Andrei Goga

This study uses single-cell RNA-sequencing to track how Pik3caH1047R mutation drives mammary tumor progression by altering epithelial and fibroblast transcriptional states.

This study identifies TACC3 as a vulnerability in MYC-overexpressing triple-negative breast cancers, showing that its inhibition induces cytotoxicity and inflammatory responses.

The paper profiles myeloid cells in breast cancer primary tumors and metastases to show how tumor heterogeneity drives shifts in myeloid cell phenotypes from anti- to pro-metastatic.

This study identifies GPT2-dependent alanine catabolism as a metabolic vulnerability in MYC-driven liver cancer, showing that inhibiting GPT2 reduces tumor growth in mouse models.

This study identifies methionine metabolism and the NOP2 methyltransferase as critical for MYC-driven liver tumorigenesis, suggesting NOP2 as a potential therapeutic target.

The paper identifies microtubule inhibitors as inducers of immunogenic cell death in MYChigh TNBC, linking MYC-dependent DAMP release to immune activation and tumor protection.

The paper shows that gap junctions between breast cancer cells and adipocytes transfer cAMP, activating lipolysis in the tumor microenvironment to support tumor growth.

This study identifies enhanced mitochondrial respiration and glutamine-dependent TCA cycle as vulnerabilities in MYChigh breast cancer cells, showing synthetic lethality with complex I inhibitors.

This study shows gut bacteria produce lactate that increases lung epithelial mitochondrial activity and worsens acute lung injury.

This study shows that YAP activation in monolayer cultures causes resistance to EGFR/KRAS/BRAF pathway inhibitors, while spheroids are more sensitive, highlighting differences in culture systems for modeling cancer progression.

This study shows MYC dysregulates mitotic spindle function, creating a dependency on TPX2, and identifies a synthetic-lethal interaction between MYC and TPX2 in cancers.