7 research outputs found

    Iterative Methods for Visualization of Implicit Surfaces on GPU

    Get PDF
    The original publication is available at www.springerlink.comInternational audienceThe ray-casting of implicit surfaces on GPU has been explored in the last few years. However, until recently, they were restricted to second degree (quadrics). We present an iterative solution to ray cast cubics and quartics on GPU. Our solution targets efficient implementation, obtaining interactive rendering for thousands of surfaces per frame. We have given special attention to torus rendering since it is a useful shape for multiple CAD models. We have tested four different iterative methods, including a novel one, comparing them with classical tessellation solution

    Whole-genome landscape of pancreatic neuroendocrine tumours

    No full text
    The diagnosis of pancreatic neuroendocrine tumours (PanNETs) is increasing owing to more sensitive detection methods, and this increase is creating challenges for clinical management. We performed whole-genome sequencing of 102 primary PanNETs and defined the genomic events that characterize their pathogenesis. Here we describe the mutational signatures they harbour, including a deficiency in G:C > T:A base excision repair due to inactivation of MUTYH, which encodes a DNA glycosylase. Clinically sporadic PanNETs contain a larger-than-expected proportion of germline mutations, including previously unreported mutations in the DNA repair genes MUTYH, CHEK2 and BRCA2. Together with mutations in MEN1 and VHL, these mutations occur in 17% of patients. Somatic mutations, including point mutations and gene fusions, were commonly found in genes involved in four main pathways: chromatin remodelling, DNA damage repair, activation of mTOR signalling (including previously undescribed EWSR1 gene fusions), and telomere maintenance. In addition, our gene expression analyses identified a subgroup of tumours associated with hypoxia and HIF signalling

    Hypermutation In Pancreatic Cancer

    Get PDF
    © 2017 AGA Institute Pancreatic cancer is molecularly diverse, with few effective therapies. Increased mutation burden and defective DNA repair are associated with response to immune checkpoint inhibitors in several other cancer types. We interrogated 385 pancreatic cancer genomes to define hypermutation and its causes. Mutational signatures inferring defects in DNA repair were enriched in those with the highest mutation burdens. Mismatch repair deficiency was identified in 1% of tumors harboring different mechanisms of somatic inactivation of MLH1 and MSH2. Defining mutation load in individual pancreatic cancers and the optimal assay for patient selection may inform clinical trial design for immunotherapy in pancreatic cancer
    corecore