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

The cellular and molecular origin of...

Franklin, Ruth Anne.

FindBook

Google Book

Amazon

博客來

The cellular and molecular origin of tumor-associated macrophages.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The cellular and molecular origin of tumor-associated macrophages./
作者:	Franklin, Ruth Anne.
面頁冊數:	205 p.
附註:	Source: Dissertation Abstracts International, Volume: 75-10(E), Section: B.
Contained By:	Dissertation Abstracts International75-10B(E).
標題:	Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3581371
ISBN:	9781321133622

The cellular and molecular origin of tumor-associated macrophages.
Franklin, Ruth Anne.

The cellular and molecular origin of tumor-associated macrophages. - 205 p.

Source: Dissertation Abstracts International, Volume: 75-10(E), Section: B.

Thesis (Ph.D.)--Cornell University, 2014.

This item is not available from ProQuest Dissertations & Theses.

Long recognized as an evolutionarily ancient cell type involved in tissue homeostasis and immune defense against pathogens, macrophages are being rediscovered as regulators of several diseases including cancer. Additionally, with the recent finding that macrophages originate from both embryonic and hematopoietic precursors, studies have begun to investigate macrophage ontogeny and the signals driving macrophage differentiation during steady state and disease. Here we show that in mice, mammary tumor growth induces the accumulation of tumor-associated macrophages (TAMs) that are phenotypically and functionally distinct from mammary tissue macrophages (MTMs). Although both macrophage populations originate from inflammatory monocytes, TAMs require fewer precursors for their maintenance due to a higher proliferative capacity compared to MTMs. TAMs express the adhesion molecule Vcam1, but do not exhibit the "alternatively activated" or "M2" macrophage phenotype that is often described in the tumor setting. Rather, MTMs appear to be phenotypically M2-polarized. TAM terminal differentiation from monocytes depends on the transcriptional regulator of Notch signaling, RBPJ; and TAM, but not MTM, depletion restores tumor-infiltrating cytotoxic T cell responses and suppresses tumor growth. These findings reveal the ontogeny of TAMs and a discrete tumor-elicited inflammatory response with a non-redundant role in promoting tumor growth, potentially providing new opportunities for cancer immunotherapy.

ISBN: 9781321133622Subjects--Topical Terms:

611031
Immunology.

The cellular and molecular origin of tumor-associated macrophages.
LDR:02464nmm a2200301 4500 001 2076076
005 20161101084233.5
008 170521s2014 ||||||||||||||||| ||eng d
020 $a 9781321133622
035 $a (MiAaPQ)AAI3581371
035 $a AAI3581371
040 $a MiAaPQ $c MiAaPQ
100 1 $a Franklin, Ruth Anne. $3 3191506
245 1 4 $a The cellular and molecular origin of tumor-associated macrophages.
300 $a 205 p.
500 $a Source: Dissertation Abstracts International, Volume: 75-10(E), Section: B.
500 $a Adviser: Ming Li.
502 $a Thesis (Ph.D.)--Cornell University, 2014.
506 $a This item is not available from ProQuest Dissertations & Theses.
520 $a Long recognized as an evolutionarily ancient cell type involved in tissue homeostasis and immune defense against pathogens, macrophages are being rediscovered as regulators of several diseases including cancer. Additionally, with the recent finding that macrophages originate from both embryonic and hematopoietic precursors, studies have begun to investigate macrophage ontogeny and the signals driving macrophage differentiation during steady state and disease. Here we show that in mice, mammary tumor growth induces the accumulation of tumor-associated macrophages (TAMs) that are phenotypically and functionally distinct from mammary tissue macrophages (MTMs). Although both macrophage populations originate from inflammatory monocytes, TAMs require fewer precursors for their maintenance due to a higher proliferative capacity compared to MTMs. TAMs express the adhesion molecule Vcam1, but do not exhibit the "alternatively activated" or "M2" macrophage phenotype that is often described in the tumor setting. Rather, MTMs appear to be phenotypically M2-polarized. TAM terminal differentiation from monocytes depends on the transcriptional regulator of Notch signaling, RBPJ; and TAM, but not MTM, depletion restores tumor-infiltrating cytotoxic T cell responses and suppresses tumor growth. These findings reveal the ontogeny of TAMs and a discrete tumor-elicited inflammatory response with a non-redundant role in promoting tumor growth, potentially providing new opportunities for cancer immunotherapy.
590 $a School code: 0058.
650 4 $a Immunology. $3 611031
650 4 $a Cellular biology. $3 3172791
650 4 $a Oncology. $3 751006
690 $a 0982
690 $a 0379
690 $a 0992
710 2 $a Cornell University. $3 530586
773 0 $t Dissertation Abstracts International $g 75-10B(E).
790 $a 0058
791 $a Ph.D.
792 $a 2014
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3581371