Biomedical Science: Postdoctoral Fellow in Cancer Biology, University of Michigan, Ann Arbor

University of Michigan

Ann Arbor, MI

Job posting number: #7057183

Posted: May 2, 2019

Application Deadline: July 2, 2019

Job Description

Postdoctoral position in biomedical science is available in Prof. Jolanta Grembecka laboratory, University of Michigan, Ann Arbor, to carry out an interdisciplinary project to study the effect of small molecules in in vitro and in vivo models of cancers and to pursue target validation studies using genetic approaches. We are seeking for a highly motivated postdoctoral fellow with extensive experience in cancer cell biology. The research will be focused on evaluation of the activity and the mechanism of action of novel small molecules blocking epigenetic proteins in cancer. This position requires the expertise in cell biology and molecular biology techniques, including PCR, qRT-PCR, Western Blotting, co-Immunoprecipitation, ChIP, ChIPSeq, flow cytometry, fluorescence microscopy, immunostaining. Prior work experience with animals such as transgenic mice and xenograft models of cancer would be desired. Successful candidate will be a part of an interdisciplinary team focused on development and pre-clinical evaluation of novel anti-cancer drug candidates.

Applicant must have PhD in biology or related field. The candidates must be a first author on at least 2-3 publications. This position requires extensive experience in cell and molecular biology techniques. Furthermore, excellent oral and written communication skills in English are required as well as the ability to conduct independent scientific investigations.

How to apply:
Please submit cover letter, CV, and contact information for 2-3 references combined into one PDF file by e-mail to:

Jolanta Grembecka, PhD, Associate Professor
Department of Pathology, University of Michigan
Ann Arbor, MI, 48109, USA

Relevant publications:
1. Borkin, D. et al., Grembecka, J., Pharmacologic inhibition of the menin-MLL interaction blocks progression of
MLL leukemia in vivo, Cancer Cell, 2015, 27 (4), 589-602.
2. He S, et; al., Grembecka J., Menin-MLL inhibitors block oncogenic transformation by MLL fusion proteins in a
fusion partner independent manner. Leukemia. 2016 Feb;30(2):508-13.
3. Kempinska K, et al, Grembecka J: Pharmacologic inhibition of the menin-MLL interaction leads to
transcriptional repression of PEG10 and blocks hepatocellular carcinoma. Mol Cancer Ther: 2018 Jan;17(1):26-

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