Bo Stenerlöw – Radiation biology and DNA repair
Our research focuses on cellular and molecular effects of ionizing radiation. We study cells’ defence signalling and DNA repair mechanisms, with the goal that our research should lead to more efficient tumour therapy and fewer adverse effects.
Ionizing radiation is used in diagnostics and tumour therapy, and is an important tool in modern health care. During tumour therapy the cancer cells are killed mainly because the radiation results in acute damage on the DNA.
The most serious DNA damage is double-strand breaks (DBS), where both DNA strands have been cut, which can prevent cell division. However, the cells, including cancer cells, have well developed defence systems that can repair most DNA damages.
Our research aims to understand how the cells’ defence signalling functions and how different repair systems can be affected or turned off.

Schematic image of how DNA strands can be repaired.
Factors that affect DNA repair
The repair of DNA damage is fundamental for the survival of a cell and an increased knowledge about DNA repair mechanisms might have future clinical implications. The complex network of repair and regulatory proteins represent a rich set of potential targets to exploit in the development of more effective chemo- and radiotherapeutic strategies in cancer therapy.
In our research projects we study how the cell handles DNA damage in the form of double-strand breaks. We examine how different types of drugs affect the repair and we try to understand how different repair systems collaborate or compete. We also develop new techniques to study these.
In one of our projects we study drugs and inhibitors that make tumour cells more sensitive to radiation. The rationale is that if it’s possible to specifically make tumour cells more radiation sensitive it could result in an increased therapeutic effect, with fewer adverse effects and less damage to normal tissues.

Mikroscope image of a cell nucleus (blue) that has be radiated with gamma radiation, showing double strand breaks as red dots.
Effects on the developing brain
Brain tumors are the most frequent solid tumors in children and the most common radiotherapy indications in pediatrics, with frequent late effects, including cognitive impairment. By using animal models designed to determine effects arising during critical phases in early brain development, we study effects of radiation- and drug-exposure on the developing brain. A better understanding of the effects and mechanism could form the basis for new clinical recommendations when pharmaceutical agents are used during radiation-exposure of the pediatric brain.
Group members
Publications
Part of Reports of Practical Oncology and Radiotherapy, p. 478-487, 2024
Impact of Proton Irradiation Depending on Breast Cancer Subtype in Patient-Derived Cell Lines
Part of International Journal of Molecular Sciences, 2024
- DOI for Impact of Proton Irradiation Depending on Breast Cancer Subtype in Patient-Derived Cell Lines
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Part of Nucleic Acids Research, 2024
- DOI for Visualizing DNA single- and double-strand breaks in the Flash comet assay by DNA polymerase-assisted end-labelling
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Part of Cell Death Discovery, 2022
- DOI for Caspase-2 is a mediator of apoptotic signaling in response to gemtuzumab ozogamicin in acute myeloid leukemia
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Ra-223 induces clustered DNA damage and inhibits cell survival in several prostate cancer cell lines
Part of Translational Oncology, 2022
- DOI for Ra-223 induces clustered DNA damage and inhibits cell survival in several prostate cancer cell lines
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Mapping the Future of Particle Radiobiology in Europe: The INSPIRE Project
Part of Frontiers in Physics, 2020
- DOI for Mapping the Future of Particle Radiobiology in Europe: The INSPIRE Project
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Part of Scientific Reports, 2020
- DOI for The HSP90 inhibitor Onalespib exerts synergistic anti-cancer effects when combined with radiotherapy: an in vitro and in vivo approach
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Part of International Journal of Molecular Sciences, 2019
- DOI for Combined Treatment with Low-Dose Ionizing Radiation and Ketamine Induces Adverse Changes in CA1 Neuronal Structure in Male Murine Hippocampi
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Part of Journal of Applied Toxicology, p. 582-589, 2019
The HSP90 inhibitor onalespib potentiates Lu-177-DOTATATE therapy in neuroendocrine tumor cells
Part of International Journal of Oncology, p. 1287-1295, 2019
- DOI for The HSP90 inhibitor onalespib potentiates Lu-177-DOTATATE therapy in neuroendocrine tumor cells
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Part of British Journal of Anaesthesia, p. 546-554, 2018
Potentiating Lu-177-DOTATATE Therapy By HSP90 Inhibition - First In Vivo Study
Part of European Journal of Nuclear Medicine and Molecular Imaging, 2018
Part of European Journal of Nuclear Medicine and Molecular Imaging, 2018
Removal of heat-sensitive clustered damaged DNA sites is independent of double-strand break repair
Part of PLOS ONE, 2018
- DOI for Removal of heat-sensitive clustered damaged DNA sites is independent of double-strand break repair
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Part of International Journal of Oncology, p. 5-14, 2017
- DOI for Different functions of AKT1 and AKT2 in molecular pathways, cell migration and metabolism in colon cancer cells
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Part of European Journal of Nuclear Medicine and Molecular Imaging, 2017
Part of Radiation Research, p. 597-604, 2017
The HSP90-inhibitor Onalespib Potentiates Lu-177-Dotatate Treatment of Neuroendocrine Tumors
Part of European Journal of Nuclear Medicine and Molecular Imaging, 2017
Part of International Journal of Radiation Biology, p. 371-379, 2016
Part of Anesthesiology, 2016
Part of European Journal of Nuclear Medicine and Molecular Imaging, p. 974-982, 2016
- DOI for Molecular imaging of EGFR and CD44v6 for prediction and response monitoring of HSP90 inhibition in an in vivo squamous cell carcinoma model.
