耍小聪明: 打小工，扛长工...

耍小聪明: 打小工，扛长工

 

闺女上周电话中透露， CollegeVine 给了她一个"小时工", 辅导高中毕业生申请学校，打小工的小时工钱比"有盼"医学院 Fan Laboratory抗长工高，三倍还有余。

 

三年前自己申请大学时，得到过"招生英雄"指定的康大一位同姓小女生认真监督和查对申请材料，花二三千美刀换个轻松平稳的经历。除了随意ED申请哥大失利外，哈&普和"有盼"被挂W - list,  进康大二年后，自己申请转学"有盼"，从经历看闺女比其他的辅导员多一次转学申请的成功经验，希望她能帮到一二位希望进好学校的小女生。

 

经过康大Lee教授Lab十个月的严格义工训练，暑假二个月去 UVA乳腺癌实验室已经可以独立做一组实验，结果还可以用，印裔女老板拿去组织文章。八月底进"有盼", 忧点欠思考走老路，又去医学院找实验室(有很多从事前沿研究的 Lab对本科学生开放), 比较仓促没有做细致的SWOT二选一进了研究脑癌的Fan Laboratory，老板项目有钱，用本科生抗长工，捡芝麻的事...

 

If 闺女能学的更聪明些，励大智琢大事，让"脚瘦"和善跑的同学们当合同工...

 

焦愚&教娱，试错和学习过程中...

 

Fan Laboratory

 

HomePeopleResearchPublicationsResourcesAbout The PI

 

HOMERESEARCHResearch

 

Glioblastoma (GBM, grade IV glioma) is the most common and most aggressive primary brain tumor in humans. GBM is among the most lethal of human malignancies with a median survival of approximately 14 months, largely due to its high resistance to standard radio- and chemotherapy. The ultimate objective of our research is to develop new, efficient therapies against GBM and other malignant tumors by targeting the cancer microenvironment. 

 

Vascular Transformation

 

Aberrant vascularization is a hallmark of cancer progression and therapy resistance. However, current anti-vascular treatments that mainly target angiogenic factors, albeit initially groundbreaking, have encountered difficulties and failure in most types of malignant tumors. Our recent studies reveal that tumor-associated endothelial cells exhibit robust plasticity, acquiring mesenchymal phenotypes to induce vascular abnormality (Huang et al, JCI 2016), which suggests endothelial de-transformation as a novel anti-cancer therapeutic strategy. We aim to decipher the key mechanisms that control cell plasticity-driven metabolic, epigenetic, and genetic reprogramming in tumor-associated endothelial cells, which serve as the targets for next-generation anti-vascular therapies. We expect these new vasculotherapies may recondition the tissue microenvironment, block cancer progression, and overcome tumor therapeutic resistance.

 

Immune Microenvironment

 

Immunotherapy holds great promise for cancer treatment. However, current immunotherapy of solid tumors, primarily by targeting tumor-associated T cells, remains a big challenge, largely due to insufficient infiltration and activation of T cells in the tumors. Our studies aim at elucidating the immunosuppressive mechanisms, by which tumor-associated macrophages and myeloid-derived suppressor cells (MDSCs) inhibit infiltration and activation of T cells and NK cells in the tumor microenvironment. We hope to develop new cancer immunotherapies by breaking microenvironment-specific immune suppression, which boosts host-tumor immunity and strengthens adoptive cellular therapy.

 

Cancer Stem Cells

 

Cancer stem cells, also known as tumor-initiating cells or tumor-propagating cells, are highly tumorigenic and able to differentiate asymmetrically to orchestrate a heterogeneous tumor mass; importantly, cancer stem cells are resistant to chemotherapy and radiation, and therefore contribute significantly to tumor resistance and relapse. Recent studies have identified a prominent population of glioma stem cells (GSCs) in GBM, which are pluripotent and radio-resistant and have the ability to repopulate tumors. The goal of our laboratory is to develop new therapies that are effective at eradicating GSCs. We employ various approaches and methods of vertebrate genetics and human genomics to dissect the convergent and divergent regulatory pathways that govern GSC stemness and resistance to chemotherapy and radiation, induced by either intrinsic signals in GSCs or extrinsic mechanisms from niche cells.

 

Radiation Biology

 

Proton therapy is an innovative radiation treatment modality that offers dosimetric advantages over conventional photon (gamma or x-ray) radiation. 

 

Contact Us

 

Fan Laboratory

 

Department of Radiation Oncology

University of Pennsylvania

3400 Civic Center Blvd

Smilow Center for Translational Research

Rm 8-132 (Office); Rm 8-167 (Lab)

Philadelphia, PA 19104

 

Email: [e-mail]

 

Lab: 215-898-0039 (lab); 215-898-9291 (office)