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This raiscd delta structurc is an ice-contact deltaic complex with a volume of ('. 4.4 .loy m', deposited c. 9500 yr BP in a shallow wide 'fjord' during the retreat o f t h e Scandinavian ice cap. The delta plain lies at an altitude of 200-223 m. It aggraded c'. 20 m above the contemporaneous sea level during a regional marine regression.The braidplain palaeochannel characteristics indicate a peak meltwater discharge of 7-9 10' m'/s. Calculations bascd on a glacial ablation model indicate a mid-summer discharge of c. 5.5 10' m3/s. However, the fluvial topset of the delta has an erosive base whose altitude decreases upstream and indicates stream incision by more the 6 m below the contemporaneous sea level. The deep scour is ascribed to episodic floods over the relatively short delta plain, which exceeded direct ablation-associated discharges. The depositional time-span of the delta is assessed to have been 70 years, calculated from coastal gradient and shoreline displacement curves. The average sedimentation rate of the delta is thereby inferred to have been extremely high, c. 6 . 10' m'lyr. The sedimentation is thought to reflect 'extreme' ice-margin conditions, where the sediment and water discharge was maximized by full-scale ablation, with simultaneous subglacial, englacial and supraglacial sediment and water supply. These conditions might further coincide with an abundant rainfall in the catchment area or the drainage of dammed waters, initiating episodic floods which eroded deep beneath sea level. As a whole, the study illustrates the hydrological conditions of proglacial sedimentation at the front of the rapidly retreating last Scandinavian ice cap. BornOslo. ISSN 0300-9483.

Infection by enveloped viruses such as HIV and influenza requires fusion of viral and host membranes. The influenza virus fuses with the membrane of the

The ability of cancer cells to detach from their neighbors, invade through local tissues, and establish distant metastases is a major contributor to cancer mortality. Epithelial-mesenchymal transition (EMT) describes a developmental process by which cells break cell-cell adhesions and gain motility. Interestingly, cells generated by EMT also bear stem cell properties and are more resistant to chemotherapeutics. EMT is triggered by a number of cellular signaling pathways, including via hepatocyte growth factor. Inappropriate signaling in epithelial tumors is thought to drive EMT, facilitating cancer metastasis. A common feature is the activation of a number of transcriptional programs. Here we report the results of transcriptomic studies that are designed to characterize transcriptional changes in cells undergoing EMT in response to HGF stimulation. MDCK cells, a normal epithelial cell line, were stimulated with HGF for different amounts of time under otherwise identical culture conditions. Since cell substrate composition affects the robustness of the HGF response, we performed this experiment on cells grown on different extracellular matrices in an attempt to better understand how cellular substrates provide context to HGF signaling. Triplicate samples of mRNA were generated from these cultures for transcriptomic sequencing and analysis. Each sample generated 20-40 million sequence reads that were assembled into known and de novo (novel) transcripts using Tuxedo Suite, allowing detection of differential transcript expression by cummeRbund and edgeR. Many of the differentially expressed genes correlated well to known cancer pathways. HGF signaling is widely accepted to play an important role in cancer progression and to be an important target for development of novel therapeutics. We previously identified a series of novel HGF pathway inhibitors using a phenotypic screening approach. Compounds were subjected to analysis of their structure-activity relationship, in vivo toxicity, and pharmacokinetic profiles. Compounds that block EMT without affecting proliferation were applied to MDCK cells prior to HGF stimulation and mRNA samples generated from these cultures. We report how these inhibitors alter the transcriptional response of MDCK cells to HGF stimulation, providing a molecular basis for how these inhibitors prevent EMT. Citation Format: Kevin J. Tuttle, Jason Burton, W Evan Johnson, Marc DH Hansen. Characterization of HGF-mediated EMT and its inhibition with novel HGF pathway inhibitors using transcriptomic analysis. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr C54.

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