摘要：
The Hemann laboratory is interested in understanding how specific anatomical sites can be inherently chemoprotective, without presenting a physical barrier to drug delivery. Their recent work has identified mechanisms by which front-line anti-cancer regimens can target most cancer cells yet, paradoxically, promote the survival of a residual tumor burden in specific microenvironments. This process involves the induction of a carefully regulated pro-survival paracrine signaling program emanating from proximal endothelial and infiltrating immune cells. These discoveries have laid a foundation to study basic mechanisms of disease persistence following chemotherapy. For example, our work has shown that the same mechanisms used to protect stem and progenitor cells from physiological stresses can be coopted by tumor cells to evade systemic drug regimens. Thus, we have been able to apply basic tenants of stem cell and developmental biology to direct hypothesis-driven experiments in the realm of cancer therapy – a field that is notoriously reliant upon empirical data.  Importantly, these experiments have also involved the development of new tractable tumor transplantation models in which cancer cells can be rapidly and extensively modified ex vivo and then transplanted into syngeneic, immunocompetent recipient mice. In the process of developing these pre-clinical models, our laboratory has pioneered the application of rapid loss of function screening approaches for use in vivo in mouse models of cancer.  Results from these studies have highlighted significant barriers to therapeutic efficacy, but have also identified new targets that, when inhibited, can potentiate the effects of currently used drug regimens
讲座人简介：
Hemann教授的工作致力于运用小鼠动物模型，结合RNAi、CRISPR等技术，研究癌症发生发展、药物治疗过程中的重要决定因素。主要的研究成果包括1）药物治疗过程中，肿瘤所处的微环境因子如何影响治疗效果（Cell 2010, 2014; Genes & Dev 2012, 2016）; 2）基于RNAi技术的一个药物机理鉴定平台，并在其基础上阐明抗癌药物组合疗法的机理（Nat Chem Bio 2011; PNAS 2013; Cancer Discovery 2014; Nat Med 2017）; 3) 基于RNAi技术的小鼠肿瘤模型筛选，发现决定肿瘤发生发展重要基因（Nat Genet 2009; Genes&Dev2015）; 4)癌细胞中哪些突变导致抗药性，以及如何对其进行针对性的逆转，以实现精准治疗（Genes & Dev 2009; PNAS 2010, 2010; Cell 2016）