A5055698507- Pancreatic and Hepatic Oncology Research
- RNA modifications and cancer
- Lung Cancer Treatments and Mutations
- Phagocytosis and Immune Regulation
- Cancer-related molecular mechanisms research
- Neuroblastoma Research and Treatments
- Immune Cell Function and Interaction
- Protein Kinase Regulation and GTPase Signaling
- Caveolin-1 and cellular processes
- Cancer-related gene regulation
- PI3K/AKT/mTOR signaling in cancer
- RNA and protein synthesis mechanisms
- Congenital heart defects research
- Hepatocellular Carcinoma Treatment and Prognosis
- Neuroendocrine Tumor Research Advances
- Mechanisms of cancer metastasis
- CAR-T cell therapy research
- Cytokine Signaling Pathways and Interactions
- Cancer, Hypoxia, and Metabolism
- Glycosylation and Glycoproteins Research
- Pancreatic function and diabetes
- CRISPR and Genetic Engineering
- Epigenetics and DNA Methylation
- Cancer Genomics and Diagnostics
- Cancer Immunotherapy and Biomarkers
University of Glasgow
2015-2020
Cancer Research UK Scotland Institute
2015
Czech Academy of Sciences, Institute of Physiology
2011
Abstract MYC is implicated in the development and progression of pancreatic cancer, yet precise level deregulation required to contribute tumor has been difficult define. We used modestly elevated expression human MYC, driven from Rosa26 locus, investigate phenotypes arising mice an approximation trisomy. show that this alone suffices drive neuroendocrine tumors, accelerate KRAS-initiated precursor lesions metastatic ductal adenocarcinoma (PDAC). Our phenotype exposed suppression type I...
KRAS is the most frequently mutated driver oncogene in human adenocarcinoma of lung. There are presently no clinically proven strategies for treatment KRAS-driven lung cancer. Activating mutations thought to confer independence from upstream signaling; however, recent data suggest that this may not be absolute. We show initiation and progression tumors require input ERBB family receptor tyrosine kinases (RTKs): Multiple RTKs expressed active earliest stages tumor development, with a...
Inducible genetically defined mouse models of cancer uniquely facilitate the investigation early events in progression, however, there are valid concerns about ability such to faithfully recapitulate human disease. We developed an inducible model progressive lung adenocarcinoma (LuAd) that combines sporadic activation oncogenic KRasG12D with modest overexpression c-MYC (KM model). Histological examination revealed a highly reproducible spontaneous transition from low-grade locally invasive...
Abstract KRAS is the most frequently mutated driver oncogene in human adenocarcinoma of lung. There are presently no clinically proven strategies for treatment KRAS-driven lung cancer. Activating mutations thought to confer independence from upstream signaling, however recent data suggest that this may not be absolute. Here we show initiation and progression tumors requires input ERBB family RTKs: Multiple RTKs expressed active earliest stages driven tumor development, with a multi-ERBB...
Inducible genetically defined mouse models of cancer uniquely facilitate the investigation early events in progression, however there are valid concerns about ability such to faithfully recapitulate human disease.  We developed an inducible model progressive lung adenocarcinoma (LuAd) that combines sporadic activation oncogenic KRasG12D with modest overexpression c-MYC (KM model). Histological examination revealed a highly reproducible transition from adenoma locally invasive within...
<p>Spreadsheet of genes co-regulated by MYC & Miz1 in KMC PDAC cells</p>
<p>6 supplementary Figures with legends under each; 3 Supplementary Tables; Methods and References</p>
<div>Abstract<p>MYC is implicated in the development and progression of pancreatic cancer, yet precise level MYC deregulation required to contribute tumor has been difficult define. We used modestly elevated expression human MYC, driven from <i>Rosa26</i> locus, investigate phenotypes arising mice an approximation <i>MYC</i> trisomy. show that this alone suffices drive neuroendocrine tumors, accelerate KRAS-initiated precursor lesions metastatic ductal...
<p>Spreadsheet of genes co-regulated by MYC & Miz1 in KMC PDAC cells</p>
<p>6 supplementary Figures with legends under each; 3 Supplementary Tables; Methods and References</p>
<div>Abstract<p>MYC is implicated in the development and progression of pancreatic cancer, yet precise level MYC deregulation required to contribute tumor has been difficult define. We used modestly elevated expression human MYC, driven from <i>Rosa26</i> locus, investigate phenotypes arising mice an approximation <i>MYC</i> trisomy. show that this alone suffices drive neuroendocrine tumors, accelerate KRAS-initiated precursor lesions metastatic ductal...
Endothelial cell damage often occurs in vascular disease such as atherosclerosis resulting loss of vasoregulation and/or thrombosis. To restore endothelial function we have established novel methods to either combine site-specific positioning with lentiviral transduction arteries or directly transduce the endothelium situ. Therefore, designed a special magnetic device obtain radially symmetric lentivirus deposition on wall. Lentivirus is coupled nanoparticles (MNPs) enabling efficient cells...