Danish Cancer Institute

Danish Cancer Institute

Forskning

Driving Breakthroughs in Cancer Research

Om os

We are dedicated to pioneering cancer breakthroughs by innovative research of the highest excellence. We aim to integrate knowledge from basic, epidemiological, translational and clinical research, generating impactful insights to reach our goals of understanding, preventing and treating cancer. We attract top scientific talent from around the world, fostering a collaborative, inclusive environment that fuels creativity. With a team of over 250 researchers representing more than 25 nationalities, we celebrate varied perspectives as a catalyst for innovation. The Danish Cancer Institute is part of the Danish Cancer Society.

Websted
https://www.cancer.dk/danish-cancer-institute/
Branche
Forskning
Virksomhedsstørrelse
201-500 medarbejdere
Hovedkvarter
Copenhagen
Type
Nonprofit

Beliggenheder

  • Primær

    Strandboulevarden 49

    Copenhagen, 2100, DK

    Se ruten

Medarbejdere hos Danish Cancer Institute

Opdateringer

  • 📢 Researchers from the 𝗥𝗲𝗱𝗼𝘅 𝗕𝗶𝗼𝗹𝗼𝗴𝘆 𝗚𝗿𝗼𝘂𝗽 𝗮𝘁 𝘁𝗵𝗲 Danish Cancer Institute have published a comprehensive review in Redox Biology, exploring the 𝗿𝗼𝗹𝗲 𝗼𝗳 𝗿𝗲𝗱𝗼𝘅 𝘀𝗶𝗴𝗻𝗮𝗹𝗶𝗻𝗴 𝗶𝗻 𝗳𝗼𝗰𝗮𝗹 𝗮𝗱𝗵𝗲𝘀𝗶𝗼𝗻 𝗱𝘆𝗻𝗮𝗺𝗶𝗰𝘀. Senior scientist and co-author of the review, Salvatore Rizza, explains: "𝘛𝘩𝘪𝘴 𝘸𝘰𝘳𝘬 𝘰𝘯 𝘳𝘦𝘥𝘰𝘹 𝘳𝘦𝘨𝘶𝘭𝘢𝘵𝘪𝘰𝘯 𝘰𝘧 𝘧𝘰𝘤𝘢𝘭 𝘢𝘥𝘩𝘦𝘴𝘪𝘰𝘯𝘴 𝘴𝘦𝘳𝘷𝘦𝘴 𝘢𝘴 𝘢𝘯 𝘪𝘮𝘱𝘰𝘳𝘵𝘢𝘯𝘵 𝘳𝘦𝘧𝘦𝘳𝘦𝘯𝘤𝘦 𝘧𝘰𝘳 𝘤𝘢𝘯𝘤𝘦𝘳 𝘳𝘦𝘴𝘦𝘢𝘳𝘤𝘩𝘦𝘳𝘴, 𝘢𝘴 𝘪𝘵 𝘶𝘯𝘳𝘢𝘷𝘦𝘭𝘴 𝘩𝘰𝘸 𝘳𝘦𝘥𝘰𝘹 𝘴𝘪𝘨𝘯𝘢𝘭𝘪𝘯𝘨 𝘪𝘯𝘵𝘳𝘪𝘤𝘢𝘵𝘦𝘭𝘺 𝘤𝘰𝘯𝘵𝘳𝘰𝘭𝘴 𝘤𝘦𝘭𝘭 𝘢𝘥𝘩𝘦𝘴𝘪𝘰𝘯 𝘢𝘯𝘥 𝘮𝘪𝘨𝘳𝘢𝘵𝘪𝘰𝘯—𝘱𝘳𝘰𝘤𝘦𝘴𝘴𝘦𝘴 𝘧𝘶𝘯𝘥𝘢𝘮𝘦𝘯𝘵𝘢𝘭 𝘵𝘰 𝘵𝘶𝘮𝘰𝘳 𝘱𝘳𝘰𝘨𝘳𝘦𝘴𝘴𝘪𝘰𝘯 𝘢𝘯𝘥 𝘮𝘦𝘵𝘢𝘴𝘵𝘢𝘴𝘪𝘴. 𝘉𝘺 𝘱𝘳𝘰𝘷𝘪𝘥𝘪𝘯𝘨 𝘯𝘦𝘸 𝘪𝘯𝘴𝘪𝘨𝘩𝘵𝘴 𝘪𝘯𝘵𝘰 𝘩𝘰𝘸 𝘰𝘹𝘪𝘥𝘢𝘵𝘪𝘷𝘦 𝘮𝘰𝘥𝘪𝘧𝘪𝘤𝘢𝘵𝘪𝘰𝘯𝘴 𝘪𝘯𝘧𝘭𝘶𝘦𝘯𝘤𝘦 𝘧𝘰𝘤𝘢𝘭 𝘢𝘥𝘩𝘦𝘴𝘪𝘰𝘯 𝘥𝘺𝘯𝘢𝘮𝘪𝘤𝘴, 𝘪𝘵 𝘰𝘱𝘦𝘯𝘴 𝘶𝘱 𝘱𝘰𝘵𝘦𝘯𝘵𝘪𝘢𝘭 𝘢𝘷𝘦𝘯𝘶𝘦𝘴 𝘧𝘰𝘳 𝘵𝘢𝘳𝘨𝘦𝘵𝘪𝘯𝘨 𝘳𝘦𝘥𝘰𝘹 𝘱𝘢𝘵𝘩𝘸𝘢𝘺𝘴 𝘪𝘯 𝘤𝘢𝘯𝘤𝘦𝘳 𝘵𝘩𝘦𝘳𝘢𝘱𝘺, 𝘰𝘧𝘧𝘦𝘳𝘪𝘯𝘨 𝘢 𝘥𝘦𝘦𝘱𝘦𝘳 𝘶𝘯𝘥𝘦𝘳𝘴𝘵𝘢𝘯𝘥𝘪𝘯𝘨 𝘰𝘧 𝘵𝘩𝘦 𝘮𝘦𝘤𝘩𝘢𝘯𝘪𝘴𝘮𝘴 𝘥𝘳𝘪𝘷𝘪𝘯𝘨 𝘤𝘢𝘯𝘤𝘦𝘳 𝘤𝘦𝘭𝘭 𝘪𝘯𝘷𝘢𝘴𝘪𝘷𝘦𝘯𝘦𝘴𝘴." The paper is 𝗼𝗽𝗲𝗻 𝗮𝗰𝗰𝗲𝘀𝘀 and can be found here: https://lnkd.in/dHHuMtvD

