Identification of genotype-specific dependencies in Keap1-deficient lung adenocarcinoma

Lung adenocarcinoma (LUAD) remains the world's leading cause of cancer related mortality with an estimated two-hundred thousand new cases arising in 2019 in the United states alone. Molecular characterization of patient tumors has identified activating mutations in the small GTPase, KRAS, encompassing ~30% of all LUAD patient samples. Efforts in therapeutic intervention for KRAS-mutant LUAD are numerous, but have been met with little clinical success. Importantly, large-scale sequencing studies have defined the genomic complexities of LUAD resulting in the need to functionally characterize frequently mutated genes in the context of tumorigenesis. The development of somatic genome editing provided by clustered regularly interspaced short palindromic repeats (CRISPR) and the endonuclease, CRISPR associated protein 9 (Cas9) has accelerated our ability to functionally interrogate putative genetic drivers in the context of mammalian cells and autochthonously arising tumors.

Name thesis:degree_name

Doctoral

Department dc:contributor.department

Massachusetts Institute of Technology. Department of Biology

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2019

Author dc:creator

• Romero, Rodrigo,Ph. D.Massachusetts Institute of Technology.

Advisor dc:contributor.advisor

• Tyler Jacks.

• Biology.

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/1721.1/122065

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/122065