Susanne Schlisio Group
Oxygen-sensing and Cancer
Our research concerns the mechanisms of how disruption of oxygen-sensing pathways can lead to cancer. Oxygen sensors enable the cell to adapt to low-oxygen environments and are critical for normal development and apoptosis. These events are often disrupted in the development of tumors. Oxygen sensing is mediated partly via prolyl hydroxylases that require molecular oxygen for enzymatic activity. Our work focuses on how prolyl hydroxylases execute apoptosis in neural precursors during development and how disruption of this process can lead to certain forms of nervous-system tumors.
The Susanne Schlisio group is currently recruiting Post Docs, please apply using the contact details below
PHD3 Regulates p53 Protein Stability by Hydroxylating Proline 359.
Cell Rep 2018 Jul;24(5):1316-1329
Combined epigenetic and differentiation-based treatment inhibits neuroblastoma tumor growth and links HIF2α to tumor suppression.
Proc. Natl. Acad. Sci. U.S.A. 2017 07;114(30):E6137-E6146
Neuroblast differentiation during development and in neuroblastoma requires KIF1Bβ-mediated transport of TRKA.
Genes Dev. 2017 05;31(10):1036-1053
The 1p36 Tumor Suppressor KIF 1Bβ Is Required for Calcineurin Activation, Controlling Mitochondrial Fission and Apoptosis.
Dev. Cell 2016 Jan;36(2):164-78
XAF1 promotes neuroblastoma tumor suppression and is required for KIF1Bβ-mediated apoptosis.
Oncotarget 2016 Jun;7(23):34229-39
RNA helicase A is a downstream mediator of KIF1Bβ tumor-suppressor function in neuroblastoma.
Cancer Discov 2014 Apr;4(4):434-51
Mutation analysis of HIF prolyl hydroxylases (PHD/EGLN) in individuals with features of phaeochromocytoma and renal cell carcinoma susceptibility.
Endocr. Relat. Cancer 2011 Feb;18(1):73-83
Neuronal apoptosis by prolyl hydroxylation: implication in nervous system tumours and the Warburg conundrum.
J. Cell. Mol. Med. 2009 Oct;13(10):4104-12
The kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor.
Genes Dev. 2008 Apr;22(7):884-93
VHL loss actuates a HIF-independent senescence programme mediated by Rb and p400.
Nat. Cell Biol. 2008 Mar;10(3):361-9
pVHL acts as an adaptor to promote the inhibitory phosphorylation of the NF-kappaB agonist Card9 by CK2.
Mol. Cell 2007 Oct;28(1):15-27
Neuronal apoptosis linked to EglN3 prolyl hydroxylase and familial pheochromocytoma genes: developmental culling and cancer.
Cancer Cell 2005 Aug;8(2):155-67
PhD, Associate Professor Susanne Schlisio
Susanne Schlisio is a cancer biologist with extensive experience in sympathoadrenal nervous system malignancies, neuronal development and cancer mouse models. She performed her PhD studies at Duke University Medical School in 2002 in cancer research. In 2008, she completed her postdoctoral research at the Dana Farber Cancer Institute at the Harvard Medical School. As a postdoctoral researcher in the laboratory of Dr. William G. Kaelin, Jr. she was part of the team discovering how cells adapt to changes in oxygen availability and how this process is directly linked to cancer-discoveries that now have been recognized with award of the Lasker Prize to Dr. Kaelin. In 2008, she was a recipient of an internationally competitive member position at the Ludwig Cancer Institute Stockholm to start her own research group. Since 2017, she is faculty at Department of Microbiology Tumor and Cell biology at Karolinska Institutet, Stockholm. Her current and future work includes the identification of novel oxygen-sensing pathways that are implicated in malignant transformation, with focus on cancer arising from the sympathoadrenal lineage, such as neuroblastoma and pheochromocytoma.
|Oscar Bedoya Reina||Postdoc|
|Wenyu Li||Graduate Student|
|Susanne Schlisio||Senior researcher|
Laboratory at Ludwig Cancer Research
- Swedish Research Council (VR)
- Swedish Childhood Cancer Foundation (BCF)
- Swedish Cancer Society (CF)
- Para Difference Foundation
- Gösta Fraenckels stiftelse för medicinsk forskning