    • Photo
Left: Giuseppe Filomeni, Group leader, Redox Biology Group, DCI
Right: Salvatore Rizza, Senior scientist, Redox Biology Group, DCI
  • Scientists from the Danish Cancer Institute, in collaboration with Dr. Shyam Sharan Deputy director of the Mouse Cancer Genetics Program at the National Cancer Institute (NCI), have taken a significant step forward in understanding which mutations in BRCA2 significantly increase the risk of breast cancer. Around 45% of women who inherit a harmful BRCA2 mutation will develop breast cancer by the age of 70. However, not all mutations are harmful. DNA testing can identify these mutations, but in many cases, results fall into a grey area labelled “variants of uncertain significance.” This leaves both patients and doctors uncertain about whether a mutation is dangerous. Now, researchers from the Danish Cancer Institute, in collaboration with international colleagues, have made a breakthrough in determining which BRCA2 mutations increase cancer risk. Using advanced CRISPR technology, a humanised mouse embryonic stem cell model and high-throughput computational mutational scans, the team analysed more than 6,500 potential mutations, creating a detailed “mutation map” that distinguishes between harmful and harmless genetic changes. Group leader Elena Papaleo at the Danish Cancer Institute explains: 💬 "We hope these findings transform uncertainty into actionable information for patients with BRCA2 variants. Many genetic tests reveal ‘variants of uncertain significance,’ leaving patients without clear guidance. Our study provides functional data to classify thousands of these variants as benign or harmful, helping clinicians interpret test results. For those with harmful variants, this could mean earlier interventions or personalised treatments, such as cisplatin or PARP inhibitors." The study, published in Nature, demonstrates the power of innovation and international collaboration in cancer research. It is exciting to see how bioinformatics, cellular biology, and clinical research are united to better understand BRCA2 and its variants, Elena Papaleo added. 💬 "The multidisciplinary nature of this project allowed us to approach the problem from multiple angles and consider real-world implications. This synergy not only made the work deeply rewarding but also highlights how science thrives when people with different expertise come together to tackle complex and meaningful questions." Sahu, S., Galloux, M., Southon, E. et al. Saturation genome editing-based clinical classification of BRCA2 variants. Nature (2025) https://lnkd.in/dh6RY9cE

    • Scientists from the Danish Cancer Institute, in collaboration with Dr. Shyam Sharan from our Mouse Cancer Genetics Program at National Cancer Institute (USA), have taken a significant step forward in understanding which mutations in BRCA2 significantly increase the risk of breast cancer.

