Tuomas Tammela

This study identifies age-acquired enhancers in mouse hearts and shows that exercise can reverse their activation.

This study identifies tumor-intrinsic stress states as modulators of CAR T cell therapy response in pancreatic cancer using CRISPR screens and single-cell genomics.

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 CXCL16 macrophages in bone metastases that transiently restrain cancer growth and G-CSF niches that promote reactivation, revealing CAF-bone-marrow interactions as a therapeutic target.

This study identifies the basal cell state in pancreatic cancer as critical for maintaining tumors through an immunosuppressive circuit, showing its ablation leads to tumor collapse.

In vivo lineage tracing and targeted ablation in autochthonous mouse lung adenocarcinoma establish the Slc4a11+ high-plasticity cell state as a bidirectional transition hub driving tumor progression and therapy resistance.

scVital integrates scRNA-seq data across species to identify conserved cell states and reduce batch effects using a variational autoencoder and discriminator.

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

The paper identifies a TNKS2-selective inhibitor that enables tumor-selective WNT suppression by exploiting 8p loss in cancer cells.

This study shows that activation of the integrated stress response (ISR) drives tumor evolution and therapy resistance by promoting dedifferentiation and stemness in lung adenocarcinoma.

This study shows aging reduces lung stem cell function and suppresses lung cancer by inducing iron deficiency through the NUPR1-lipocalin-2 pathway.