Charles M. Rudin

P-selectin-targeted fucoidan nanoparticles carrying Navitoclax or dBET6 deplete a senescent-like, lipid-associated macrophage subset, reverse mouse liver and lung fibrosis with less toxicity, and restore checkpoint therapy response in fibrotic tumors.

The paper identifies SMARCA4/STK11/KEAP1 triple mutant lung adenocarcinoma as a poor prognosis subset and links it to TGF-β pathway activation.

The paper introduces Suco and Compocyte to classify immune cells from 3,965 patients, identifying new macrophage and monocyte states and T cell memory erosion in metastases.

The paper analyzes the evolutionary trajectories of high-level copy-number amplifications in cancer cell genomes to distinguish between extrachromosomal and intrachromosomal amplification mechanisms.

The paper identifies metabolic differences between ASCL1-high and low SCLC cells, showing that ASCL1-high cells resist ferroptosis via BH4/BH2 antioxidants and are vulnerable to combined cysteine depletion and BH4/BH2 inhibition.

This paper develops antibody-drug conjugates targeting L1CAM to treat metastatic cancer, showing potent tumor control and extended survival in mouse models.

The paper identifies basal cells as the origin of neuroendocrine-tuft-like tumors in SCLC, revealing lineage plasticity and transcriptional states that mirror human cancer and normal cell injury responses.

The paper identifies L1CAM-driven planar cell polarity signaling as a mechanism promoting SOX2+ metastatic progenitors in lung adenocarcinoma.

This study shows that dopamine D2 receptor agonists reduce angiogenesis and inhibit chemotherapy-refractory small cell lung cancer progression by targeting tumour-associated endothelial cells.

This study identifies MAPK activation and cellular plasticity as complementary resistance mechanisms to EGFR TKI in lung adenocarcinoma using single-nuclei RNA sequencing and clinical data.

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

This study identifies a therapeutic vulnerability in POU2F-POU2AF-driven cancers by showing that targeting the mSWI/SNF complex with a PROTAC degrader reduces tumor growth in preclinical models.

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.

SCHAF generates spatially resolved single-cell transcriptomes from H&E histology images using vision transformers and adversarial learning, showing good agreement with ground-truth data.

The paper identifies TMEM41B as a host factor required for flavivirus infection and shows SNPs in TMEM41B reduce infection in East Asian populations.

The paper identifies inherited rare, deleterious ATM variants as risk factors for lung adenocarcinoma, showing increased odds ratios in case-control studies and population cohorts.

The paper describes the development and clinical application of MSK-ACCESS, a liquid biopsy assay that improves the specificity of somatic variant detection in cell-free DNA by using paired normal sequencing.