Jorge Silvio Gutkind

This study identifies a reversible GNAS-PKA-RUNX2 checkpoint that governs skeletal stem cell fate in fibrous dysplasia and shows PKA inhibition can reverse disease features.

This study shows that mTOR inhibition with everolimus enhances antitumor immune responses in TP53-mutant HNSCC by altering the tumor microenvironment.

This study shows that knocking out PKA regulatory subunits RI and RII leads to distinct metabolic and phosphorylation changes, with RI KO increasing Tau phosphorylation linked to Alzheimer's disease.

This paper develops a targeted radiosensitizer drug conjugate that enhances tumor control and immune responses while minimizing toxicity to normal tissues.

This paper investigates the effects of Gαs ablation in the pancreas, showing reduced β-cell mass, exocrine defects, and attempted β-cell regeneration from ducts, suggesting potential therapeutic strategies for diabetes.

This study identifies the COX2-PGE2-PKA axis as a negative regulator of mtDNA-STING signaling, which suppresses antiviral immunity by inhibiting STING activation through mitophagy.

This study predicts 3D structures of human GPCR-G protein complexes using AlphaFold3 and uses machine learning to predict coupling potency, revealing new signaling mechanisms and coupling preferences across GPCR subtypes.

This study identifies hyperactivation of YAP/TEAD signaling in EACSCC and shows that targeting TEAD or PITX2 can suppress tumor growth and predict poor prognosis.

The paper identifies collagen remodeling as a mechanism that activates a GPCR-mediated immune checkpoint in ADGRG1+ CD8+ T cells, influencing response to immunotherapy.

This study shows CD47 blockade combined with anti-PD1 and radiotherapy improves tumor response in HNSCC by enhancing antigen presentation and immune cell infiltration.

This study shows that delivering CXCL10 into tumors enhances immune cell infiltration, activation, and anti-tumor responses, and improves the effectiveness of immunotherapy in head and neck squamous cell carcinoma.

This study shows LSD1 inhibition enhances antitumor immunity in HNSCC by upregulating MHC-I and activating the IFNγ-CXCL9-CXCR3 axis through dendritic cells and CD8+ T cells.

The paper identifies antigenic cancer persister cells that survive direct T cell attack by leveraging apoptosis to avoid inflammatory death and acquiring mutations for immune resistance.

The paper identifies YAP-driven reprogramming of oral epithelial stem cells into tumor-initiating cells using single-cell multiomics, revealing conserved transcriptional programs linked to poor patient survival.

The paper refines gene expression signatures using multi-omics data to improve enrichment analysis by addressing lack of coordinate expression in gene sets.

This study identifies endothelial RhoA activation as a key driver of tumor cell transendothelial migration and metastasis, showing it can be inhibited to reduce metastatic potential.

This study identifies mTOR inhibition as a way to prevent adaptive resistance to CDK4/6 blockade in HNSCC by targeting cell cycle pathways.

The paper analyzes GPCR signaling dysregulation in cancer transcriptomics data to identify therapeutic targets and survival-associated signaling axes.

This study identifies structural changes in P-Rex1 upon activation by PIP3 and inhibition by IP4, revealing how these interactions regulate its GEF activity.

The paper analyzes pan-cancer single-cell transcriptomes to evaluate and identify new CAR targets for head and neck cancer, finding five promising targets with superior selectivity and safety.

The paper identifies 71,946 genetic interactions in cancer using a novel method, revealing non-synthetic-lethal interactions that explain driver gene specificity and drug response.