Yizhou Hu

• Principal Researcher, Department of Laboratory Medicine, Karolinska Institutet, Sweden
• Docent in Systems Biology (approved by the docentship committee, 2025/01/28), Faculty of Medicine, University of Helsinki 
• University Researcher, Faculty of Medicine at University of Helsinki & Wihuri Institute,   Finland
• Postdoctoral researcher from 2017, SSMF fellowship (2020-2022),   Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Sweden
• Ph.D. in Pathology (Oncology and Molecular Cell Biology), 2017, , Research Programs Unit, Faculty of Medicine, University of Helsinki, Finland
• M.Sc. in Genetics (Human Genetics and Bioinformatics),  2011,   Faculty of Biological and Environmental Sciences, University of Helsinki, Finland

1.    Developmental Plasticity in Nervous System Cancers: Insights from Glioblastoma and Neuroblastoma
Developmental plasticity plays a key role in cancer progression. Glioblastoma and high-risk neuroblastoma remain major clinical challenges. However, we still do not fully understand how neural crest-derived mesenchymal trajectories influence tumor development in these cancers. Recent studies show that reactivating developmental programs increases tumor heterogeneity and aggressiveness. Our research aims to uncover the cellular and molecular mechanisms driving these processes.
We focus on identifying the specific developmental states that drive high-risk neuroblastoma and glioblastoma. In neuroblastoma, we have identified distinct states characterized by extensive epigenetic priming and dynamic interactions with the tumor microenvironment. In glioblastoma, our work shows that a subset of tumors mirrors a neural crest–brain-perivascular lineage. To investigate these processes, we use a range of cutting-edge techniques, including single-cell MultiOmics, spatial MultiOmics, our own built deep-learning analytics (scCAMEL), and genetically modified animal models. Our overarching goal is to understand how developmental trajectories contribute to cellular heterogeneity and malignancy in nervous system cancers. By doing so, we aim to advance the development of targeted therapies that disrupt these pathways and improve patient outcomes.

2.    Immune priming of non-immune cells in psoriatic skin
Psoriasis is a chronic inflammatory skin disease. Our research shows that non-immune cells—such as neural crest–derived Schwann cells, dermal papilla cells, and various keratinocyte types—can become immune-primed. We built an integrated single-cell transcriptomics atlas of human psoriatic skin. This atlas revealed unique, tissue-based regulatory mechanisms that drive immune activation in these cells. Our findings have significantly advanced the understanding of immune pathways in psoriatic skin and have been widely cited. Our goal is to identify key gene regulatory drivers that could lead to the development of targeted therapies.

*Software:*
scCAMEL, Deep learning-based single-cell analysis toolkits,
website: https://sccamel.readthedocs.io/ 

*Dataset visualization:*

1. "Single cell transcriptional zonation of human psoriasis skin identifies an alternative immunoregulatory axis", <Cell Death Dis.>, 2021 May 6;12(5):450.

Gene Expression Omnibus: GSE162183

Shinyapps website: https://yz-studio.shinyapps.io/shinyapph5ad/

2. "Integrative single-cell transcriptomic investigation unveils long non-coding RNAs associated with localized cellular inflammation in psoriasis" <Front Immunol>2023 Sep 26:14:1265517.
Integrated dataset: 106, 675 cells from 11 healthy human skin and 79, 887 cells from 9 psoriatic human skin

Shinyapps website:  https://yz-studio.shinyapps.io/psoriaticskincellatlas2/