Rev7 is a novel regulator of chemotherapeutic response in drug-resistant lung cancer

Most malignant cancers are treated with chemotherapeutic agents that target and damage cellular DNA While genotoxic chemotherapies have proven to be highly effective agents for cancer therapy, it is well known that intrinsic and acquired cancer drug resistance is a problem that severely limits the successful elimination of a wide range of malignancies. This point is particularly important in the context of genotoxic chemotherapies, because the DNA damaging agents used in cancer treatment induce a diverse spectrum of toxic lesions that are recognized by a variety of DNA damage response (DDR) mechanisms. In this thesis I used CRISPR-Cas9 gene-editing and other molecular biology and biochemical techniques to examine the functional relevance of that Rev7, a multi-functional translesion synthesis (TLS) DNA damage tolerance protein in drug-resistant cancers.

Name thesis:degree_name

Doctoral

Department dc:contributor.department

Massachusetts Institute of Technology. Department of Biological Engineering

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2018

Author dc:creator

• Vassel, Faye-Marie.

Advisor dc:contributor.advisor

• Graham C. Walker and Michael T. Hemann.

• Biological Engineering.

Statement dc:rights

• 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.

Licence dc:rights.uri

• http://dspace.mit.edu/handle/1721.1/7582

Language dc:language.iso

eng

Handle dc:identifier.uri

https://hdl.handle.net/1721.1/122837

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/122837