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About me

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.



2002: PhD, Duke University Medical School, Durham, N.C., USA, 2002

1999: MSc, Humboldt University, Berlin, Germany

Research description

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.


PHD3 Regulates p53 Protein Stability by Hydroxylating Proline 359
Rodriguez J, Herrero A, Li S, Rauch N, Quintanilla A, Wynne K, et al
Cell reports 2018;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
Proceedings of the National Academy of Sciences of the United States of America 2017;114(30):E6137-E6146

High levels of EPAS1 are closely associated with key features of low-risk neuroblastoma
Westerlund I, Shi Y, Toskas K, Fell Sm, Li Sj, Sodersten E, et al

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 & development 2017;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
Developmental cell 2016;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 (Auckland, N.Z.) 2016;4():15-27

XAF1 promotes neuroblastoma tumor suppression and is required for KIF1B beta-mediated apoptosis
Choo Z, Koh Ryl, Wallis K, Koh Tjw, Kuick Ch, Sobrado V, et al
ONCOTARGET 2016;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 discovery 2014;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

Neuronal apoptosis by prolyl hydroxylation: implication in nervous system tumours and the Warburg conundrum
Schlisio S
Journal of cellular and molecular medicine 2009;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 & development 2008;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
Nature cell biology 2008;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
Molecular cell 2007;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;8(2):155-67

The v-Jun point mutation allows c-Jun to escape GSK3-dependent recognition and destruction by the Fbw7 ubiquitin ligase
Wei W, Jin J, Schlisio S, Harper Jw, Kaelin Wg
Cancer cell 2005;8(1):25-33

A role for E2F6 in distinguishing G1/S- and G2/M-specific transcription
Giangrande Ph, Zhu W, Schlisio S, Sun X, Mori S, Gaubatz S, et al
Genes & development 2004;18(23):2941-51

Interaction of YY1 with E2Fs, mediated by RYBP, provides a mechanism for specificity of E2F function
Schlisio S, Halperin T, Vidal M, Nevins Jr
The EMBO journal 2002;21(21):5775-86

The Bacillus subtilis regulator protein SpoIIE shares functional and structural similarities with eukaryotic protein phosphatases 2C
Schroeter R, Schlisio S, Lucet I, Yudkin M, Borriss R
FEMS microbiology letters 1999;174(1):117-23

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