An essential role of the immune system in remodeling the tumor microenvironment upon oncogene inactivation

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Abstract/Contents

Abstract
Oncogene addiction is thought to occur cell autonomously. Immune effectors are implicated in the initiation and restraint of tumorigenesis, but their role in oncogene inactivation-mediated tumor regression is unclear. Here, we show that an intact immune system, specifically CD4+ T cells, is required for the induction of cellular senescence, shutdown of angiogenesis, and chemokine expression resulting in sustained tumor regression upon inactivation of the MYC or BCR-ABL oncogenes in mouse models of T cell acute lymphoblastic lymphoma and pro-B cell leukemia, respectively. Moreover, immune effectors knocked out for thrombospondins failed to induce sustained tumor regression. Hence, CD4+ T cells are required for the remodeling of the tumor microenvironment through the expression of chemokines, such as thrombospondins, in order to elicit oncogene addiction.

Description

Type of resource text
Form electronic; electronic resource; remote
Extent 1 online resource.
Publication date 2011
Issuance monographic
Language English

Creators/Contributors

Associated with Rakhra, Kavya
Associated with Stanford University, Department of Immunology.
Primary advisor Felsher, Dean (Dean Walton)
Thesis advisor Felsher, Dean (Dean Walton)
Thesis advisor Krams, Sheri Michele
Thesis advisor Kuo, Calvin Jay
Thesis advisor Levy, Ronald, 1941 December 6-
Advisor Krams, Sheri Michele
Advisor Kuo, Calvin Jay
Advisor Levy, Ronald, 1941 December 6-

Subjects

Genre Theses

Bibliographic information

Statement of responsibility Kavya Rakhra.
Note Submitted to the Department of Immunology.
Thesis Ph.D. Stanford University 2011
Location electronic resource

Access conditions

Copyright
© 2011 by Kavya Rakhra
License
This work is licensed under a Creative Commons Attribution Non Commercial 3.0 Unported license (CC BY-NC).

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