Kjetil Tasken

• Fagereng, Gro Live; Abel, Edvard; Consortium, CAN.HEAL; Casolino, Raffaella; Maria, Ruggero De & Fröhling, Stefan [Vis alle 30 forfattere av denne artikkelen] (2026). Landscape of cancer genomics and precision oncology in Europe. The Lancet Regional Health - Europe. doi: 10.1016/j.lanepe.2026.101841. Fulltekst i vitenarkiv
• Casolino, Raffaella; Mateo, Joaquin; Vries, Elisabeth G E de; Johns, Amber; Courtot, Melanie & Lawlor, Rita T [Vis alle 56 forfattere av denne artikkelen] (2026). Accelerating equitable cancer genomics and precision oncology in health care and research: a Lancet Oncology Commission. The Lancet Oncology. ISSN 1470-2045. doi: 10.1016/s1470-2045(26)00302-5. Fulltekst i vitenarkiv
• Yaqub, Sheraz; Valberg, Morten; Bjørnbeth, Bjørn Atle; Angelsen, Jon-Helge; Brudvik, Kristoffer Watten & Eilertsen, Ina [Vis alle 43 forfattere av denne artikkelen] (2026). Aspirin after curative-intent treatment of colorectal cancer liver metastases (ASAC): a multicentre, phase 3, randomised, double-blind, placebo-controlled trial. The Lancet Gastroenterology and Hepatology. ISSN 2468-1253. doi: 10.1016/s2468-1253(26)00260-8. Fulltekst i vitenarkiv Vis sammendrag

  Background Colorectal cancer frequently metastasises to the liver. Recurrence after curative-intent treatment of colorectal cancer liver metastases is common. Aspirin has shown preventive and antitumour effects in colorectal cancer, but its role after treatment of metastatic disease is uncertain. We aimed to establish whether adjuvant aspirin improves disease-free survival after curative-intent treatment of colorectal cancer liver metastases. Methods In this phase 3, randomised, double-blind, placebo-controlled trial conducted at 14 centres in Norway, Sweden, and Denmark, patients who had undergone curative-intent treatment for colorectal cancer liver metastases were randomly assigned (1:1), stratified by study site using a centrally generated computerised sequence with variable block sizes, to aspirin 160 mg per day or matching placebo for up to 3 years or until recurrence, death, or treatment discontinuation. The primary outcome was disease-free survival in the full analysis set, comprising all patients who initiated study treatment. The trial is completed and this is the final analysis. This trial is registered with ClinicalTrials.gov, NCT03326791, and EudraCT, 2014-003601-15. Findings Between Dec 15, 2017, and Jan 27, 2022, 466 patients were randomly assigned, of whom 428 initiated study treatment and were included in the full analysis set (217 assigned aspirin and 211 assigned placebo); 272 (64%) were male, 156 (36%) were female, and the mean age was 62·2 years. 269 disease-free survival events occurred (138 in the aspirin group and 131 in the placebo group). Aspirin did not improve disease-free survival (hazard ratio [HR] for recurrence or death 1·08 [95·44% CI 0·85–1·38]; p=0·58). Median disease-free survival was 1·13 years (95·44% CI 0·92–1·44) with aspirin and 1·40 years (1·11–1·69) with placebo. Overall survival at 36 months was 76% (95% CI 69·4–82·7) with aspirin and 85% (79·5–90·8) with placebo (HR for death 1·64 [95% CI 1·01–2·65]; p=0·045). Time to recurrence did not differ between groups (adjusted cause-specific HR 1·06 [95% CI 0·83–1·35]; p=0·64). 24 serious adverse events occurred in 17 (8%) of 217 patients in the aspirin group and five serious adverse events occurred in four (2%) of 211 patients in the placebo group. Clinically relevant adverse events and serious adverse events that occurred more commonly in the aspirin group than in the placebo group were myocardial infarction (two vs 0), epistaxis (four vs 0), duodenal ulcer (two vs 0), and cerebral haemorrhage (two vs 0). There were no treatment-related deaths. Interpretation Adjuvant aspirin did not improve disease-free survival and was associated with lower overall survival and more serious adverse events. These findings do not support routine use of aspirin after curative-intent treatment of colorectal cancer liver metastases.

