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Crosstalk between endothelial cells ...

Neiva, Kathleen Gaboardi.

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Crosstalk between endothelial cells and tumor cells in head and neck cancer.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Crosstalk between endothelial cells and tumor cells in head and neck cancer./
作者:	Neiva, Kathleen Gaboardi.
面頁冊數:	121 p.
附註:	Source: Dissertation Abstracts International, Volume: 71-02, Section: B, page: 0812.
Contained By:	Dissertation Abstracts International71-02B.
標題:	Biology, Molecular. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3392922
ISBN:	9781109596519

Crosstalk between endothelial cells and tumor cells in head and neck cancer.
Neiva, Kathleen Gaboardi.

Crosstalk between endothelial cells and tumor cells in head and neck cancer. - 121 p.

Source: Dissertation Abstracts International, Volume: 71-02, Section: B, page: 0812.

Thesis (Ph.D.)--University of Michigan, 2009.

Tumor angiogenesis is necessary for cancer progression and requires active interaction between endothelial cells and tumor cells. It is well established that cancer cells secrete angiogenic factors to recruit and sustain tumor vascular networks. However, little is known about the effect of endothelial cell-secreted factors on the phenotype and behavior of tumor cells. The identification and characterization of signaling events initiated by tumor-associated endothelial cells may have important implications in cancer therapy. The hypothesis underlying this dissertation is that factors secreted by endothelial cells initiate signaling pathways in head and neck squamous cell carcinoma (HNSCC) cells that enhance tumor growth.

ISBN: 9781109596519Subjects--Topical Terms:

1017719
Biology, Molecular.

Crosstalk between endothelial cells and tumor cells in head and neck cancer.
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100 1 $a Neiva, Kathleen Gaboardi. $3 1682763
245 1 0 $a Crosstalk between endothelial cells and tumor cells in head and neck cancer.
300 $a 121 p.
500 $a Source: Dissertation Abstracts International, Volume: 71-02, Section: B, page: 0812.
500 $a Adviser: Jacques Eduardo Nor.
502 $a Thesis (Ph.D.)--University of Michigan, 2009.
520 $a Tumor angiogenesis is necessary for cancer progression and requires active interaction between endothelial cells and tumor cells. It is well established that cancer cells secrete angiogenic factors to recruit and sustain tumor vascular networks. However, little is known about the effect of endothelial cell-secreted factors on the phenotype and behavior of tumor cells. The identification and characterization of signaling events initiated by tumor-associated endothelial cells may have important implications in cancer therapy. The hypothesis underlying this dissertation is that factors secreted by endothelial cells initiate signaling pathways in head and neck squamous cell carcinoma (HNSCC) cells that enhance tumor growth.
520 $a Here, we observed that soluble mediators from primary human dermal microvascular endothelial cells activate STAT3, Akt, and ERK signaling in HNSCC cells. HNSCC cells adjacent to blood vessels showed increased phosphorylation of STAT3, Akt, and ERK in xenograft human tumors. IL-6, CXCL8, and EGF are upregulated in endothelial cells co-cultured with HNSCC, and blockade of endothelial cell-derived IL-6, CXCL8, or EGF inhibited the activation of STAT3, Akt, or ERK in tumor cells, respectively. Notably, activation of these pathways by endothelial cells enhanced migration and inhibited anoikis of tumor cells. It is known that Bc1-2 is upregulated in tumor microvessels of patients with HNSCC. Here, we observed that Bcl-2 signaling induces expression of IL-6, CXCL8, and EGF, providing a mechanism for the upregulation of these cytokines in tumor-associated endothelial cells.
520 $a We also observed that endothelial cell-induced Akt or ERK signaling in HNSCC has a compensatory effect whereas STAT3 pathway is activated independent of Akt or ERK. Among these three pathways, STAT3 presented the higher phosphorylation levels, and was mainly induced by endothelial cell-secreted IL-6. Interestingly, downregulation of IL-6 in tumor-associated endothelial cells inhibited tumor growth in xenograft human tumors. These results suggest that patients with HNSCC might benefit from targeted inhibition of signaling events initiated by tumor associated-endothelial cells.
520 $a Collectively, this work expands the contribution of vascular endothelial cells to the pathobiology of cancer. It shows that endothelial cells function as the initiators of molecular signaling events that enhance head and neck tumor growth.
590 $a School code: 0127.
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650 4 $a Health Sciences, Dentistry. $3 1019378
650 4 $a Health Sciences, Oncology. $3 1018566
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710 2 $a University of Michigan. $3 777416
773 0 $t Dissertation Abstracts International $g 71-02B.
790 1 0 $a Nor, Jacques Eduardo, $e advisor
790 $a 0127
791 $a Ph.D.
792 $a 2009
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