, PI3K, p38, and ERK1/2. E2 signaling did not involve Jak2, but was particularly sensitive to inhibition of PI3K and ERK1/2. PRL and E2 increased the dynamic phosphorylation of ERK1/2, and levels of phosphorylated c-Fos. The enhanced AP-1 activity resulting from the interaction of these hormones would increase expression of many target genes that are critical for oncogenesis and may be important for neoplastic progression. These findings will provide insight for the design of new drug therapies for the treatment of breast cancer.
590 $a School code: 0262.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Oncology. $3 1018566
650 4 $a Health Sciences, Toxicology. $3 1017752
690 $a 0379
690 $a 0992
690 $a 0383
710 2 0 $a The University of Wisconsin - Madison. $3 626640
773 0 $t Dissertation Abstracts International $g 65-04B.
790 1 0 $a Schuler, Linda A., $e advisor
790 $a 0262
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3127971