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Plos Genetics : Modulating the Strength and Threshold of Notch Oncogenic Signals by Mir-181A-1, Volume 8

By Grimes, H. Leighton

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Book Id: WPLBN0003941930
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos Genetics : Modulating the Strength and Threshold of Notch Oncogenic Signals by Mir-181A-1, Volume 8  
Author: Grimes, H. Leighton
Volume: Volume 8
Language: English
Subject: Journals, Science, Genetics
Collections: Periodicals: Journal and Magazine Collection (Contemporary), PLoS Genetics
Historic
Publication Date:
Publisher: Plos

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Grimes, H. L. (n.d.). Plos Genetics : Modulating the Strength and Threshold of Notch Oncogenic Signals by Mir-181A-1, Volume 8. Retrieved from http://www.nationalpubliclibrary.com/


Description
Description : Oncogenes, which are essential for tumor initiation, development, and maintenance, are valuable targets for cancer therapy. However, it remains a challenge to effectively inhibit oncogene activity by targeting their downstream pathways without causing significant toxicity to normal tissues. Here we show that deletion of mir-181a-1/b-1 expression inhibits the development of Notch1 oncogene-induced T cell acute lymphoblastic leukemia (T-ALL). mir-181a-1/b-1 controls the strength and threshold of Notch activity in tumorigenesis in part by dampening multiple negative feedback regulators downstream of NOTCH and pre-T cell receptor (TCR) signaling pathways. Importantly, although Notch oncogenes utilize normal thymic progenitor cell genetic programs for tumor transformation, comparative analyses of mir-181a-1/b-1 function in normal thymocyte and tumor development demonstrate that mir-181a-1/b-1 can be specifically targeted to inhibit tumor development with little toxicity to normal development. Finally, we demonstrate that mir-181a-1/b-1, but not mir-181a-2b-2 and mir-181-c/d, controls the development of normal thymic T cells and leukemia cells. Together, these results illustrate that NOTCH oncogene activity in tumor development can be selectively inhibited by targeting the molecular networks controlled by mir-181a-1/b-1.

 

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