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Part of Behavioural Brain Research, p. 11-19, 2016
Formation and repair of clustered damaged DNA sites in high LET irradiated cells
Part of International Journal of Radiation Biology, p. 820-826, 2015
Part of European Journal of Nuclear Medicine and Molecular Imaging, 2015
Part of Oncotarget, p. 35652-35666, 2015
- DOI for The novel HSP90 inhibitor AT13387 potentiates radiation effects in squamous cell carcinoma and adenocarcinoma cells
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Part of European Journal of Nuclear Medicine and Molecular Imaging, 2014
Part of PLOS ONE, 2014
- DOI for Evaluation of cancer stem cell markers CD133, CD44, CD24: association with AKT isoforms and radiation resistance in colon cancer cells.
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Part of PLOS ONE, 2014
- DOI for Ionising Radiation Immediately Impairs Synaptic Plasticity-Associated Cytoskeletal Signalling Pathways in HT22 Cells and in Mouse Brain: An In Vitro/In Vivo Comparison Study
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Part of Neurotoxicology, p. 48-55, 2014
Part of Mutation research, p. 1-10, 2014
- DOI for Suppression of DNA-dependent protein kinase sensitize cells to radiation without affecting DSB repair
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Part of Molecular Neurodegeneration, p. 57, 2014
- DOI for The cognitive defects of neonatally irradiated miceare accompanied by changed synaptic plasticity,adult neurogenesis and neuroinflammation
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The influence of AKT isoforms on radiation sensitivity and DNA repair in colon cancer cell lines
Part of Tumor Biology, p. 3525-3534, 2014
- DOI for The influence of AKT isoforms on radiation sensitivity and DNA repair in colon cancer cell lines
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Part of Cellular Microbiology, p. 98-113, 2013
Radiation response in colorectal cancer cells
Part of International Journal of Molecular Medicine, 2012
Part of International Journal of Oncology, p. 176-184, 2012
- DOI for The effect of a dimeric Affibody molecule (ZEGFR:1907)2 targeting EGFR in combination with radiation in colon cancer cell lines
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(125)I-Labeled Quercetin as a Novel DNA-Targeted Radiotracer
Part of Cancer Biotherapy and Radiopharmaceuticals, p. 469-475, 2011
Part of Neurotoxicology, p. 223-229, 2010
Myc is required for activation of the ATM-dependent checkpoints in response to DNA damage
Part of PLoS ONE, 2010
Radical formation in lithium formate EPR dosimeters after irradiation with protons and nitrogen ions
Part of Radiation Research, p. 251-257, 2010
Part of Molecular & Cellular Proteomics, p. 1117-1129, 2009
Differences in radiosensitivity between three HER2 overexpressing cell lines
Part of European Journal of Nuclear Medicine and Molecular Imaging, p. 1179-1191, 2008
Repair of Radiation-Induced Heat-Labile Sites is Independent of DNA-PKcs, XRCC1 and PARP-1
Part of Radiation Research, p. 506-512, 2008
Part of Current radiopharmaceuticals, p. 225-233, 2008
Part of BMC Molecular Biology, p. 97, 2007
Part of Radiation Research, p. 175-182, 2007
Progress in Dosimetry of Neutrons and Light Nuclei
Part of Radiation Protection Dosimetry, p. 1-2, 2007
Part of Radiation Research, p. 312-318, 2007
Part of Molecular Cancer Therapeutics, p. 2303-2309, 2007
Part of Radiation Research, p. 917-927, 2006
Part of Biochemical and Biophysical Research Communications - BBRC, p. 1211-7, 2006
Radiation-induced bystander effects
Part of Acta Oncologica, p. 373-4, 2006
Part of Letters in Drug Design & Discovery, p. 357-368, 2006
Cellular internalization of cytolethal distending toxin: a new end to a known pathway
Part of Cellular Microbiology, p. 921-34, 2005
Part of International Journal of Radiation Biology, p. 261-72, 2005
Part of Radiat Res, p. 1, 2004
Part of Radiat Res, p. 517-27, 2004