An essential role of the immune system in remodeling the tumor microenvironment upon oncogene inactivation
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 |
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Form | electronic; electronic resource; remote |
Extent | 1 online resource. |
Publication date | 2011 |
Issuance | monographic |
Language | English |
Creators/Contributors
Associated with | Rakhra, Kavya | |
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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 |
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Bibliographic information
Statement of responsibility | Kavya Rakhra. |
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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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