Àlvaro Quintanal-Villalonga

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 study identifies genotype-specific immune and metabolic vulnerabilities in lung adenocarcinoma through cross-species analysis of human and mouse tumors.

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 introduces inDrops-2, a cost-efficient scRNA-seq platform that profiles clinical samples with sensitivity comparable to commercial systems and demonstrates its utility in analyzing lung carcinoma samples.