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Juraj Bies, Ph.D.

Laboratory of Cellular Oncology
Leukemogenesis Section
Staff Scientist
Center for Cancer Research
National Cancer Institute
Building 37, Room 4124
Bethesda, MD 20892
Phone:  
301-402-9229
Fax:  
301-594-3996
E-Mail:  
jb5o@nih.gov

Biography

Dr. Bies received a M.Sc. in Biochemistry and Molecular Biology from the Comenius University Bratislava, and a Ph.D. in Experimental Oncology from the Cancer Research Institute Slovak Academy of Sciences studying the specific role of the c-Myb and B-Myb proteins in differentiation of myeloid cells. In 1992, Dr. Bies began post-doctoral training in the Laboratory of Genetics under the guidance of Dr. Linda Wolff at NCI NIH, where he continued his studies on the regulation of the c-Myb transcription factor by posttranslational modifications. In 1997, he returned to the Cancer Research Institute in Slovakia where he worked as an investigator. He was recruited in 2006 as a Staff Scientist into Laboratory of Cellular Oncology. His current research interests focus on transcription factors regulation and tumor suppressors.

Research

Our research projects are focused on the development of model systems to study acute myeloid leukemia (AML) using knockout mice and retroviruses. In addition we also study regulation of activity of oncogenes and tumor suppressors involved in the development of AML.

The c-myb oncogene

The c-Myb transcription factor is essential for the development of hematopoietic cells and plays a role in proliferation, differentiation and apoptosis. We have discovered that c-myb can be activated to transform myeloid cells either by overexpression at the transcriptional level or by protein truncation that removes sequences critical for phosphorylation-induced degradation via the ubiquitin/26S-proteasome pathway. More recently we have identified conjugation of SUMO to the negative regulatory domain of c-Myb as an important posttranslational modification that regulates activity of this transcription factor. Currently we are investigating a possible physiological relationship between c-Myb and the Polycomb group (PcG) proteins.

p15INK4B tumor suppressor

The p15Ink4b protein is member of a family of cyclin-dependent kinase inhibitors (CDKIs) that control G1/S transition at the restriction point through inhibition of the Rb pathway. The expression of the ink4b gene is induced in response to cytokines that force cell differentiation and/or growth arrest. The tumor suppressor p15INK4B plays an important role in human hematopoietic neoplasia, since its inactivation by hypermethylation is detected in more than 80% of acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL). We have developed a murine model in which deletion of the p15Iin4b in myeloid compartment accelerates retrovirus-induced myeloid leukemia. Currently, using inverse PCR and ligation-mediated PCR techniques, we are identifying genes that cooperate with the loss of p15Ink4b in the induction of AML in our model systems.


This page was last updated on 2/21/2013.