C. M. Rudin

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.

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.

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.

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.

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.

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.

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.

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.

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

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.

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

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

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

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.