David G. McFadden

This study combines Msh2 depletion and proofreading-deficient DNA polymerase ε expression to enhance mutagenesis, enabling identification of drug resistance mutations and cytotoxin mechanisms in SCLC cells.

The paper identifies germline mutations in complex I subunits as a driver of Warburg metabolism in oncocytic thyroid carcinoma through loss of heterozygosity.

This study creates inducible EWSR1-FLI1 degron alleles in tumor cell lines to control fusion oncoprotein expression, showing reversible cell cycle arrest and tumor growth suppression in xenografts.

This study identifies two resistance mechanisms to LDH inhibitors in complex I-mutant HTC models through forward genetic screens.