• Panagopoulos, Ioannis; Stranger, Ane; Sveen, Anita; Jareid, Mie Linnea; Kidd, Susanne Gundersen & Bischof, Katharina [Vis alle 12 forfattere av denne artikkelen] (2026). Fusion gene heterogeneity and kinase enrichment in high-grade serous carcinomas. Neoplasia. ISSN 1522-8002. 79, s. 101332–101332. doi: 10.1016/j.neo.2026.101332. Fulltekst i vitenarkiv
• Agudo, Maria Martin; Pol, Henk Van der; Stav, Gabriel Bratseth; Kringelbach, Tina; Puco, Katarina & Flobak, Åsmund [Vis alle 10 forfattere av denne artikkelen] (2026). ‘Crossing borders’ in data standardisation: application of OMOP CDM in an international clinical trial network in precision cancer medicine. Acta Oncologica. ISSN 0284-186X. 65, s. 163–163. doi: 10.2340/1651-226x.2026.45120. Fulltekst i vitenarkiv
• Nakken, Sigve; Edsjö, Anders; Lehtiö, Janne; Nygaard, Vigdis; Roepman, Paul & Rosenquist, Richard [Vis alle 69 forfattere av denne artikkelen] (2026). Towards an ecosystem of clinical decision support tools for precision cancer medicine. NPJ precision oncology. doi: 10.1038/s41698-026-01551-6. Fulltekst i vitenarkiv Vis sammendrag

  Molecular tumor boards are supported by clinical decision support system (CDSS) tools for the interpretation of complex molecular data towards personalized treatments. Current CDSS tools are genomics-focused and characterized by tight couplings between data ingestion, guideline-based reasoning logic and curated knowledgebases. Next-generation CDSS solutions should integrate multimodal data and learn from outcomes in an interoperable ecosystem, leveraging explainable, trustworthy output from AI models through rigorous clinical validation processes.

• Solli, Elise; Bevilacqua, Alessio; Wenes, Mathias; Migliorini, Denis; Veen, Lars van der & Skånland, Sigrid [Vis alle 8 forfattere av denne artikkelen] (2026). The PI3Kδ inhibitor roginolisib (IOA-244) preserves T-cell function and activity. Molecular Oncology. ISSN 1574-7891. doi: 10.1002/1878-0261.70203. Fulltekst i vitenarkiv
• Henkel, Pia Sofie; Pedersen, Kine; Tasken, Kjetil; Hult, Ebba Hallersjö; Gelderblom, Hans & Fagereng, Gro Live [Vis alle 8 forfattere av denne artikkelen] (2026). Precision cancer medicine in Europe: a mixed-methods study on infrastructure for extended molecular diagnostics. Journal of Cancer Research and Clinical Oncology. ISSN 0171-5216. 152. doi: 10.1007/s00432-026-06468-y. Fulltekst i vitenarkiv Vis sammendrag

  Purpose Precision cancer medicine (PCM), targeting cancer treatment to patients’ individual genomic profiles, has the potential to improve diagnosis and outcomes substantially. Implementing PCM in healthcare systems requires that extended molecular diagnostics are accessible as part of routine practice. We conducted a mixed-methods study to identify and inform the infrastructure necessary for the implementation of extended molecular diagnostics as part of the health care system. Methods To identify and inform relevant categories of necessary infrastructure, we combined a survey, a structured literature search, and expert interviews. The survey included questions on reimbursement and technology assessment of diagnostics for PCM. Findings from the structured literature search were grouped to identify categories of infrastructure together with emerging themes in interviews with experienced oncologists, pathologists, and health technology assessment experts. Results 44 respondents from 20 countries participated in our survey. We identified and included 45 published papers, and seven experts were interviewed. We identified six key categories for implementing PCM as part of the healthcare system: physical, financial, organisational, competency, data and legal infrastructure. Our combined data sources revealed several themes to promote implementation, including the importance of centralisation of testing, the need for sustainable reimbursement, engagement of relevant stakeholders, interoperability of data infrastructure, and inter-disciplinary collaboration. Conclusion Our results highlight the need for interdisciplinary approaches and the value of initiatives to establish infrastructure within and across countries. While several European countries have come a long way in implementing diagnostics for PCM, considerable work remains to ensure equitable access for patients in need.

