K. Politi

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.

Chitinase 3-like-1 (CHI3L1) in the Pathogenesis of Epidermal Growth Factor Receptor Mutant Non-Small Cell Lung Cancer

This study shows CHI3L1 is induced by EGFR activation in NSCLC and promotes EGFR signaling, with anti-CHI3L1 antibodies reversing TKI resistance and inhibiting metastasis.

EGFR+ lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth

This study shows EGFR-mutant lung adenocarcinomas exploit alveolar macrophage metabolism via GM-CSF--PPARγ signaling to support tumor growth and EGFR signaling, suggesting new therapeutic strategies combining statins and PPARγ inhibition.

Overexpressed Malat1 Drives Metastasis through Inflammatory Reprogramming of Lung Adenocarcinoma Microenvironment

This study shows that overexpressed Malat1 promotes lung adenocarcinoma metastasis by reprogramming the tumor microenvironment through Ccl2-driven inflammation.

Autologous humanized PDX modeling for immuno-oncology recapitulates the human tumor microenvironment

This study develops an autologous humanized PDX model to study tumor-immune interactions and demonstrates its utility in preclinical testing by showing VEGF-A inhibition reduces tumor growth.

Stromal remodeling regulates dendritic cell abundance and activity in the tumor microenvironment

The paper shows that stromal remodeling generates signals that regulate dendritic cell survival and activity, enhancing T-cell inflammation in the tumor microenvironment.

Multimodal Analysis Reveals Differential Immuno-Metabolic Features in Lung Squamous Cell Carcinoma and Adenocarcinoma

This study compares immunometabolic features of lung adenocarcinoma and squamous cell carcinoma using multimodal data, finding distinct metabolic and immune patterns between the two tumor types.

Targeting de novo lipogenesis and the Lands cycle induces ferroptosis in KRAS-mutant lung cancer

This study identifies FASN as a therapeutic target in KRAS-mutant lung cancer by showing its role in lipid metabolism and ferroptosis induction.

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.

YES1 amplification: a mechanism of acquired resistance to EGFR inhibitors identified by transposon mutagenesis and clinical genomics

This study identifies YES1 amplification as a novel mechanism of resistance to EGFR inhibitors in lung cancer using transposon mutagenesis and clinical genomic analysis.

Tumor regression mediated by oncogene withdrawal or erlotinib stimulates infiltration ofinflammatory immune cells in EGFR mutant lung tumors

The paper shows that erlotinib and oncogene withdrawal in EGFR mutant lung tumors increase infiltration of inflammatory immune cells, suggesting immunostimulatory effects of tumor regression.