Around 45% of women who inherit a harmful BRCA2 mutation will develop breast cancer by the age of 70. However, not all mutations are harmful. DNA testing can identify these mutations, but in many cases, results fall into a grey area labelled “variants of uncertain significance.” This leaves both patients and doctors uncertain about whether a mutation is dangerous.

Now, researchers from the Danish Cancer Institute, in collaboration with international colleagues, have made a breakthrough in determining which BRCA2 mutations increase cancer risk.

Using advanced CRISPR technology, a humanised mouse embryonic stem cell model and high-throughput computational mutational scans, the team analysed more than
  • 🌟 Earlier this week, everyone at the Danish Cancer Institute gathered for the DCI Annual Retreat. This year was special as we were joined by 55 new colleagues, four new research groups, who will be joining us here at the DCI next month 🌟 The annual retreat is a great way to strengthen our collaboration and team spirit. A big shoutout to all colleagues for contributing such great science, lively discussions, great posters, intense networking, and a wonderful time together. Also a big thank you to guest speaker Professor Jens Juul Holst for a fascinating lecture on the study of GLP-1. We are thrilled to welcome our new colleagues and groups to the team 🤩 Thank you to everyone who made this year's DCI Annual Retreat a memorable event 🙏 The energy and insights from the retreat have left us all inspired and ready for the challenges ahead 🚀

  • 📰 NEWS: Research from the Danish Cancer Institute has revealed a vital role for the E3 ligase Pellino 3 (PELI3) in regulating autophagy, a process by which cells recycle nutrients during periods of stress.   This study highlights how PELI3 supports liver health by maintaining lipid balance and preventing harmful fat accumulation, particularly during nutrient deprivation.   This new insight into the mechanisms of autophagy also provides important information for diseases such as cancer, where cellular stress responses play a critical role.   Group leader Lisa Frankel and her team are continuing their research into PELI3, investigating a critical role for this protein and its influence on cancer progression in the near future. In this video Lisa Frankel explains more 👇 Read the findings in full here: https://lnkd.in/dgUcJvMw

  • What a brilliant way to start 2025! 🌟 🚀   We’re delighted to share that a groundbreaking research initiative led by the Danish Cancer Institute's Professor Jiri Bartek has been awarded an impressive 30 million kr. grant from the Lundbeckfonden / Lundbeck Foundation's Collaborative Projects programme. This funding will drive vital research into the role of Human Cytomegalovirus (HCMV) in brain cancer, with a particular focus on glioblastoma.   Glioblastoma, the most common and aggressive form of brain cancer, remains a challenge in oncology due to the lack of effective treatments. The research team aims to uncover how HCMV— a DNA virus that latently infects most of the global population and is frequently detected in brain tumours — might contribute to the onset and progression of this devastating disease.   The project will explore how HCMV variant viruses disrupt brain cell metabolism, cause genetic instability, and promote tumour growth. The goal is to uncover vulnerabilities in glioblastoma cells.   Professor Bartek explains:    💬 “We are thrilled and deeply grateful for this opportunity to explore HCMV’s role in glioblastoma pathogenesis. By understanding these mechanisms, we hope to uncover new therapeutic avenues to combat this malignant disease.”   This ambitious project is a collaboration between leading scientists from the DCI, the Karolinska Institutet in Stockholm and the University of Turku in Finland, led by Professor Cecilia Soderberg-Naucler.

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  • Drug resistance is one of the biggest challenges in treating melanoma, leaving many patients without effective solutions. Researchers at the Danish Cancer Institute are at the forefront of research that has the potential to transform melanoma treatment. A new project will focus on understanding how the activation of the protein FAK1 contributes to drug resistance in melanoma. Team leader of the Melanoma Research Team at the DCI, Daniela De Zio, explains why this research is so critical: "Drug resistance is one of the biggest challenges in treating melanoma, leaving many patients without effective solutions. By understanding the role of FAK1 in resistance, we can tackle a key problem that prevents therapies from working, opening the door to better and longer-lasting treatment strategies." This research, funded by the Novo Nordisk Foundation, aims to identify biomarkers that can predict patient responses to FAK1 inhibitors and guide the development of more effective, targeted therapies. "By identifying predictive biomarkers to guide the use of FAK1 inhibitors, we aim to offer a lifeline to patients with resistant tumors. This approach can lead to more personalised, effective therapies, reduce treatment failures, and ultimately improve survival and quality of life for melanoma patients," Daniela de Zio says.

