王中王鉄算盘开奖结果，2013年10月8日，美国杜兰大学医学院生化与分子生物学系教授、系主任，杜兰大学医学院肿瘤中心转化肿瘤学Reynolds and Ryan Families教授及医学院执行委员会委员卢华博士应邀访问研究所并举办学术讲座。讲座的题目为：A double edged sword: the ribosomal stress-p53 pathway。朱冰博士主持讲座。
王中王算盘三期必开奖，2012年2月21日，美国得克萨斯大学西南医学院内科教授Theodora S. Ross博士应邀访问研究所并举办学术讲座。讲座的题目为：Tyrosine Kinases, Cancer and their Connection to HIP1。陈良博士主持讲座。
The major theme of my talk is about how the newly identified nucleolar or ribosomal stress-p53 pathway plays an anti-cancer role in protecting mammalian cells from tumorigenesis on one hand, while plays a pathogenic role in inherited human diseases specifically in bone marrow disorders, such as some types of ribosomopathies, on the other hand. Also, this molecular pathway could be utilized for either anti-cancer drug discovery or anti-ribosompathy drug discovery.
For many years we have investigated the basic mechanisms of transformation of normal cells into cancer cells and the resistance of cancer cells to targeted drugs .More specifically, our research has focused on 1) understanding how cancer cells hijack clathrin trafficking pathways to increase signals from multiple growth factor receptors in parallel (Rao et al., Cancer Cell 2003; 3:471) and 2) understanding how tyrosine kinase oncogene induced cancers resist targeted therapiesin vivo(Oravecz-wilson et al, Cancer Cell 2009; 16:137). In my talk I will touch on how the clathrin binding protein Huntingtin Interacting Protein 1 has been implicated in tumorigenesis and normal cell physiology.We have found that HIP1 is elevated in many cancers and have evaluated the clinical implications of this in prostate cancer patients and found that HIP1 expression is a strong marker of tumor progression.We have shown that HIP1’s expression is necessary for some normal and cancer cells to survive in vivo and that it directly transforms fibroblasts as a result of altered levels of multiple growth factor receptors.In addition HIP1 knockout mice have a general “cell loss” or degenerative phenotype as evidenced by hematopoietic defects, testicular degeneration, spinal defects, diminished prostate tumorigenesis and cataracts.The putative regulation of endocytic pathways by HIP1 and HIP1r could explain our observations.I.e. alteration of these pathways may be the reason for the altered growth characteristics during overexpression or knockout of HIP1 and HIP1r.Because it was originally linked to neoplasia by our discovery of the oncogenic HIP1/PDGFβR fusion protein that resulted from a t chromosomal translocation in a patient with leukemia, I will also discuss our work towards a better understanding the transforming biology of HIP1/PDGFβR and other tyrosine kinase oncogenes that cause chronic leukemias.We have generated and are analyzing HIP1/PDGFβR and Bcr/Abl conditional knock-in mice.Using these “high-end” mouse models we are in a unique position to define common pathways of leukemogenesis by fusion tyrosine kinases in vivo.These knock-in mice are being used to rigorously test the tumorigenic stem cell hypothesis in the setting of realistic expression of human oncogenes, to understand mechanisms of transformation by HIP1/PDGFβR and Bcr/Abl and to make sense of therapeutic resistance to tyrosine kinase inhibitors (e.g. imatinib, nilotinib and desatinib) or further downstream signal transduction pathway inhibitors .In sum, much of the laboratory focus is to understand the necessary role of the HIP1 family in modulation of fundamental cellular pathways in the biology of normal and neoplastic cells.