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Role of cancer-associated fibroblast...

Salzler, Gregory G.

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Role of cancer-associated fibroblasts in tumorigenesis in non-small cell lung cancer.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Role of cancer-associated fibroblasts in tumorigenesis in non-small cell lung cancer./
Author:	Salzler, Gregory G.
Description:	45 p.
Notes:	Source: Masters Abstracts International, Volume: 53-03.
Contained By:	Masters Abstracts International53-03(E).
Subject:	Oncology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1525721
ISBN:	9781321133592

Role of cancer-associated fibroblasts in tumorigenesis in non-small cell lung cancer.
Salzler, Gregory G.

Role of cancer-associated fibroblasts in tumorigenesis in non-small cell lung cancer. - 45 p.

Source: Masters Abstracts International, Volume: 53-03.

Thesis (M.S.)--Cornell University, 2014.

Cancer-associated fibroblasts (CAFs) are a genetically stable subpopulation of cells residing in the tumor microenvironment that have been found to have a profound pro-tumorigenic effect in many types of cancer. We sought to confirm the difference in tumor-promoting capability in CAFs and NFs from patients with non-small cell lung cancer (NSCLC) and then link the results to both metabolic and genomic profiling data, hoping that the differences found would lead to a better understanding of the stromal effects on the development and progression of NSCLC. We found that the ability to promote tumor growth was in fact not limited to CAFs, as fibroblasts isolated from adjacent normal lung tissue in many cases promoted larger tumors than CAFs did, and in some cases fibroblasts isolated directly from tumors, or "CAFs" by established definitions, did not promote enhanced tumor growth. We further found that though there were significant increases in tumor growth when co-injecting both CAFs and NFs, no human fibroblasts were present in the tumors at the time of resection, indicating that fibroblasts seem to have an important role in setting up a tumor-promoting environment but are not necessary for the subsequent sustained tumor growth. Finally, we performed metabolomic profiling of our fibroblasts using mass spectrometry, however, rather than grouping fibroblasts by their isolation location, we instead grouped them by their ability to promote tumorigenesis in our in vivo model. Utilizing this novel grouping, we discovered several metabolic pathways were indeed different between pro- and non-tumorigenic fibroblasts. Though there are undoubtedly differences between CAFs and NFs, our work provides evidence that this framework should be revised, grouping fibroblasts as either pro- or non-tumorigenic instead of grouping them based on the location from which they were isolated.

ISBN: 9781321133592Subjects--Topical Terms:

751006
Oncology.

Role of cancer-associated fibroblasts in tumorigenesis in non-small cell lung cancer.
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520 $a Cancer-associated fibroblasts (CAFs) are a genetically stable subpopulation of cells residing in the tumor microenvironment that have been found to have a profound pro-tumorigenic effect in many types of cancer. We sought to confirm the difference in tumor-promoting capability in CAFs and NFs from patients with non-small cell lung cancer (NSCLC) and then link the results to both metabolic and genomic profiling data, hoping that the differences found would lead to a better understanding of the stromal effects on the development and progression of NSCLC. We found that the ability to promote tumor growth was in fact not limited to CAFs, as fibroblasts isolated from adjacent normal lung tissue in many cases promoted larger tumors than CAFs did, and in some cases fibroblasts isolated directly from tumors, or "CAFs" by established definitions, did not promote enhanced tumor growth. We further found that though there were significant increases in tumor growth when co-injecting both CAFs and NFs, no human fibroblasts were present in the tumors at the time of resection, indicating that fibroblasts seem to have an important role in setting up a tumor-promoting environment but are not necessary for the subsequent sustained tumor growth. Finally, we performed metabolomic profiling of our fibroblasts using mass spectrometry, however, rather than grouping fibroblasts by their isolation location, we instead grouped them by their ability to promote tumorigenesis in our in vivo model. Utilizing this novel grouping, we discovered several metabolic pathways were indeed different between pro- and non-tumorigenic fibroblasts. Though there are undoubtedly differences between CAFs and NFs, our work provides evidence that this framework should be revised, grouping fibroblasts as either pro- or non-tumorigenic instead of grouping them based on the location from which they were isolated.
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