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  • 📢 New publication:  Researchers from the Genome Integrity research group at the Danish Cancer Institute has just published an article in Nature Cell Biology. The work is done in collaboration with international colleagues, and the results show how alterations in six genes, including FAT1, result in defective homologous recombination (HR) repair of DNA damage among non-small cell lung cancer, one of the leading causes of death in both men and women. In particular, loss of FAT1 caused severe chromosomal instability and whole-genome doubling, i.e. features that lead to tumour progression and resistance to therapy.    In the video below you can hear professor and research group leader, Jiri Bartek, explain the exciting results 👇   The new results are published here (link in comments): Lu WT. et al.: TRACERx analysis identifies a role for FAT1 in regulating chromosomal instability and whole-genome doubling via Hippo signalling. Nat Cell Biol. 2024 Dec 30. DOI: 10.1038/s41556-024-01558-w. Online ahead of print.

  • 🌟 Introducing the Genome Integrity Group 🌟    Led by Professor Jiri Bartek this group focuses on various mechanistic aspects of the DDR and DNA repair pathways. Their work aims to improve the understanding of cancer development and identify vulnerabilities in cancer cells.   Scroll through the pictures below to learn more about the GIG group and their research work 👇

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  • ⭐ Into the unknown: Groth and van Oudenaarden laboratories receive Novo Nordisk Foundation Synergy Grant for Epigenome Fidelity   How reliably are patterns or markers on DNA (that don’t change the genetic code itself) passed from a one cell to its daughter cells? The Groth lab at the Danish Cancer Institute and CPR, University of Copenhagen (Leonie Kollenstart and Anja Groth) and the van Oudenaarden lab at the Hubrecht Institute in the Netherlands (Jeroen van den Berg and Alexander van Oudenaarden) have been awarded a Novo Nordisk Foundation Synergy Grant of DKK 15 million (approximately 2 million EUR) to answer this question. Both teams will use this grant to develop and apply novel technology to study the robustness of copying non-genetic information known as the epigenome. A better understanding of these processes can open new strategies to prevent diseases like cancer and combat ageing.  In this project, the researchers will develop new technologies to study epigenome inheritance on individual DNA molecules as well as single cells. Together with computational models, they aim to determine the fidelity of epigenome inheritance and identify hotspots for epigenome alterations. This knowledge will be applied in models of cancer, tissue regeneration and rejuvenation to understand how epigenomes evolve or mutate across human lifespan. Congratulations to all the researchers on this amazing news. On the picture is seen: Above: scEdU-seq for two cellular models (in cyan and purple) showing distinct replication timing profiles. Below: Researchers from the Groth Lab: Anja Groth and Leonie Kollenstart and the Hubrecht Institute: Alexander van Oudenaarden and Jeroen van den Berg.

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  • ⭐ Scientific Achievements in 2024 ⭐ 🔟 This year, The Cancer Structural Biology (CSB) team achieved a major breakthrough with the first use of a novel structure-based protocol linking genetic variant pathogenicity to cellular mechanisms. This approach focused on lysosomal acid sphingomyelinase (ASM), a crucial enzyme in lipid metabolism linked to genetic disorders and cancer. By integrating molecular dynamics simulations with pathogenicity predictions, the team developed a structural atlas of over 400 ASM variants, validated through experiments on 100+ cases. These findings advance our understanding of ASM-related diseases and open the door to therapies such as enzyme replacement therapy. The article “𝑨𝑺𝑴 𝒗𝒂𝒓𝒊𝒂𝒏𝒕𝒔 𝒊𝒏 𝒕𝒉𝒆 𝒔𝒑𝒐𝒕𝒍𝒊𝒈𝒉𝒕: 𝑨 𝒔𝒕𝒓𝒖𝒄𝒕𝒖𝒓𝒆-𝒃𝒂𝒔𝒆𝒅 𝒂𝒕𝒍𝒂𝒔 𝒇𝒐𝒓 𝒖𝒏𝒓𝒂𝒗𝒆𝒍𝒊𝒏𝒈 𝒑𝒂𝒕𝒉𝒐𝒈𝒆𝒏𝒊𝒄 𝒎𝒆𝒄𝒉𝒂𝒏𝒊𝒔𝒎𝒔 𝒊𝒏 𝒍𝒚𝒔𝒐𝒔𝒐𝒎𝒂𝒍 𝒂𝒄𝒊𝒅 𝒔𝒑𝒉𝒊𝒏𝒈𝒐𝒎𝒚𝒆𝒍𝒊𝒏𝒂𝒔𝒆” was published in Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease in October 2024.

    ASM variants in the spotlight: A structure-based atlas for unraveling pathogenic mechanisms in lysosomal acid sphingomyelinase

    ASM variants in the spotlight: A structure-based atlas for unraveling pathogenic mechanisms in lysosomal acid sphingomyelinase

    sciencedirect.com

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