語系:
繁體中文
English
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
The Role of Hyperinsulinemia in Brea...
~
Zelenko, Zara.
FindBook
Google Book
Amazon
博客來
The Role of Hyperinsulinemia in Breast Cancer Progression.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
The Role of Hyperinsulinemia in Breast Cancer Progression./
作者:
Zelenko, Zara.
面頁冊數:
125 p.
附註:
Source: Dissertation Abstracts International, Volume: 77-12(E), Section: B.
Contained By:
Dissertation Abstracts International77-12B(E).
標題:
Oncology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10129345
ISBN:
9781339872360
The Role of Hyperinsulinemia in Breast Cancer Progression.
Zelenko, Zara.
The Role of Hyperinsulinemia in Breast Cancer Progression.
- 125 p.
Source: Dissertation Abstracts International, Volume: 77-12(E), Section: B.
Thesis (Ph.D.)--Icahn School of Medicine at Mount Sinai, 2016.
Women with Type 2 diabetes (T2D) have a 49% increase in breast cancer related mortality compared to women without T2D. Epidemiological studies report that increased endogenous insulin levels and increased insulin receptor (IR) expression are associated with poor survival in breast cancer patients. Therefore, it is essential to investigate the role of endogenous hyperinsulinemia on breast cancer progression. Presented in this thesis are contributions to understanding the effect of insulin in a mouse model of hyperinsulinemia (MKR mouse). First, data is shown that highlights the significant increase in primary MVT-1 tumors and pulmonary metastasis in the MKR mouse compared to Wild Type mice. The studies presented show that the primary tumors from the MKR mice have significantly higher Vimentin protein expression compared to primary tumors from control mice. Next, the studies determine that silencing Vimentin expression in the tumor cells leads to either decreased number of pulmonary metastasis in the hyperinsulinemic mice. The work in this thesis also establishes a novel immunodeficient hyperinsulinemic (Rag/MKR) mouse model that enabled the study of the effects of endogenous insulin on the progression of human cancer cells. The hyperinsulinemia of the Rag/MKR mice promoted a significant increase in tumor growth of MDA-MB-231 and LCC6 cells. The knockdown of the insulin receptor in the LCC6 cells led to primary tumors that were significantly smaller in both the hyperinsulinemic Rag/MKR and Rag/WT control mice compared to the tumors from the LCC6 control cells. Finally, it is shown for the first time that the knockdown of the IR promotes a reversal of the epithelial-mesenchymal phenotype by repressing mesenchymal markers and re-expressing epithelial markers in the LCC6 insulin receptor knockdown tumors. The data presented in this thesis highlight a potential contribution to the understanding of the role of insulin in the setting of hyperinsulinemia and provide potential targets for therapy to improve survival in women with breast cancer and hyperinsulinemia.
ISBN: 9781339872360Subjects--Topical Terms:
751006
Oncology.
The Role of Hyperinsulinemia in Breast Cancer Progression.
LDR
:02984nmm a2200289 4500
001
2076013
005
20161101084214.5
008
170521s2016 ||||||||||||||||| ||eng d
020
$a
9781339872360
035
$a
(MiAaPQ)AAI10129345
035
$a
AAI10129345
040
$a
MiAaPQ
$c
MiAaPQ
100
1
$a
Zelenko, Zara.
$3
3191441
245
1 4
$a
The Role of Hyperinsulinemia in Breast Cancer Progression.
300
$a
125 p.
500
$a
Source: Dissertation Abstracts International, Volume: 77-12(E), Section: B.
500
$a
Adviser: Derek LeRoith.
502
$a
Thesis (Ph.D.)--Icahn School of Medicine at Mount Sinai, 2016.
520
$a
Women with Type 2 diabetes (T2D) have a 49% increase in breast cancer related mortality compared to women without T2D. Epidemiological studies report that increased endogenous insulin levels and increased insulin receptor (IR) expression are associated with poor survival in breast cancer patients. Therefore, it is essential to investigate the role of endogenous hyperinsulinemia on breast cancer progression. Presented in this thesis are contributions to understanding the effect of insulin in a mouse model of hyperinsulinemia (MKR mouse). First, data is shown that highlights the significant increase in primary MVT-1 tumors and pulmonary metastasis in the MKR mouse compared to Wild Type mice. The studies presented show that the primary tumors from the MKR mice have significantly higher Vimentin protein expression compared to primary tumors from control mice. Next, the studies determine that silencing Vimentin expression in the tumor cells leads to either decreased number of pulmonary metastasis in the hyperinsulinemic mice. The work in this thesis also establishes a novel immunodeficient hyperinsulinemic (Rag/MKR) mouse model that enabled the study of the effects of endogenous insulin on the progression of human cancer cells. The hyperinsulinemia of the Rag/MKR mice promoted a significant increase in tumor growth of MDA-MB-231 and LCC6 cells. The knockdown of the insulin receptor in the LCC6 cells led to primary tumors that were significantly smaller in both the hyperinsulinemic Rag/MKR and Rag/WT control mice compared to the tumors from the LCC6 control cells. Finally, it is shown for the first time that the knockdown of the IR promotes a reversal of the epithelial-mesenchymal phenotype by repressing mesenchymal markers and re-expressing epithelial markers in the LCC6 insulin receptor knockdown tumors. The data presented in this thesis highlight a potential contribution to the understanding of the role of insulin in the setting of hyperinsulinemia and provide potential targets for therapy to improve survival in women with breast cancer and hyperinsulinemia.
590
$a
School code: 1734.
650
4
$a
Oncology.
$3
751006
650
4
$a
Molecular biology.
$3
517296
650
4
$a
Cellular biology.
$3
3172791
690
$a
0992
690
$a
0307
690
$a
0379
710
2
$a
Icahn School of Medicine at Mount Sinai.
$b
Biomedical Sciences.
$3
3191442
773
0
$t
Dissertation Abstracts International
$g
77-12B(E).
790
$a
1734
791
$a
Ph.D.
792
$a
2016
793
$a
English
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10129345
筆 0 讀者評論
館藏地:
全部
電子資源
出版年:
卷號:
館藏
1 筆 • 頁數 1 •
1
條碼號
典藏地名稱
館藏流通類別
資料類型
索書號
使用類型
借閱狀態
預約狀態
備註欄
附件
W9308881
電子資源
11.線上閱覽_V
電子書
EB
一般使用(Normal)
在架
0
1 筆 • 頁數 1 •
1
多媒體
評論
新增評論
分享你的心得
Export
取書館
處理中
...
變更密碼
登入