C. M. Rudin

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.

Functional Characterisation of the ATOH1 Molecular Subtype Indicates a Pro-Metastatic Role in Small Cell Lung Cancer

The paper identifies ATOH1 as a pro-metastatic oncogenic driver in SCLC by showing its role in cell survival and metastasis suppression upon depletion.

Alveolar differentiation drives resistance to KRAS inhibition in lung adenocarcinoma

This study shows that KRAS inhibition in lung adenocarcinoma leads to an AT1-like cell state that drives resistance, and targeting these cells improves treatment response.

Tumor-intrinsic LKB1-LIF signaling axis establishes a myeloid niche to promote immune evasion and tumor growth

This study identifies a LKB1-LIF signaling axis in tumors that promotes immune evasion by reprogramming myeloid cells, and shows that inhibiting LIF signaling reduces tumor growth.

Glutamine antagonist DRP-104 suppresses tumor growth and enhances response to checkpoint blockade in KEAP1 mutant lung cancer

This study shows that DRP-104, a glutamine antagonist, suppresses KEAP1 mutant lung tumor growth and enhances response to checkpoint blockade by inhibiting glutamine metabolism and improving T cell function.

In vivo metabolomics identifies CD38 as an emergent vulnerability in LKB1-mutant lung cancer

The paper identifies CD38 as a therapeutic target in LKB1-mutant lung cancer through in vivo metabolomics and shows that targeting CD38 inhibits tumor growth.

Actin dysregulation induces neuroendocrine plasticity and immune evasion: a vulnerability of small cell lung cancer

This study shows that CRACD, an actin regulator, suppresses neuroendocrine plasticity and immune evasion in SCLC by modulating NOTCH1 and EZH2 pathways, suggesting EZH2 blockade as a potential therapy.

CD39 Identifies Tumor-Reactive CD8 T cells in Patients With Lung Cancer

This study identifies CD39 as a marker for tumor-reactive CD8 T cells in lung cancer, showing its association with clinical outcomes and response to immune checkpoint therapy.

Regulation of Neuroendocrine Plasticity by the RNA-Binding Protein ZFP36L1

This study identifies ZFP36L1 as an LSD1 target gene that regulates neuroendocrine plasticity in SCLC by destabilizing mRNAs of lineage transcription factors.

Regional and clonal T cell dynamics at single cell resolution in immune checkpoint blockade

This study uses scTCR/RNA-seq to analyze T cell dynamics in lung cancer patients before and after ICB, finding regional heterogeneity and clonal persistence associated with clinical responses.

KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance

This study shows KEAP1 mutations in lung adenocarcinoma lead to immune evasion by reducing dendritic cell and T cell responses, contributing to immunotherapy resistance.

Genomic characterization of metastatic patterns from prospective clinical sequencing of 25,000 patients

The paper analyzes genomic data from 25,000 patients to identify associations between genomic alterations and metastatic patterns across 50 tumor types, finding chromosomal instability correlates with metastatic burden in some cancers.

Multi-omic analysis of lung tumors defines pathways activated in neuroendocrine transformation

The paper identifies molecular mechanisms of neuroendocrine transformation in lung cancer using multi-omic analysis of tumors and clinical samples.

Single cell profiling reveals novel tumor and myeloid subpopulations in small cell lung cancer

The paper profiles single-cell transcriptomes of SCLC subtypes to identify novel tumor and myeloid subpopulations and their associations with metastasis and immune microenvironment changes.

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.

Direct genome editing of patient-derived xenografts using CRISPR-Cas9 enables rapid in vivo functional genomics

This study develops a CRISPR-Cas9 lentiviral platform for genome editing of patient-derived xenografts to analyze genetic dependencies and drug resistance mechanisms in vivo.