18 research outputs found

    Genome sequence of Aedes aegypti, a major arbovirus vector

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    We present a draft sequence of the genome of Aedes aegypti, the primary vector for yellow fever and dengue fever, which at approximately 1376 million base pairs is about 5 times the size of the genome of the malaria vector Anopheles gambiae. Nearly 50% of the Ae. aegypti genome consists of transposable elements. These contribute to a factor of approximately 4 to 6 increase in average gene length and in sizes of intergenic regions relative to An. gambiae and Drosophila melanogaster. Nonetheless, chromosomal synteny is generally maintained among all three insects, although conservation of orthologous gene order is higher (by a factor of approximately 2) between the mosquito species than between either of them and the fruit fly. An increase in genes encoding odorant binding, cytochrome P450, and cuticle domains relative to An. gambiae suggests that members of these protein families underpin some of the biological differences between the two mosquito species

    Pancreatic cancer genomics

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    Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with the worst prognosis among all solid tumors [1]. Although surgical resection offers the only hope for cure, it is possible in only 20% of patients that present with local disease [2]. Indeed, most patients are diagnosed at an advanced stage, when the disease is inoperable. Whether dismal prognosis is a result of late diagnosis or early dissemination to distant organ is still a debate. Systemic chemotherapy provides temporary benefits in controlling advanced disease and prolonging survival in the adjuvant setting but this happens in a small proportion of patients. Several factors are supposed to contribute variably to the intrinsic chemotherapic resistance of pancreatic cancer and include: (i) the presence of a dense stromal component (termed desmoplastic reaction) that significantly reduces drug delivery [3]; (ii) the transformation of epithelial cells into a mesenchymal phenotype (referred to as epithelial to mesenchymal transition, EMT) [4]; and (iii) the presence of pancreatic cancer stem cells [5]. To complicate our understanding of chemoresistance, there is the marked molecular heterogeneity among primary tumors and metastatic deposits (discussed in details below) [6]. \ua9 2013 Springer Science+Business Media Dordrecht. All rights are reserved
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