Georgios Kanellos
A5035369322- PI3K/AKT/mTOR signaling in cancer
- Colorectal Cancer Treatments and Studies
- Explainable Artificial Intelligence (XAI)
- Stock Market Forecasting Methods
- RNA modifications and cancer
- Cellular Mechanics and Interactions
- Cell Adhesion Molecules Research
- Synthesis and Biological Activity
- Biochemical and Molecular Research
- Forecasting Techniques and Applications
- Hippo pathway signaling and YAP/TAZ
- Peptidase Inhibition and Analysis
- RNA and protein synthesis mechanisms
- Signaling Pathways in Disease
- Epigenetics and DNA Methylation
- Mast cells and histamine
- Protein Kinase Regulation and GTPase Signaling
- Pancreatic and Hepatic Oncology Research
- Virus-based gene therapy research
- Polyamine Metabolism and Applications
- RNA Research and Splicing
- Imbalanced Data Classification Techniques
- Nuclear Structure and Function
- Ubiquitin and proteasome pathways
Cancer Research UK
2023-2024
Cancer Research UK Scotland Institute
2020-2023
Glasgow Life
2023
European Central Bank
2021
Edinburgh Cancer Research
2015-2016
Western General Hospital
2015-2016
Genetic co-depletion of the actin-severing proteins ADF and CFL1 triggers catastrophic loss adult homeostasis in multiple tissues. There is impaired cell-cell adhesion skin keratinocytes with dysregulation E-cadherin, hyperproliferation differentiated cells, ultimately apoptosis. Mechanistically, primary consequence depleting both uncontrolled accumulation contractile actin stress fibers associated enlarged focal adhesions at plasma membrane, as well reduced rates membrane protrusions. This...
Abstract KRAS-mutant colorectal cancers are resistant to therapeutics, presenting a significant problem for ∼40% of cases. Rapalogs, which inhibit mTORC1 and thus protein synthesis, significantly less potent in cancer. Using Kras-mutant mouse models mouse- patient-derived organoids, we demonstrate that KRAS with G12D mutation fundamentally rewires translation increase both bulk mRNA-specific initiation. This occurs via the MNK/eIF4E pathway culminating sustained expression c-MYC. By genetic...
The genomic landscape of colorectal cancer (CRC) is shaped by inactivating mutations in tumour suppressors such as APC, and oncogenic mutant KRAS. Here we used genetically engineered mouse models, multimodal mass spectrometry-based metabolomics to study the impact common genetic drivers CRC on metabolic intestine. We show that untargeted profiling can be applied stratify intestinal tissues according underlying alterations, use spectrometry imaging identify tumour, stromal normal adjacent...
Abstract Increased protein synthesis supports growth of established tumours. However, how mRNA translation contributes to early tumorigenesis remains unclear. Here we show that following oncogene activation, hepatocytes enter a non-proliferative/senescent-like phase characterized by α5β1 integrin-dependent deposition fibronectin-rich extracellular matrix (ECM) niches. These niches then promote exit from oncogene-induced senescence permit progression proliferating hepatocellular carcinoma...
Abstract Dysregulated translation is a hallmark of cancer. Targeting the translational machinery represents therapeutic avenue which being actively explored. eIF4A inhibitors target both eIF4A1, promotes as part eIF4F complex, and eIF4A2, can repress via CCR4–NOT complex. While high eIF4A1 expression associated with poor patient outcome, role eIF4A2 in cancer remains unclear. Furthermore, on-target toxicity targeting specific paralogues healthy tissue under-explored. We show that while loss...
Abstract Increased protein synthesis drives proliferation of established tumours. However, how mRNA translation contributes to early tumorigenesis remains unclear. Following oncogene activation, hepatocytes enter a senescent phase characterized by deposition extracellular matrix (ECM) niches which promote subsequent progression hepatocellular carcinoma (HCC). We demonstrate an inverse relationship between rates and transition from this oncogene-induced state proliferating HCC. have found...
<div>Abstract<p><i>KRAS</i>-mutant colorectal cancers are resistant to therapeutics, presenting a significant problem for ∼40% of cases. Rapalogs, which inhibit mTORC1 and thus protein synthesis, significantly less potent in <i>KRAS</i>-mutant cancer. Using <i>Kras</i>-mutant mouse models mouse- patient-derived organoids, we demonstrate that KRAS with G12D mutation fundamentally rewires translation increase both bulk mRNA-specific initiation....
<div>Abstract<p><i>KRAS</i>-mutant colorectal cancers are resistant to therapeutics, presenting a significant problem for ∼40% of cases. Rapalogs, which inhibit mTORC1 and thus protein synthesis, significantly less potent in <i>KRAS</i>-mutant cancer. Using <i>Kras</i>-mutant mouse models mouse- patient-derived organoids, we demonstrate that KRAS with G12D mutation fundamentally rewires translation increase both bulk mRNA-specific initiation....
<p>All supplemental figures and legends</p>
<p>All supplemental figures and legends</p>
Explainable AI constitutes a fundamental step towards establishing fairness and addressing bias in algorithmic decision-making. Despite the large body of work on topic, benefit solutions is mostly evaluated from conceptual or theoretical point view usefulness for real-world use cases remains uncertain. In this work, we aim to state clear user-centric desiderata explainable reflecting common explainability needs experienced statistical production systems European Central Bank. We link...