• Wei, Qian; Hajjar, Ehsan; Cornillot‐Clément, Selma; Solli, Elise; Diaz, Nuria Garcia & Landskron, Johannes [Vis alle 9 forfattere av denne artikkelen] (2026). High-Throughput Phenotypic Screen to Identify FoxP3 Regulators in Primary T Cells. ACS Chemical Biology. ISSN 1554-8929. 21(4), s. 764–778. doi: 10.1021/acschembio.5c01019. Fulltekst i vitenarkiv Vis sammendrag

  FoxP3+ regulatory T cells (Tregs) maintain immune homeostasis by suppressing excessive antiself-immunity of effector T cells (Teffs) and thereby regulate autoimmunity and inhibit antitumor immune responses. Thus, Treg-targeting is a popular therapeutic strategy for both autoimmune diseases and cancer treatment. However, specific regulators of Tregs are needed to bypass adverse effects elicited by strategies that target molecules with overlapping expression between Tregs and other T cell subsets. We aim to identify small molecules that specifically target the key Treg lineage-defining transcription factor FoxP3. Here, we describe a high-throughput, flow-cytometry-based phenotypic screening assay, its data processing pipeline, and downstream methods for compound validation. We developed a set of algorithms to easily exclude compounds with high toxicity and to filter out autofluorescent compounds. Our screening assay is performed on human primary T cells by measuring FoxP3 levels in CD4+ T cells, using an automated liquid handling pipeline. Selected hit candidates from the screening were validated and assessed through functional analyses. From screening a library of approved drugs, we identified several candidates that regulate Treg functions through FoxP3. Seventeen chemical analogs of one hit compound were identified and characterized in cell-based assays, revealing structure–activity relationships and identifying compounds with more potent effects on the regulation of FoxP3 levels and Treg function. We conclude that this novel screening method could successfully identify FoxP3 regulators with an effect on Treg functions.

• Pol, Henk van der; Kringelbach, Tina; Agudo, Maria Martin; Stav, Gabriel Bratseth; Fagereng, Gro Live & Fiocco, Marta [Vis alle 24 forfattere av denne artikkelen] (2026). Procedures of data merging in precision cancer medicine: the PRIME-ROSE project. Acta Oncologica. ISSN 0284-186X. 65, s. 1–8. doi: 10.2340/1651-226X.2026.44889. Fulltekst i vitenarkiv
• Slørdahl, Kathinka Schmidt; Puco, Katarina; Falk, Ragnhild Sørum; Dyvik, Ingrid; Brabrand, Sigmund & Niehusmann, Pitt [Vis alle 19 forfattere av denne artikkelen] (2026). Clinical outcomes of genomically guided trametinib monotherapy across cancer types: results from the IMPRESS-Norway trial. Acta Oncologica. ISSN 0284-186X. 65, s. 90–96. doi: 10.2340/1651-226X.2026.45086. Fulltekst i vitenarkiv Vis sammendrag

