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 role of TLE4 as a tumor suppress...

Shin, Thomas Hyungsup.

FindBook

Google Book

Amazon

博客來

The role of TLE4 as a tumor suppressor in acute myeloid leukemia and regulator of hematopoietic and bone development.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The role of TLE4 as a tumor suppressor in acute myeloid leukemia and regulator of hematopoietic and bone development./
作者:	Shin, Thomas Hyungsup.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2016,
面頁冊數:	167 p.
附註:	Source: Dissertation Abstracts International, Volume: 78-08(E), Section: B.
Contained By:	Dissertation Abstracts International78-08B(E).
標題:	Medicine. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10189205
ISBN:	9781369569544

The role of TLE4 as a tumor suppressor in acute myeloid leukemia and regulator of hematopoietic and bone development.
Shin, Thomas Hyungsup.

The role of TLE4 as a tumor suppressor in acute myeloid leukemia and regulator of hematopoietic and bone development. - Ann Arbor : ProQuest Dissertations & Theses, 2016 - 167 p.

Source: Dissertation Abstracts International, Volume: 78-08(E), Section: B.

Thesis (Ph.D.)--Boston University, 2016.

The presence of AML1-ETO (RUNX1-CBF2T1), a fusion oncoprotein resulting from a t(8;21) chromosomal translocation, is a necessary but insufficient event in the development of a subset of acute myeloid leukemias (AML). Although AML1-ETO is able to block differentiation and immortalize hematopoietic stem cells, other contributory events are required for cell proliferation and leukemogenesis, suggesting that specific tumor suppressor genes may counteract the leukemic potential of AML1-ETO.

ISBN: 9781369569544Subjects--Topical Terms:

641104
Medicine.

The role of TLE4 as a tumor suppressor in acute myeloid leukemia and regulator of hematopoietic and bone development.
LDR:03473nmm a2200337 4500 001 2124007
005 20171023101704.5
008 180830s2016 ||||||||||||||||| ||eng d
020 $a 9781369569544
035 $a (MiAaPQ)AAI10189205
035 $a AAI10189205
040 $a MiAaPQ $c MiAaPQ
100 1 $a Shin, Thomas Hyungsup. $3 3285970
245 1 4 $a The role of TLE4 as a tumor suppressor in acute myeloid leukemia and regulator of hematopoietic and bone development.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2016
300 $a 167 p.
500 $a Source: Dissertation Abstracts International, Volume: 78-08(E), Section: B.
500 $a Advisers: George J. Murphy; David A. Sweetser.
502 $a Thesis (Ph.D.)--Boston University, 2016.
520 $a The presence of AML1-ETO (RUNX1-CBF2T1), a fusion oncoprotein resulting from a t(8;21) chromosomal translocation, is a necessary but insufficient event in the development of a subset of acute myeloid leukemias (AML). Although AML1-ETO is able to block differentiation and immortalize hematopoietic stem cells, other contributory events are required for cell proliferation and leukemogenesis, suggesting that specific tumor suppressor genes may counteract the leukemic potential of AML1-ETO.
520 $a In studying del(9q), one of the most common concomitant chromosomal abnormalities with t(8;21), we identified the loss of TLE4 as a key cooperating event in the development of AML1-ETO AML, leading to increased cell proliferation, blocked apoptosis and differentiation, as well as cytarabine resistance in leukemic cells. This suggested TLE4 functions as a tumor suppressor gene in AML.We found these effects are mediated by the loss of TLE4 regulation of a COX-Wnt inflammatory axis. These effects were consequently reversible by Wnt signaling and cyclooxygenase inhibition, pointing towards anti-inflammatory agents as potentially new therapeutic and adjuvant strategies for AML.
520 $a While studies in Drosophila implicate TLE/Groucho as a key mediator of various signaling pathways, including receptor tyrosine kinase/Ras/MAPK, Notch, Myc, and Wnt pathways, there is surprisingly little known about the role of TLE in mammalian development. Using a Tle4 knockout (T4KO) mouse, we identified previously unknown roles for Tle4 in regulating vertebrate mammalian hematopoietic and bone development. T4KO mice manifest leukocytopenia and defective hematopoietic stem cell populations. Using serial transplantation and stromal co-culture, we find that these hematopoietic deficiencies arise due to both intrinsic dysfunction of hematopoietic stem cells as well as defective extrinsic regulation of hematopoiesis by the stem cell niche. Additionally, T4KO mice are severely runted and exhibit markedly decreased bone mineralization concomitant with defective osteoblast function and decreased mineral apposition rates.
520 $a Many of the pathways regulated by TLE are aberrant in cancer, which has led to increasing studies connecting TLE with various malignancies, including synovial cell sarcoma and glioblastoma. Our findings have great implications for current understanding of TLE function in not only cancer, but also bone and hematopoietic development.
590 $a School code: 0017.
650 4 $a Medicine. $3 641104
650 4 $a Oncology. $3 751006
650 4 $a Molecular biology. $3 517296
690 $a 0564
690 $a 0992
690 $a 0307
710 2 $a Boston University. $b Molecular and Translational Medicine GMS. $3 3285971
773 0 $t Dissertation Abstracts International $g 78-08B(E).
790 $a 0017
791 $a Ph.D.
792 $a 2016
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10189205