M. M. Winslow

Efficient and multiplexed somatic genome editing with Cas12a mice

This study develops transgenic Cas12a mice to enable efficient, multiplexed somatic genome editing for studying complex genetic interactions in vivo.

Combinatorial in vivo genome editing identifies widespread epistasis during lung tumorigenesis

The paper uses in vivo genome editing to study genetic interactions in lung cancer, finding widespread negative epistasis among tumor suppressor genes.

A Lung Cancer Mouse Model Database

The paper establishes a database of lung cancer mouse models to improve data comparison and translational relevance by aligning mouse mutations with human lung cancer mutations.

Oncogenic context shapes the fitness landscape of tumor suppression

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

Fully accessible fitness landscape of oncogene-negative lung adenocarcinoma

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.

A multiplexed in vivo approach to identify driver genes in small cell lung cancer

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.

Combinatorial tumor suppressor inactivation efficiently initiates lung adenocarcinoma with therapeutic vulnerabilities

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.

Neuronal mimicry generates an ecosystem critical for brain metastatic growth of SCLC

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

Multiplexed identification of RAS paralog imbalance as a driver of lung cancer growth

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.

LKB1 inactivation modulates chromatin accessibility to drive metastatic progression

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

Genetic determinants of EGFR-Driven Lung Cancer Growth and Therapeutic Response In Vivo

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

miR-200 deficiency promotes lung cancer metastasis by activating cancer-associated fibroblasts

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

G-baToN: a versatile reporter system for cancer cell-stromal cell interactions.

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.

Quantitative in vivo analyses reveal a complex pharmacogenomic landscape in lung adenocarcinoma

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