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Susanne Schlisio Group

The research in our group concerns the mechanisms of how disruption of oxygen-sensing pathways can lead to cancer.

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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.

Publications

EglN3 hydroxylase stabilizes BIM-EL linking VHL type 2C mutations to pheochromocytoma pathogenesis and chemotherapy resistance.
Li S, Rodriguez J, Li W, Bullova P, Fell SM, Surova O, et al
Proc. Natl. Acad. Sci. U.S.A. 2019 Aug;116(34):16997-17006

PHD3 Regulates p53 Protein Stability by Hydroxylating Proline 359.
Rodriguez J, Herrero A, Li S, Rauch N, Quintanilla A, Wynne K, et al
Cell Rep 2018 07;24(5):1316-1329

Combined epigenetic and differentiation-based treatment inhibits neuroblastoma tumor growth and links HIF2α to tumor suppression.
Westerlund I, Shi Y, Toskas K, Fell SM, Li S, Surova O, et al
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.
Fell SM, Li S, Wallis K, Kock A, Surova O, Rraklli V, et al
Genes Dev. 2017 05;31(10):1036-1053

The 1p36 Tumor Suppressor KIF 1Bβ Is Required for Calcineurin Activation, Controlling Mitochondrial Fission and Apoptosis.
Li S, Fell SM, Surova O, Smedler E, Wallis K, Chen ZX, et al
Dev. Cell 2016 Jan;36(2):164-78

The 2-oxoglutarate analog 3-oxoglutarate decreases normoxic hypoxia-inducible factor-1α in cancer cells, induces cell death, and reduces tumor xenograft growth.
Koivunen P, Fell SM, Lu W, Rabinowitz JD, Kung AL, Schlisio S
Hypoxia (Auckl) ;4():15-27

XAF1 promotes neuroblastoma tumor suppression and is required for KIF1Bβ-mediated apoptosis.
Choo Z, Koh RY, Wallis K, Koh TJ, Kuick CH, Sobrado V, et al
Oncotarget 2016 Jun;7(23):34229-39

RNA helicase A is a downstream mediator of KIF1Bβ tumor-suppressor function in neuroblastoma.
Chen ZX, Wallis K, Fell SM, Sobrado VR, Hemmer MC, Ramsköld D, et al
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.
Astuti D, Ricketts CJ, Chowdhury R, McDonough MA, Gentle D, Kirby G, et al
Endocr. Relat. Cancer 2011 Feb;18(1):73-83

Neuronal apoptosis by prolyl hydroxylation: implication in nervous system tumours and the Warburg conundrum.
Schlisio S
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.
Schlisio S, Kenchappa RS, Vredeveld LC, George RE, Stewart R, Greulich H, et al
Genes Dev. 2008 Apr;22(7):884-93

VHL loss actuates a HIF-independent senescence programme mediated by Rb and p400.
Young AP, Schlisio S, Minamishima YA, Zhang Q, Li L, Grisanzio C, et al
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.
Yang H, Minamishima YA, Yan Q, Schlisio S, Ebert BL, Zhang X, et al
Mol. Cell 2007 Oct;28(1):15-27

Neuronal apoptosis linked to EglN3 prolyl hydroxylase and familial pheochromocytoma genes: developmental culling and cancer.
Lee S, Nakamura E, Yang H, Wei W, Linggi MS, Sajan MP, et al
Cancer Cell 2005 Aug;8(2):155-67

Group members

Research group leader

Susanne Schlisio

PhD, Associate Professor

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 Nobel 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.

All group members

Laboratory at Ludwig Cancer Research

Susanne Schlisio laboratory at Ludwig Cancer Research

Funding

  • H2020 European Research Commission ERC-2019-SyG
  • Knut och Alice Wallenbergs Stiftelse
  • Swedish Research Council (VR)
  • Swedish Childhood Cancer Foundation (BCF)
  • Swedish Cancer Society (CF)
  • Para Difference Foundation
  • Gösta Fraenckels stiftelse för medicinsk forskning

Contact

Susanne Schlisio

PhD, Associate Professor
C1 Department of Microbiology, Tumor and Cell Biology

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