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学术报告
Profs. Isaac P. Witz与Menashe Bar-Eli学术报告
威尼斯官网: 2012-11-13 来源: 浏览次数:

 应生命科学技术学院与前沿科学技术研究院转化医学研究中心主任陆五元教授邀请,以色列特拉维夫大学免疫学教授兼国际癌症微环境协会主席Isaac P. Witz和美国德克萨斯大学MD Anderson癌症研究中心教授Menashe Bar-Eli将于11月19日下午3点在主楼B303面向全校师生做学术报告,欢迎广大师生届时参加。 

学术报告时间:11月19日下午3:00
学术报告地点:主楼B303
学术报告人:
 

一) Prof. Isaac P. Witz
Department of Cell Research and Immunology
Tel Aviv University, Tel Aviv, Israel
学术报告题目:The Tumor Microenvironment and Metastasis
学术报告摘要:A solid tumor is composed of tumor cells, resident and infiltrating non-tumor cells, and molecules present in proximity to these cells. This ecosystem can be collectively described as the tumor microenvironment. Both the tumor cells as well as the neighboring non-tumor cells take part in establishing the specific conditions existing in the microenvironmental milieu.
It is well established that the tumor microenvironment serves as an interaction ground between microenvironmental components and tumor cells. Each of the interactive partners is capable of regulating gene expression in all the other partners, thereby shaping their phenotype. As such, the tumor microenvironment operates primarily as an active “educational/inductive/selection” venue in which the tumor is directed into one of several molecular evolution pathways. In other words, by exerting regulatory functions and selective pressures, the tumor microenvironment determines and shapes the malignancy phenotype of cancer cells and as such drives tumor progression and metastasis.

(二) Prof. Menashe Bar-Eli
Department of Cancer Biology
The University of Texas MD Anderson Cancer Center
, Houston, Texas 77030, USA
学术报告题目:Driving Genes in Melanoma Metastasis
学术报告摘要:The molecular changes associated with the transition of melanoma cells from radial growth phase (RGP) to vertical growth phase (VGP) and the metastatic phenotype are not very well defined.  However, some of the genes involved in this process and their transcriptional regulation are beginning to be elucidated.  For example, the switch from RGP to VGP and the metastatic phenotype is associated with loss of the AP-2α transcription factor.  AP-2α regulates the expression of c-KIT, MMP-2, VEGF, and the adhesion molecule MCAM/MUC18.  Recently, we reported that AP-2α also regulates two G-protein coupled receptors (GPCRs) PAR-1 and PAFR.  In turn, the thrombin receptor, PAR-1, regulates the expression of the gap junction protein Connexin-43 and the tumor suppressor gene Maspin.  Activation of PAR-1 also leads to overexpression and secretion of proangiogenic factors such as IL-8, uPA, VEGF, PDGF, as well certain integrins.  PAR-1 also cooperates with PAFR to regulate the expression of MCAM/MUC18 via phosphorylation of CREB.  The ligands for these GPCRs, thrombin and PAF, are secreted by stromal cells, emphasizing the importance of the tumor microenvironment in melanoma metastasis.  We have developed novel systemic delivery of nano-particles encapsulated with siRNA to PAR-1 or to IL-8 and utilized them to inhibit melanoma growth and metastasis in vivo.  The metastatic phenotype of melanoma is also associated with overexpression and function of CREB/ATF-1.  Loss of AP-2α and overexpression of CREB/ATF-1 results in the overexpression of MCAM/MUC18 which by itself contributes to melanoma metastasis by regulating the inhibitor of DNA binding-1 (Id-1). CREB/ATF-1 also regulates the angiogenic factor CYR-61.  Our recent data indicate that CREB/ATF-1 regulates the expression of AP-2α, thus, supporting the notion that CREB is an important “master switch” in melanoma progression.

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