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Conference Student Scholarships: Dendritic Cells and the Initiation of Adaptive Immunity
Scholarship Deadline: October 13, 2010 (Midnight US Mountain Standard Time)
Current studies of Dendritic Cells (DCs) have confirmed not only their major role as antigen presenting cells in adaptive immunity but also their important functions in maintaining tolerance and in the initiation of the innate resistance and inflammatory responses. Thus, DCs function as an important bridge between innate resistance and adaptive immunity either through cellular interactions or secretion of pro-inflammatory and immunoregulatory cytokines. The origin and migration pattern of DCs, their cell biological mechanisms of action, their functional diversity, their specializations and activities in specific tissue contexts, as well as their sharing of hematopoietic lineages, functions, and receptors with other phagocytic cell types such as monocytes and macrophages are subjects of intense investigation. Increasingly, the role of dendritic cells in disease pathology and as potential therapeutic targets is being explored both in the laboratory and in the clinic. This is particularly true in human cancer, where both active and passive immunotherapies involving dendritic cells are finally being put to the test in a systematic fashion. In this symposium, each of these aspects of dendritic cell biology and immunological function will be explored in detail, including taking a number of “in depth” looks at functions (such as innate activation mechanisms) that are key to understanding how dendritic cells perform their many remarkable tasks. In addition, this symposium will combine and synergize with a second, jointly organized symposium entitled "Cancer Control by Tumor Suppressors and Immune Effectors", thereby emphasizing emerging concepts concerning the role of the immune response in cancer and cancer therapy.
Keystone Symposia is offering scholarships to students and post-docs this conference season. These scholarships, of up to $1000 each, are to be used to help defray the expenses associated with conference attendance, including air (on a U.S. air carrier), ground transportation and lodging costs. Receipts will be required to receive reimbursement.
Abstracts submitted for poster presentation will be used as the basis for awarding the scholarships. Conference organizers will select the scholarship recipients based on the quality of science of the abstract and the relevance of the abstract to the conference topic. Only one application per abstract is accepted.
Keystone Symposia 221 Summit Place #272 PO Box 1630 Silverthorne, CO 80498 www.keystonesymposia.org
Financial Assistance / Student Scholarships Phone: +1 (800) 253-0685 or Ksenia Shambarger - +1 (970) 262-1230 extension 140 Fax: +1 (970) 262-0311
Conference Student Scholarships: Cancer Control by Tumor Suppressors and Immune Effectors
The changes in the cell biology of tumor cells are conditioned by epigenetic and genetic reprogramming, genomic instability being an essential feature of both oncogenesis and tumor progression despite intrinsic tumor suppressing barriers. These modifications of cancer cells can be accompanied by the emission of “danger signals” that can be perceived by the innate and cognate immune systems. Likewise, promoting tumor cell death or autophagy may enhance or probe the activation of the immune system. Therefore, unravelling the links between the intrinsic barriers against tumor progression and the extrinsic anticancer checkpoints may contribute to unravelling the key molecular sensors of the host-tumor equilibrium and create novel therapeutic targets. The major objectives will be as follows: 1) examine the molecular links between tumor intrinsic checkpoints (p53, NF-Kappa B, autophagy, DNA damage response…) and immunity or immunosuppression, 2) explore the indirect effects of anticancer therapies (conventional or targeted) on the immune system, 3) describe the rationale for and the potential benefit of novel strategies of cancer vaccines or immunotherapies exploiting this knowledge.
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