2017 The Cell Biology of Megakaryocytes & Platelets Gordon Research Conference & Gordon Research Seminar

项目摘要/摘要 两年一度的细胞生物学戈登研究会议(GRC)和戈登研究研讨会(GRS) 巨核细胞和血小板将现任领导人、初级调查人员和受训人员聚集在一起 巨核细胞系的发育和紊乱。它是世界上最重要的 菲尔德。正在进行的长期科学任务是弥合不同研究人员之间的差距 血统的各个方面，即干细胞、巨核细胞和血小板。这项任务比以往任何时候都更加重要， 随着每种细胞类型之间的相互依赖日益明显，例如，巨核细胞在 干细胞发展，以及炎症对巨核细胞生长和血小板生成的影响。 GRC的主要目的是让该领域的现任和新兴领导人进行交流 未公布的数据，从而教育同事、促进讨论和促进合作。 具体地说，目的是：1.突出在先天性血小板紊乱方面取得的非凡进展。 在2000年，这些情况中约5%是已知的致因性病变。现在这一比例超过了50%。其影响 这些关于诊断、治疗和开辟新的治疗可能性的知识将是 讨论2.传播最新的未发表的研究，将这种血统与免疫和炎症联系起来。它 越来越明显的是，血小板可以促进炎症，炎症和感染可以 影响止血并引发出血。这表明了一系列新的治疗切入点，将 被大力开发。 3.促进癌症中血小板领域的扩大。这包括血小板在调节肿瘤中的作用。 转移，以及癌症相关炎症、血小板生成增加和 血栓形成。尽管进行了几十年的研究，但直到现在才有一些潜在的治疗切入点 开始浮出水面。为实现这些目标，2017年全球资源中心做出了以下承诺： 1.在本次会议的前几次会议中，会议的重点是血小板或巨核细胞，会议 基本上被分成两半。在GRC 2017年，该计划混合了关于巨核细胞的会议 或具有处理更广泛地影响/涉及血统的过程或疾病的会议的血小板。 2.2017年，我们将压缩咖啡休息时间，并削减主旨演讲时间，以便有12次演讲 从摘要中挑选。高级调查人员将绝对准时，抽象的谈话将是 与特邀演讲者混杂在一起，使初级调查人员的出席率最大化。 3.将强调多学科性质，例如关于以下各种方法和技术的会议 被用于先天性血小板疾病，包括图谱、外显子组测序和GWAS。 4.将解决该领域在多个领域的治疗潜力，并就c-mpl突变在 骨髓增殖性肿瘤、白血病中的AURKA抑制剂和血栓形成中的PI3K抑制剂。

PROJECT SUMMARY / ABSTRACT The biennial Gordon Research Conference (GRC) and Gordon Research Seminar (GRS) on the Cell Biology of Megakaryocytes and Platelets brings together current leaders, junior investigators and trainees working on the development and disorders of the megakaryocyte lineage. It is the premier international meeting in the field. The ongoing, long-term scientific mission is to bridge the gap between researchers working on different aspects of the lineage, i.e. stem cells, megakaryocytes and platelets. This mission is more relevant than ever, as the interdependence between each cell type becomes increasingly clear, e.g. the role of megakaryocytes in stem cell development, and the impact of inflammation on megakaryocyte growth and platelet production. The overarching, aim of the GRC is to allow current and emerging leaders of the field to communicate unpublished data, thereby educating colleagues, promoting discussions and fostering collaborations. Specifically, the aims are to:1. Highlight the extraordinary progress being made in congenital platelet disorders. In 2000, the causative lesion was known for ~5% of these conditions. This is now more than 50%. The impact this knowledge is having on diagnosis, treatment and the opening up of novel therapeutic possibilities will be discussed.2. Disseminate the latest unpublished research linking the lineage to immunity and inflammation. It is increasingly apparent that platelets can promote inflammation, and that inflammation and infection can impact on hemostasis and trigger hemorrhage. This suggests a range of new therapeutic entry points that will be vigorously explored. 3. Promote the expanding field of platelets in cancer. This includes the role platelets play in mediating tumor metastasis, and the link between cancer-associated inflammation, elevated platelet production, and thrombosis. Despite decades of research, only now are some of the potential therapeutic entry points beginning to emerge. To achieve these aims, the 2017 GRC has made the following commitments: 1. In the earlier iterations of this meeting, sessions focused on platelets or megakaryocytes, and the meeting was essentially divided into two halves. For GRC 2017, the program intermixes sessions on megakaryocytes or platelets with sessions dealing with processes or diseases affecting/involving the lineage more broadly. 2. In 2017 we will be compressing the coffee breaks and trimming keynote speaker times to allow 12 talks to be selected from abstracts. Senior investigators will be kept absolutely to time, and the abstract talks will be intermixed with invited speakers so that attendance is maximized for junior investigators. 3. Multidisciplinarity will be emphasized, e.g. the session on the various approaches and technologies that are being brought to bear on congenital platelet disorders, including mapping, exome sequencing, and GWAS. 4. The therapeutic potential of the field in multiple areas will be tackled, with talks on c-Mpl mutations in myeloproliferative neoplasms, agents such as AURKA inhibitors in leukemia, and PI3K inhibitors in thrombosis.