Nijman
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[[Image:Cancer vs crab.jpg|200px|right]] In the post-genomic era, a major challenge is to understand the molecular networks that allow the cell perform it's physiological function. Within the Nijman lab the aim is to contribute to the understanding of the cellular circuitry in health and disease with a particular focus on cancer. In addition, we try to find new angles for cancer therapy. In order to achieve these goals, the lab employs state-of-the-art technology, [[genomics]] and bioinformatics. | [[Image:Cancer vs crab.jpg|200px|right]] In the post-genomic era, a major challenge is to understand the molecular networks that allow the cell perform it's physiological function. Within the Nijman lab the aim is to contribute to the understanding of the cellular circuitry in health and disease with a particular focus on cancer. In addition, we try to find new angles for cancer therapy. In order to achieve these goals, the lab employs state-of-the-art technology, [[genomics]] and bioinformatics. | ||
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''Figure (right). Breast cancer in a mastectomy specimen (top). The cancerous tumour (pale yellow) resembles the figure of a crab, giving the disease its name. | ''Figure (right). Breast cancer in a mastectomy specimen (top). The cancerous tumour (pale yellow) resembles the figure of a crab, giving the disease its name. | ||
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==Projects== | ==Projects== | ||
Revision as of 09:26, 21 September 2010
Contents |
About
The Nijman lab is at the Center for Molecular Medicine (CeMM, pronounce \sam\) in Vienna, Austria . We have recently moved into our new research building right next to Vienna General Hospital, one of the largest academic hospitals in Europe. CeMM is an international, independent and interdisciplinary research of the Austrian Academy of Sciences dedicated to research with a human focus.
“From the clinic to the clinic”
CeMM’s mission is to combine insight obtained from basic and clinical research and use it to implement the development of innovative therapeutic and diagnostic strategies – from the clinic to the clinic.
In the Nijman lab we are particularly interested in cancer and try to understand the cellular circuitry that is misregulated in this disease. In addition, we wish to identify new angles for patient stratified cancer therapy using genomics strategies, such as genetic and compound screens.
Research scope
Figure (right). Breast cancer in a mastectomy specimen (top). The cancerous tumour (pale yellow) resembles the figure of a crab, giving the disease its name.
Projects
Synthetic lethal interactions in mammalian cells
During the last 5 years, in vitro human cell genetics has become within reach for many laboratories around the world. One of the challenges for the coming years is to use the available tools in new and creative ways to fully exploit the power of experimental genetics. In this context, a major focus of the lab is the high-throughput assessment of synthetic lethal/sick (SSL) interactions using chemical compounds and RNAi. In particular we are trying to identify genotype-specific cancer vulnerabilites or "Achilles' heels". However, the identification of SSL interactions can be useful for the study of any cell biological process and is thus not limited to the study of cell growth.
Cell circuits and cancer
Ubiquitin dynamics
Other projects in the lab are generally focussed on cancer-relevant pathways and signaling dynamics, such as ubiquitination/deubiquitination. To identify deubiquitinating enzymes (DUBs) in pathways or processes of interest we employ RNAi libraries directed against all DUBs in the human genome. Using this approach we have previously identifid DUBs in NF-kappaB signaling, DNA repair and hypoxia signaling.
Figure (right). Ribbon representation of ubiquitin protein, highlighting the secondary structure. α-helices are coloured in blue and the β-sheet in green. The typical attachment point for a further ubiquitin molecule in polyubiquitin chain formation, lysine 48, is shown in pink.
Genetic screens
The lab also employs genome wide gain-of-function and loss-of-function screens using cDNA and shRNA libraries.
Figure (left). Colony formation assay showing that overexpression of TFE3 can by-pass the temperature sensitive growth arrest induced by pRB. Figure taken from Nijman et. al. JBC (2006) Free access.
For instance, we identified the transcription factor TFE3 as a regulator of cell-cycle arrest induced by the Retinoblastoma tumor suppressor gene (pRB).
Collaborations
Collaborations are crucial for modern day science!
Listed here are some (science) friends and collaborators:
Tony Huang (NYU)
Thijn Brummelkamp (MIT, Whitehead Institute)
Rene Bernards (Netherlands Cancer Institute)
Todd Golub (Broad Institute, MIT/Harvard)
Dave Root (Broad Institute, MIT/Harvard)
In the news
Sebastian Nijman wins "Future of Vienna award" (Wiener Zukunftspreis) See also CeMM News
