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Tyler E. Jacks and Phillip A. Sharp. Thai, Kevin K. (Kevin Kinh) Massachusetts Institute of Technology. Department of Biology. Massachusetts Institute of Technology. Department of Biology 2018-05-23T16:30:37Z 2018-05-23T16:30:37Z 2018 2018 http://hdl.handle.net/1721.1/115694 1036985783 Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2018. Cataloged from PDF version of thesis. "G̳1̳2̳D̳" in the title on title page appears as superscript. Curriculum Vitae of author on page 2. Includes bibliographical references. Cancer is a disease of normal healthy cells that have accumulated genetic aberrations that contribute to uncontrolled cell divisions. Generally, cancer cells have acquired gain of function mutations in oncogenes that positively promote cell proliferation and growth. Simultaneously, mutations in tumor suppressor genes are frequently detected, allowing cells to evade cell cycle checkpoints, resulting in the inhibition of cell death signals. Therefore, identifying genetic abnormalities that promote tumor initiation and progression is imperative in the development of targeted therapeutics. This thesis focuses on the role of Argonaute-2 in promoting cellular transformation in mouse model systems, highlighting novel oncogenic functions associated with AGO2 overexpression. In short, we have determined that AGO2 overexpression promotes metastasis in an autochthonous mouse model of non-small cell lung cancer while elevated AGO2 levels in B cells contribute to the initiation and maintenance of activated B cell-like diffuse large B cell lymphoma (ABC-like DLBCL), both in the context of KRAS activation and Tp53 deletion. by Kevin K. Thai. Ph.D. 236 pages eng Massachusetts Institute of Technology MIT theses are protected by copyright. They may be viewed, downloaded, or printed from this source but further reproduction or distribution in any format is prohibited without written permission. http://dspace.mit.edu/handle/1721.1/7582 Biology. AGO2 in overexpression exhibits oncogenic functions KrasG̳1̳2̳D̳ -associated mouse tumor models Argonaute-2 in overexpression exhibits oncogenic functions KrasG12D -associated mouse tumor models Thesis application/pdf false Publication unknown unknown <Publication xmlns="https://www.openaire.eu/cerif-profile/1.1/" id="a40b0c70-a05f-4283-b591-5be87ac5a49f"> <Type xmlns="https://www.openaire.eu/cerif-profile/vocab/COAR_Publication_Types">http://purl.org/coar/resource_type/c_1843</Type> <Language>eng</Language> <Title>AGO2 in overexpression exhibits oncogenic functions KrasG̳1̳2̳D̳ -associated mouse tumor models</Title> <Subtitle>Argonaute-2 in overexpression exhibits oncogenic functions KrasG12D -associated mouse tumor models</Subtitle> <PublishedIn> <Publication> </Publication> </PublishedIn> <PublicationDate>2018</PublicationDate> <Authors> <Author> <DisplayName>Thai, Kevin K. (Kevin Kinh)</DisplayName> <Affiliation> <OrgUnit> </OrgUnit> </Affiliation> </Author> </Authors> <Editors> </Editors> <Publishers> <Publisher> <DisplayName>Massachusetts Institute of Technology</DisplayName> <OrgUnit /> </Publisher> </Publishers> <License>http://dspace.mit.edu/handle/1721.1/7582</License> <Keyword>Biology.</Keyword> <Abstract>Cancer is a disease of normal healthy cells that have accumulated genetic aberrations that contribute to uncontrolled cell divisions. Generally, cancer cells have acquired gain of function mutations in oncogenes that positively promote cell proliferation and growth. Simultaneously, mutations in tumor suppressor genes are frequently detected, allowing cells to evade cell cycle checkpoints, resulting in the inhibition of cell death signals. Therefore, identifying genetic abnormalities that promote tumor initiation and progression is imperative in the development of targeted therapeutics. This thesis focuses on the role of Argonaute-2 in promoting cellular transformation in mouse model systems, highlighting novel oncogenic functions associated with AGO2 overexpression. In short, we have determined that AGO2 overexpression promotes metastasis in an autochthonous mouse model of non-small cell lung cancer while elevated AGO2 levels in B cells contribute to the initiation and maintenance of activated B cell-like diffuse large B cell lymphoma (ABC-like DLBCL), both in the context of KRAS activation and Tp53 deletion.</Abstract> <Access xmlns="http://purl.org/coar/access_right" > </Access> </Publication>