Institute for Cancer Research has since its foundation in 1954 played a central role within the field of cancer research both in Norway and internationally. The Institute has seven research departments and more than 380 employees. About 70% of the employees and projects are externally funded. Read more
Mitochondria are essential for cellular energy production and homeostasis, and their selective degradation through mitophagy is critical for maintaining cell function. However, the molecular mechanisms governing this process remain incompletely understood.
Now, Laura Trachsel-Moncho and co-workers in Anne Simonsen’s group identify the endosomal protein SNX10 as a modulator of piecemeal mitophagy, a process involving the selective degradation of mitochondrial components. They show that SNX10 localizes to early endosomes in normal conditions but associates with mitochondria-containing endosomal structures under hypoxia-mimicking stress. Loss of SNX10 leads to increased turnover of specific mitochondrial proteins, reduced mitochondrial respiration, and elevated reactive oxygen species (ROS) levels. Furthermore, zebrafish larvae lacking Snx10 exhibit reduced COX-IV levels and increased oxidative stress and cell death, demonstrating the physiological relevance of Snx10 in mitochondrial homeostasis.
These findings uncover an unexpected role for SNX10 in mitochondrial quality control and highlight its importance in cellular adaptation to metabolic stress.
Mev Dominquez-Valentin from the Department of Tumor Biology at the Institute for Cancer Research is senior author on a study recently published in the prestigious journal Clinical Gastroenterology and Hepatology, entitled: "Characterization of Screening Strategies for Lynch Syndrome in Latin America.” The study involves the collaborations of more than 50 investigators from 24 representative genetic cancer registries/center of 8 countries from Latin America, highlighting the significant insights we've gained into Lynch Syndrome (LS) screening methods across the region. The results emphasize challenges in hereditary cancer syndrome screening in Latin America and the need for enhanced strategies. Other OUS researchers involved in the study are Eivind Hovig, Pål Møller and Vessela Kristensen.
Do you have an innovative idea based on your research for a new product or service, but need funding to develop your early-stage technology or service further? Apply for seed funding from The UiO Growth House! Application deadline: 20 March 2025.
The European doctoral network Mac4Me (Macrophage Targets for Metastatic Treatment) is a 48-month project that addresses both technical and social challenges in cancer metastasis, focusing on three tumour types that show poor response to current immunotherapies: neuroblastoma, breast, and prostate cancer. Mac4Me is a Horizon Europe MSCA (Marie Sklodowska-Curie Actions) Doctoral Network. The network will train 18 Doctoral Candidates to study the tumour microenvironment at metastatic sites. The project is led by a consortium of 14 partners, that includes Oslo University Hospital. Tero Aittokallio, leader of the Computational Systems Medicine research group at the Institute for Cancer Research, is one of the supervisors, who were selected for their exceptional academic qualifications. The doctoral researcher at OUS will apply multi-modal AI algorithms to define new targets for improved immunotherapy.
Sigrid S. Skånland and co-author Johanne U. Hermansen
Drug resistance remains a major challenge in chronic lymphocytic leukemia (CLL). A study led by Martina Seiffert (German Cancer Research Center) in collaboration with Sigrid S. Skånland (Institute for Cancer Research) suggests that alterations in the proteasome activity drive resistance to the BTK inhibitor ibrutinib, and that proteasome inhibitors are effective in ibrutinib resistant or refractory CLL.
Treatment with ibrutinib can induce remissions for several years, yet development of drug resistance represents a major challenge. Mutations in BTK and the downstream protein PLCG2 are commonly detected in resistant disease, while mechanisms of resistance that are not explained by these mutations have not yet been understood.
From major journals, first or last author from the Institute for Cancer Research
Avershina E, Qureshi AI, Winther-Larsen HC, Rounge TB(2025) Challenges in capturing the mycobiome from shotgun metagenome data: lack of software and databases Microbiome, 13(1), 66 DOI 10.1186/s40168-025-02048-3, PubMed 40055808
Trachsel-Moncho L, Veroni C, Mathai BJ, Lapao A, Singh S, Asp NT, Schultz SW, Pankiv S, Simonsen A(2025) SNX10 functions as a modulator of piecemeal mitophagy and mitochondrial bioenergetics J Cell Biol, 224(5) DOI 10.1083/jcb.202404009, PubMed 40052924
Campos-Segura AV, Alvarez K, Murillo Carrasco AG, Rossi BM, Bohorquez M, Spirandelli F, Benavides C, Balto A, Della Valle A, Bruno LI, Lopez-Kostner F, Cruz-Correa M, Del Monte JS, Rugeles J, Ramirez JM, Nascimento I, Forones NM, Cock-Rada AM, Reyes-Silva C, Avila S, Apolinario L, Rossi NT, Martin C, Sulcahuaman Y, Vaccaro CAet al.(2025) Characterization of screening strategies for Lynch syndrome in Latin America Clin Gastroenterol Hepatol(in press) DOI 10.1016/j.cgh.2024.12.026, PubMed 40010418
Trachsel-Moncho L, Veroni C, Mathai BJ, Lapao A, Singh S, Asp NT, Schultz SW, Pankiv S, Simonsen A(2025) SNX10 functions as a modulator of piecemeal mitophagy and mitochondrial bioenergetics J Cell Biol, 224(5) DOI 10.1083/jcb.202404009, PubMed 40052924
Avershina E, Qureshi AI, Winther-Larsen HC, Rounge TB(2025) Challenges in capturing the mycobiome from shotgun metagenome data: lack of software and databases Microbiome, 13(1), 66 DOI 10.1186/s40168-025-02048-3, PubMed 40055808
D'Altri T, Freeberg MA, Curwin AJ, Alonso A, Freitas AT, Capella-Gutierrez S, Gadelha L, Hagwall A, Hovig E, Kerry G, Kirli K, Kochel K, Kohlbacher O, Korbel JO, Leinonen J, Marciniak B, Oliveira JS, Petersen K, Silva MJ, Stegle O, Valencia A, Viklund J, Guigo R, Parkinson H, Navarro Aet al.(2025) The Federated European Genome-Phenome Archive as a global network for sharing human genomics data Nat Genet(in press) DOI 10.1038/s41588-025-02101-9, PubMed 40033058