This may be due to the fact that in solid tumors repeated episodes of hypoxia followed by reoxygenation is a common phenomenon. This so called “intermittent hypoxia” is described to regulate stem-like characteristics. The occurrence of intermittent hypoxic episodes varies significantly in rapidly growing malignant tumors. In phases of normoxia when EMT-inducing signals are removed CSClow cells that have been induced to EMT may revert to the epithelial state similar by undergoing mesenchymal epithelial transition as has been reported to occur in some carcinoma cells. Additional new data provide insights into how dynamic interactions among epithelial, self-renewal, and mesenchymal gene programs determine the plasticity of CSC in switching between epithelial and mesenchymal states. These findings suggest that CSClow cells may differentiate to CSC-like cells upon induction of EMT by hypoxia and dedifferentiate upon withdrawal of hypoxia. In contrast, CSChigh cells with already basal enhanced EMT features may only partially undergo MET upon reversal of hypoxia. As a result the cells keep their high migratory potential in a normoxic tumor microenvironment and upon a new cycle of hypoxia they upregulate EMT signaling along with enhanced migratory activity faster. A higher basal EMT signaling and the ability to respond faster to EMT may provide a survival advantage to CSChigh cells. In consequence, this may lead to enrichment of CSCs during intermittent hypoxia in tumor progression and subsequently to enhanced invasion and metastasis. In conclusion, we show that a hypoxic environment predominantly increases the migratory capacity of PDA cells with elevated stem cell characteristics. This is of important clinical relevance with respect to the pronounced hypoxic tumor-microenvironment of PDA. Bevacizumab or Avastin and the observed pro-invasive adaption to such anti-angiogenic therapy. The results of the present study together with recent findings of other authors suggest the development of new treatment protocols to target tumor hypoxia. Neuronal activity has been shown to play an important role in the development, maintenance and modulation of these circuits. Animals exhibiting simple behaviors have often been used to understand mechanisms underlying neural circuit development and function. Our interest is to identify individual ICG-001 components of the neural circuits required for insect flight, through a genetic and cellular approach in the fruit fly, Drosophila melanogaster. Triggering of flight by the giant-fiber mediated escape response pathway has been relatively well studied in Drosophila. Escape response pathways are activated under conditions perceived as a threat by the animal, such as a bright flash of light. The organization of these circuits is usually less complex because speed of response is critical for survival. Insect flight can also be initiated by non-threatening stimuli like a gentle puff of air. Air-puff stimulated flight is thought to be mediated by an alternate pathway. A requirement for the biogenic amines, octopamine and tyramine in modulation of insect flight has been shown from studies in locusts, Manduca and other moths. More recently, using an octopaminergic neuronal driver, dTdc-2GAL4, octopamine has been shown to play a modulatory role in Drosophila flight. Although the neural components of air-puff stimulated flight, measured in tethered flies, remain largely unknown, previous studies have shown that serotonergic and dopaminergic neurons.