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 reactive astrocytes in t...
~
Lin, Qingtang.
FindBook
Google Book
Amazon
博客來
The role of reactive astrocytes in the resistance of melanoma brain metastasis to chemotherapy.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
The role of reactive astrocytes in the resistance of melanoma brain metastasis to chemotherapy./
作者:
Lin, Qingtang.
面頁冊數:
104 p.
附註:
Source: Dissertation Abstracts International, Volume: 71-02, Section: B, page: 0809.
Contained By:
Dissertation Abstracts International71-02B.
標題:
Biology, Molecular. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3394954
ISBN:
9781109630459
The role of reactive astrocytes in the resistance of melanoma brain metastasis to chemotherapy.
Lin, Qingtang.
The role of reactive astrocytes in the resistance of melanoma brain metastasis to chemotherapy.
- 104 p.
Source: Dissertation Abstracts International, Volume: 71-02, Section: B, page: 0809.
Thesis (Ph.D.)--The University of Texas Graduate School of Biomedical Sciences at Houston, 2009.
Brain metastasis is resistant to chemotherapy while the leaky blood-brain-barrier in brain metastasis can not be the underlying reason. Metastatic tumor cells ("seed") exploit the host microenvironment ("soil") for survival advantages. Astrocytes which maintain the homeostasis of the brain microenvironment become reactive subsequent to brain damages and protect neurons from various injuries. We observed reactive astrocytes surrounding and infiltrating into brain metastasis in both clinical specimen and experimental animal model, thus raising a possibility that reactive astrocytes may protect tumor cells from cytotoxic chemotherapeutic drugs.
ISBN: 9781109630459Subjects--Topical Terms:
1017719
Biology, Molecular.
The role of reactive astrocytes in the resistance of melanoma brain metastasis to chemotherapy.
LDR
:04183nam 2200337 4500
001
1403503
005
20111118095941.5
008
130515s2009 ||||||||||||||||| ||eng d
020
$a
9781109630459
035
$a
(UMI)AAI3394954
035
$a
AAI3394954
040
$a
UMI
$c
UMI
100
1
$a
Lin, Qingtang.
$3
1682767
245
1 4
$a
The role of reactive astrocytes in the resistance of melanoma brain metastasis to chemotherapy.
300
$a
104 p.
500
$a
Source: Dissertation Abstracts International, Volume: 71-02, Section: B, page: 0809.
500
$a
Adviser: Isaiah J. Fidler.
502
$a
Thesis (Ph.D.)--The University of Texas Graduate School of Biomedical Sciences at Houston, 2009.
520
$a
Brain metastasis is resistant to chemotherapy while the leaky blood-brain-barrier in brain metastasis can not be the underlying reason. Metastatic tumor cells ("seed") exploit the host microenvironment ("soil") for survival advantages. Astrocytes which maintain the homeostasis of the brain microenvironment become reactive subsequent to brain damages and protect neurons from various injuries. We observed reactive astrocytes surrounding and infiltrating into brain metastasis in both clinical specimen and experimental animal model, thus raising a possibility that reactive astrocytes may protect tumor cells from cytotoxic chemotherapeutic drugs.
520
$a
To test this hypothesis, we first generated an immortalized astrocyte cell line from H-2Kb-tsA58 mice. The immortal mouse astrocytes expressed specific markers including GFAP. Scanning electron microscopy demonstrated that astrocytes formed direct physical contact with tumor cells. Moreover, the expression of GFAP by astrocytes was up-regulated subsequent to co-culture with tumor cells, indicating that the co-culture of astrocytes and tumor cells may serve as a model to recapitulate the pathophysiological situation of brain metastasis.
520
$a
In co-culture, astrocytes dramatically reduced apoptosis of tumor cells produced by various chemotherapeutic drugs. This protection effect was not because of culturing cells from different species since mouse fibroblasts did not protect tumor cells from chemotherapy. Furthermore, the protection by astrocytes was completely dependent on a physical contact.
520
$a
Gap junctional communication (GJC) served as this physical contact. Tumor cells and astrocytes both expressed the major component of gap junctional channel---connexin 43 and formed functional GJC as evidenced by the "dye transfer" assay. The blockage of GJC between tumor cells and astrocytes by either specific chemical blocker carbenoxolone (CBX) or by genetically knocking down connexin 43 on astrocytes reversed the chemo-protection.
520
$a
Calcium was the signal molecule transmitted through GJC that rescued tumor cells from chemotherapy. Accumulation of cytoplasmic calcium preceded the progress of apoptosis in tumor cells treated with chemotherapeutic drugs. Furthermore, chelation of accumulated cytoplasmic calcium inhibited the apoptosis of tumor cells treated with chemotherapeutic drugs. Most importantly, astrocytes could "shunt" the accumulated cytoplasmic calcium from tumor cells (treated with chemotherapeutic drug) through GJC. We also used gene expression micro-array to investigate global molecular consequence of tumor cells forming GJC with astrocytes. The data demonstrated that astrocytes (but not fibroblasts), through GJC, up-regulated the expressions of several well known survival genes in tumor cells.
520
$a
In summary, this dissertation provides a novel mechanism underlying the resistance of brain metastasis to chemotherapy, which is due to protection by astrocytes through GJC. Interference with the GJC between astrocytes and tumor cells holds great promise in sensitizing brain metastasis to chemotherapy and improving the prognosis for patients with brain metastasis.
590
$a
School code: 2034.
650
4
$a
Biology, Molecular.
$3
1017719
650
4
$a
Health Sciences, Oncology.
$3
1018566
690
$a
0307
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
71-02B.
790
1 0
$a
Fidler, Isaiah J.,
$e
advisor
790
$a
2034
791
$a
Ph.D.
792
$a
2009
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3394954
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
W9166642
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