Understanding and precision targeting of malfunctioning gene regulatory elements in human cancer and other enhanceropathies.
Understanding and precision targeting of malfunctioning gene regulatory elements in human cancer and other enhanceropathies.
The Precision Cancer Epigenomics laboratory at NCMBM (Nordic-EMBL Partnership Institute) at the University of Oslo, Norway started in September 2022.
The Enhancer Biology lab started in June 2019 in the Applied Tumor Genomics research program of the Faculty of Medicine at the University of Helsinki, Finland.
We have a total of 16 group members in both our Oslo and Helsinki groups, lead by Dr Biswajyoti Sahu, and we are looking forward to grow in the coming days!
Our goal is to understand the molecular mechanisms of chromatin reprogramming by transcription factors in cell fate control and in cancer operating through the non-coding regulatory genome.
We use state-of-the-art functional genomics methods both bulk and single-cell for transcription factor binding, enhancer activity by massively parallel reporter assays, chromatin accessibility and genome editing by CRISPR-Cas9 tools.
We employ computational tools and machine learning methods to integrate genome wide datasets from several multiomics assays utilising next-generation sequencing.
We use novel cell fate conversion methods to study the early regulatory events in pancreatic cancer – one of the most lethal cancer types currently lacking clear diagnostic markers and effective treatment options.
Here our goal is to find key transcription factors, their gene regulatory networks and the downstream signaling pathways that are important in metastasis and treatment response in pancreatic and ovarian cancers.
Our goal is to understand the human gene regulatory elements such as promoters and enhancers in defining the regulatory logic of human DNA sequence. We use a plethora of functional genomics methods and computational analysis to decipher this logic.
Here our aim is to understand how transcription factors decode and specify the regulatory grammar and also utilize the transposable elements as oncogenic enhancers in cancer.
To understand the cellular states and transcriptional adaptation in cancer mediated by epigenome reprogramming, we are using hospital biobank samples for pancreatic and ovarian cancers from primary and distal metastatic sites.
We perform deep molecular profiling using bulk/single-cell multiomics and spatial methods together with functional validation using cellular models including cell lines and organoid co-cultures and xenografts.
To achieve our research objectives, we utilize various cutting-edge genome-wide techniques based on next generation sequencing and their computational analysis from bulk samples to single cell and single molecule resolution.
I lead the Precision Cancer Epigenomics laboratory in Oslo and the Enhancer Biology laboratory in Helsinki. I am genomics scientist by training and the primary goal of my research is to understand the role of transcription factors and the non-coding regulatory genome in human enhanceropathies such as cancer.
I am a Group Leader in Precision Medicine at the Centre for Molecular Biosciences and Medicine (NCMBM, a Nordic-EMBL Partnership Institute) at the University of Oslo, Norway. I also hold an Adjunct Researcher position at the Oslo University Hospital in the Department of Cancer Genetics at the Institute of Cancer Research in Norway.
I am also a Principal Investigator at the Applied Tumor Genomics program of the Research Programs Unit at the Faculty of Medicine, University of Helsinki, Finland. I also hold the title of Docent (Adjunct Professor) in Molecular Genetics from the Faculty of Medicine at the University of Helsinki, Finland.
Here we show that classical enhancers, embedded within multipartite super-enhancer structures, act as determinant regulatory elements that initiate the gene regulatory cascade by linking DNA sequence recognition to 3D chromatin architecture.
In this study, we developed a novel statistical toolkit, IonStats, to profile DNA adducts in nanopore sequencing data.
Here, we identify that KSHV hijacks the pioneering function of the endothelial-specific transcription factor SOX18 to facilitate persistence of viral episomes.
If you’d like to get in touch, please use the contact form, call us by phone or visit our lab in Oslo or Helsinki.
Feel free to contact us about possible collaboration opportunities! We are always looking for motivated researchers!!
Master’s thesis students who are interested in bioinformatics and computational analysis of NGS and single-cell omics datasets can always contact us about available thesis projects and positions.
