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Tudor Oprea is Principal Investigator at the University of New Mexico and coordinator of the Illuminating Tudor Oprea "Dan Rich worked on HIV protease inhibitors. Tudor Oprea "If you only make big enough numbers, big enough networks, big enough algorithms, suddenly Our guests were Maria Waldhoer , Tudor I. Oprea , Thomas Sakmar , Aurelien Rizk & Yaroslav Nikolaev .

are dramatically upregulated in cancer-associated fibroblasts, creating feedback loops between the tumor adrenergic receptor biology to purinergic receptors and, most recently, proton-sensing GPCRs in the tumor microenvironment — Proton-sensing receptors, cancer-associated fibroblasts, and the role of low pH in tumor The tumor signals fibroblasts to raise GPR68 expression, and the low pH of the tumor microenvironment It is a positive feedback loop that exploits the acidic environment tumors naturally create. 3.

four subtypes, their G protein coupling profiles, and why ubiquity creates selectivity problems The tumor Tumor cells use adenosine receptors to silence the immune response In the tumor microenvironment, adenosine receptors expressed on immune cells - and that activation suppresses the immune response, allowing tumors pharmacology and the challenge of targeting four subtypes 16:56 A2A vs A2B - affinity differences, tumor

polyadenylation as a targetable driver of pancreatic cancer, and 2) dysregulation of the pancreatic tumor Ricky's group at UPenn to explore the GPCR side of the lab, which led to the discovery of potential tumor had a discussion about their research on GPCRs, specifically focusing on GPR68 and its role in the tumor his team's current focus on alprazolam, an anti-anxiety medication that has unexpected effects in the tumor his experiments and discoveries about GPR161 in mammary epithelial cells, the effect of alprazolam on tumors

Roughly 20% of tumors now show mutations in GPCRs or their coupled G proteins, and specific cancers — Roughly 20% of tumors carry mutations in GPCRs or G proteins, with striking hotspots in GαQ, GαS, and Beyond this driver, the tumor has only a handful of additional mutations — more like a pediatric cancer A synthetic lethality analysis performed entirely in silico revealed that GαQ tumors depend not only

Attention Now Twenty years ago, cancer biologists dismissed GPCRs: they weren't oncogenic and didn't kill tumor The shift came through the tumor microenvironment — immune cells, chemokine receptors, adenosine signaling — where GPCRs now sit at the center of immuno-oncology strategies that tumor-intrinsic target lists

Richard Vile's lab at Mayo Clinic where she aided the evaluation of tumor-specific oncolytic viruses.

signaling in cancer biology, head and neck squamous cell carcinoma, and the molecular circuitry that drives tumor

signaling — one of the most fundamental pathways in vertebrate development, stem cell renewal, and tumor