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アメリカ中西部に位置しますUniversity of Colorado School of Medicineの藤田研究室でポスドクを募集しています。ボス(私)はアメリカ在住20年。アメリカの医師免許も持ち、外来で患者さんを診ながら研究室を運営しています。悪性黒色腫(melanoma,ほくろの癌で悪性度が高い)の患者さんの癌組織をマウスで継代し、その遺伝子、癌幹細胞や炎症を研究しています。詳細は下記に英語で記してあります。





Mayumi Fujita, M.D., Ph.D.
Associate Professor, Dept of Dermatology
University of Colorado School of Medicine
Aurora, CO 80045
(303) 724-4045 (office phone)

The position is offered in Dr. Mayumi Fujita’s laboratory through the Department of Dermatology. Dr. Fujita’s lab has been studying tumor biology, cancer stem cells and tumor inflammation in human melanoma (http://www.ucdenver.edu/academics/colleges/medicalschool/departments/Dermatology/adultderm/clinicfaculty/Pages/Fujita.aspx).

A position is available to study molecular and cell biology in melanoma and cancer stem cells at the University of Colorado Denver, School of Medicine. Specifically, the projects are focused on the genomic changes involved in the invasion of human melanoma tumors and the role of alpha-1 antitrypsin.

The candidate will perform the investigation as follows:
1) Genomic study of human melanoma to identify tumor suppressor genes: We established patient-derived tumor xenografts (PDTX), a unique preclinical model of human melanoma (J Invest Dermatol 132(10); 2440-50, 2012). We hypothesize that metastatic driver genes will be identified by sequentially analyzing tumors from this model. We finished array experiments and identified several interesting candidate tumor suppressor genes. We will focus on 1) genes pre-programmed into primary tumors and 2) genes related with cancer stem cells. We will perform functional and mechanistic study of the genes.
2) The role of alpha-1 antitrypsin in melanoma: Alpha1-antitrypsin (AAT) is a serine protease inhibitor that protects normal tissues from degradation by proteases. AAT has been shown to inhibit pro-inflammatory cytokines and inflammation whereas it also induces immune tolerance. With a collaboration of Charles A Dinarello (Infectious Dis, Internal Medicine), we have a transgenic mouse expressing human AAT under a human surfactant protein C promoter. In this model, small amount of AAT (physiological level) is circulating in the blood. We found that tumorigenesis was dramatically inhibited in this mouse model. We will analyze the role of AAT in tumor microenvironment.

Experience in cell and molecular biology is required.
Experience in working with small animal cancer models is required.
Experience in immunology and cancer biology is highly desirable.


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