M. M. Winslow

The paper models tumor suppression fitness landscapes across four oncogenic contexts and finds context-specific tumor suppressor effects.

This study characterizes the fitness landscapes of tumor suppressor genes in oncogene-negative lung adenocarcinoma, finding that multiple mutations can drive tumor growth with minimal constraints on mutational order.

The paper develops a multiplexed in vivo approach to identify driver genes in SCLC using CRISPR/Cas9 and lentiviral barcoding, finding TSC1 as a robust tumor suppressor.

This study identifies RAS/PI3K pathway activation as a common driver in oncogene-negative lung adenocarcinomas and shows these tumors are vulnerable to targeted therapy.

This study shows SCLC cells mimic neurons to promote brain metastasis by recruiting astrocytes through factors like Reelin and SERPINE1.

This study identifies HRAS and NRAS as suppressors of KRASG12D-driven lung cancer using CRISPR screens in mouse models and confirms their role in human cell lines.

This study shows that LKB1 inactivation alters chromatin accessibility, promoting metastatic progression in lung cancer through SOX17 activation.

This study investigates how genetic alterations affect EGFR-driven lung cancer growth and therapy response using a mouse model and CRISPR-Cas9 editing.

This study shows that miR-200 deficiency in lung cancer cells promotes metastasis by activating cancer-associated fibroblasts through Notch signaling.

This paper introduces G-baToN, a reporter system that labels cell-cell interactions through fluorescent protein transfer, enabling study of cancer-stromal cell interactions and other biological processes.

The paper uses a quantitative platform and statistical methods to map pharmacogenomic responses in lung cancer, revealing complex genotype-specific therapeutic interactions.