PhD positions in Molecular Biology of Childhood Cancer

Location
Children´s Cancer Research Institute, St. Anna Children´s Hospital, Medical University Vienna
Salary
EUR 28.631 gross per year, including social security
Posted
January 25 2017
Position Type
Full Time
Job Type
PhD Studentship

PhD positions in Molecular Biology of Childhood Cancers

at the Children´s Cancer Research Institute, Vienna, Austria

 

Topic: Tumor susceptibility and translational stress response

The Children´s Cancer Research Institute (CCRI) (http://science.ccri.at) is a multidisciplinary academic research institution closely affiliated with Austria´s leading pediatric cancer center, St. Anna Children´s Hospital, and thus associated with the Medical University of Vienna. The paramount aim of the CCRI is to improve treatment outcome of malignant diseases in children and adolescents by performing basic, translational and clinical research. The institute is located in the heart of Vienna, a European metropolis full of history, music and fine arts.

We are inviting applications for two PhD positions funded by the Austrian Research Fund in a project exploring the molecular basis of tumor susceptibility, and the role of long non-coding RNA and translational stress response in the pathogenesis of Ewing sarcoma, a bone cancer in children and adolescents. You will work in the group of Heinrich Kovar, Scientific Director of the CCRI and an international leader in the field of Ewing sarcoma research. Recent publications of the group related to the subject are listed below.

You will be enrolled in the PhD program N094 “Malignant Diseases” of the Medical University of Vienna. Funding will be according to the salary scheme of the Austrian Science Fund (https://www.fwf.ac.at/en/research-funding/personnel-costs/).

Highly motivated, talented candidates with profound theoretical and practical molecular biological knowledge, team spirit and excellent communication skills are invited to submit their application with a motivation letter, CV and three addresses for reference to heinrich.kovar@ccri.at no later than March 6 2017.

References

Ban J, et al. (2014) Suppression of deacetylase SIRT1 mediates tumor-suppressive NOTCH response and offers a novel treatment option in metastatic Ewing sarcoma. Cancer Res. 15,74:6578-88.

Tomazou EM, et al. (2015). Epigenome mapping reveals distinct modes of gene regulation and widespread enhancer reprogramming by the oncogenic fusion protein EWS-FLI1. Cell Reports, 10:1-14.

Schwentner R, et al. (2015) EWS-FLI1 employs an E2F switch to drive target gene expression. Nucleic Acids Res. 43:2780-9

Schwentner R, et al. (2016) The role of miR-17-92 in the miRegulatory landscape of Ewing sarcoma. Oncotarget. 2016 Dec 22. [Epub ahead of print]

Sheffield NC, et al. (2017)  DNA methylation heterogeneity in Ewing sarcoma defines an epigenetic disease spectrum underlying a genetically homogeneous developmental cancer. Nature Med., in press.