A5072507966- Glioma Diagnosis and Treatment
- Cancer-related Molecular Pathways
- Cancer Genomics and Diagnostics
- Cancer, Hypoxia, and Metabolism
- PI3K/AKT/mTOR signaling in cancer
- Epigenetics and DNA Methylation
- RNA modifications and cancer
- MicroRNA in disease regulation
- Microtubule and mitosis dynamics
- Ubiquitin and proteasome pathways
- Cancer-related molecular mechanisms research
- Lung Cancer Treatments and Mutations
- HER2/EGFR in Cancer Research
- Ocular Oncology and Treatments
- Cancer Mechanisms and Therapy
- Monoclonal and Polyclonal Antibodies Research
- Cancer-related gene regulation
- Renal and related cancers
- Protein Degradation and Inhibitors
- Circular RNAs in diseases
- Genomics and Chromatin Dynamics
- Cell Adhesion Molecules Research
- Neuroblastoma Research and Treatments
- RNA Research and Splicing
- Extracellular vesicles in disease
University of California, San Diego
2016-2025
Ludwig Cancer Research
2015-2024
University of San Diego
2024
La Jolla Alcohol Research
2013-2023
Moores Cancer Center
2011-2019
University of Minnesota
2019
Ludwig Cancer Research
1994-2015
Virginia Commonwealth University
2000-2014
The Ohio State University
2011-2014
Memorial Sloan Kettering Cancer Center
2014
The epidermal growth factor receptor (EGFR) is frequently amplified, overexpressed, or mutated in glioblastomas, but only 10 to 20 percent of patients have a response EGFR kinase inhibitors. mechanism responsiveness glioblastomas these inhibitors unknown.
Although genetic analysis has demonstrated that members of the winged helix, or forkhead, family transcription factors play pivotal roles in regulation cellular differentiation and proliferation, both during development adult, little is known mechanisms underlying their regulation. Here we show activation phosphatidylinositol 3 (PI3) kinase by extracellular growth induces phosphorylation, nuclear export, transcriptional inactivation FKHR1, a member FKHR subclass forkhead factors. Protein B...
The development and neoplastic progression of human astrocytic tumors appears to result through an accumulation genetic alterations occurring in a relatively defined order. One such alteration is amplification the epidermal growth factor receptor (EGFR) gene. This episomal occurs 40-50% glioblastomas, which also normally express endogenous receptors. Moreover, significant fraction amplified genes are rearranged specifically eliminate DNA fragment containing exons 2-7 gene, resulting in-frame...
Genetic analysis in Caenorhabditis elegans has uncovered essential roles for DAF-16 longevity, metabolism, and reproduction. The mammalian orthologs of DAF-16, the closely-related FOXO subclass forkhead transcription factors (FKHR/FOXO1, FKHRL1/FOXO3a, AFX/FOXO4), also have important cell cycle arrest, apoptosis stress responses vitro, but their vivo physiological are largely unknown. To elucidate role normal development physiology, we disrupted each Foxo genes mice. Foxo1-null embryos died...
Deregulation of signaling by the epidermal growth factor receptor (EGFR) is common in human malignancy progression. One mutant EGFR (variously named ΔEGFR, de2-7 EGFR, or EGFRvIII), which occurs frequently cancers, lacks a portion extracellular ligand-binding domain due to genomic deletions that eliminate exons 2 7 and confers dramatic enhancement brain tumor cell tumorigenicity <i>in vivo</i>. In order dissect molecular mechanisms this activity, we analyzed location, autophosphorylation,...
Playing Hide and Seek Targeted cancer therapies have shown promising results in patients, but few of these drugs provide long-term benefits because tumor cells rapidly develop drug resistance. Nathanson et al. (p. 72 , published online 5 December) show that glioblastoma can become resistant to erlotinib, an epidermal growth factor receptor (EGFR)–targeted drug, by eliminating extrachromosomal copies the mutant EGFR gene. After a period withdrawal, gene reappears on DNA resensitized. The...
Overexpression of c-Myc is one the most common alterations in human cancers, yet it not clear how this transcription factor acts to promote malignant transformation. To understand molecular targets function, we have used an unbiased genome-wide location-analysis approach examine genomic binding sites Burkitt's lymphoma cells. We find that together with its heterodimeric partner, Max, occupy >15% gene promoters tested these cancer The DNA and Max correlates extensively expression...