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

项目总结/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） 巨核细胞和血小板聚集在一起，目前的领导人，初级研究人员和学员的工作， 巨核细胞谱系的发育和紊乱。这是世界上最重要的国际会议， 领域正在进行的长期科学使命是弥合研究人员之间的差距， 谱系的各个方面，即干细胞、巨核细胞和血小板。这次使命比以往任何时候都重要 随着每种细胞类型之间的相互依赖性变得越来越清楚，例如巨核细胞在 干细胞发育以及炎症对巨核细胞生长和血小板产生的影响。 GRC的首要目标是让该领域的当前和新兴领导者能够交流 这些数据是未公布的数据，从而教育同事，促进讨论和促进合作。 具体而言，目标是：1.强调在先天性血小板疾病方面取得的非凡进展。 在2000年，已知这些疾病的病因病变约为5%。现在这个比例超过了50%。的影响 这些知识对诊断、治疗和开辟新的治疗可能性的作用将是 讨论。传播最新未发表的研究，将谱系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， 积极探索。 3.促进血小板在癌症中的应用领域不断扩大。这包括血小板在介导肿瘤中的作用。 转移，以及癌症相关炎症，血小板生成增加， 血栓形成尽管进行了数十年的研究，但直到现在才发现一些潜在的治疗切入点 开始出现。为了实现这些目标，2017年GRC做出了以下承诺： 1.在这次会议的早期迭代中，会议集中在血小板或巨核细胞上， 基本上被分成了两半。对于GRC 2017，该计划混合了关于巨核细胞的会议 或血小板与处理更广泛地影响/涉及谱系的过程或疾病的会议。 2.在2017年，我们将压缩咖啡休息时间和削减主旨发言人的时间，使12个会谈， 从摘要中选出。高级调查人员将绝对准时，抽象的谈话将是 与特邀发言者混合，以便最大限度地提高初级调查员的出席率。 3.将强调多学科性，例如，关于各种方法和技术的会议， 被带到承担先天性血小板疾病，包括映射，外显子组测序，和GWAS。 4.该领域在多个领域的治疗潜力将得到解决，并将讨论c-Mpl突变， 骨髓增生性肿瘤、药物如白血病中的AURKA抑制剂和血栓形成中的PI 3 K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 The overarching, aim of the GRC is to allow current and emerging leaders of the field to communicate unpublished data, thereby educating colleagues, promoting discussions and fostering collaborations.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 Disseminate the latest unpublished research linking the lineage to immunity and inflammation.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.