  Background and purpose: Molecular profiling guides cancer treatment, by identifying actionable genomic alterations. The IMPRESS-Norway trial (NCT04817956) is a nation-wide precision medicine trial evaluating the efficacy of approved cancer drugs on a novel indication in patients with advanced cancers harbouring potentially actionable alterations. Trametinib, a selective MEK1/2 inhibitor targeting the Mitogen-Activated Protein Kinase (MAPK) signalling pathway, is approved for BRAF V600 mutant melanoma but may also show activity in tumours with other alterations. This sub-study aimed to assess the efficacy of trametinib monotherapy across tumour types with alterations activating the MAPK signalling pathway. Patient/material and methods: In the IMPRESS-Norway trial patients are screened with the TruSight Oncology 500 panel or circulating tumour DNA profiling. Eligible patients are offered biomarker matched targeted therapies. In this subgroup analysis, we identified patients treated with trametinib monotherapy. Primary endpoints were disease control rate (DCR) after 16 weeks and safety. Secondary endpoints included progression-free survival (PFS) and overall survival (OS). Results: DCR after 16 weeks of treatment was 39% in 52 response evaluable patients, with four patients (8%) experiencing partial response, and 16 (31%) stable disease. Responses were seen in tumours harbouring BRAF fusions, GNA11, GNAQ, KRAS, NF1, and NRAS alterations, most frequently in low-grade serous ovarian cancer, central nervous system tumours, and uveal melanoma. Forty-eight percent of patients experienced treatment-related adverse events, including two treatment related deaths. Median PFS and OS were 4 and 9 months, respectively. Interpretation: Trametinib monotherapy achieved a 39% DCR in patients lacking standard options, supporting further studies to confirm efficacy and identify predictive biomarkers for treatment response.

• Frisell, Oskar; Aas, Eline; Henkel, Pia Sofie; Fagereng, Gro Live; Tasken, Kjetil & Hult, Ebba Hallersjö [Vis alle 8 forfattere av denne artikkelen] (2026). A conceptual health economic modelling framework to assess the cost-effectiveness of molecular target–driven treatment regimens in oncology. Acta Oncologica. ISSN 0284-186X. 65, s. 141–147. doi: 10.2340/1651-226x.2026.45088. Fulltekst i vitenarkiv Vis sammendrag

  Background and purpose: Molecularly targeted cancer therapies challenge conventional health economic evaluation frameworks that are structured around tumour-specific indications, comparators, and trial designs. Existing models often rely on pooled estimates from heterogeneous early-phase evidence or single-indication analyses, creating uncertainty for reimbursement decision-makers. We propose a conceptual modelling framework that aligns cost-effectiveness analyses with the biological rationale of precision oncology, evaluating therapies according to shared molecular alterations across tumour types. Patient/material and methods: We examined the methodological limitations of conventional partitioned survival models (PSMs) commonly applied in oncology and evaluated their suitability for tumour-agnostic indications. Based on the collected literature, we developed a dynamic, modular PSM framework that integrates multiple tumour sites expressing a common biomarker. The framework supports pooled and tumour-specific analysis of cost-effectiveness and enables progressive disaggregation of subgroups as additional evidence becomes available. Results: The proposed modelling approach facilitates transparent synthesis of heterogeneous evidence across tumour types using epidemiologically informed weighting, while preserving the ability to estimate tumour-specific cost-effectiveness where data permit. It addresses key challenges in tumour-agnostic evaluation, including variation in standard of care, treatment effects, and resource use across cancer sites. The modular design promotes internal consistency, reduces duplication of analytical effort, and enables iterative re-assessment of both overall and subgroup-specific cost-effectiveness. Interpretation: A dynamic, weighted multi-site modelling framework represents a coherent and adaptable extension of current health-technology assessment-practice for tumour-agnostic therapies. By structuring evidence around molecular targets, the framework can improve transparency and robustness of cost-effectiveness estimates, thereby supporting more equitable and efficient reimbursement decisions in the context of precision oncology.

• Pol, Henk van der; Kringelbach, Tina; Fagereng, Gro Live; Stav, Gabriel Bratseth; Agudo, Maria Martin & Mohammad, Soemeya Fooziye Haj [Vis alle 20 forfattere av denne artikkelen] (2025). Procedure for pooling clinical outcome data from DRUP-like clinical trials using the OMOP model. Journal of Clinical Oncology. ISSN 0732-183X. 43, s. e23165–e23165. doi: 10.1200/JCO.2025.43.16_suppl.e23165. Fulltekst i vitenarkiv
• Våtsveen, Thea Kristin; Giliberto, Mariaserena; Björnsdottir, Valgerdur; Centonze, Federica Grazia; Besse, Andrej & Frey, Yannick [Vis alle 19 forfattere av denne artikkelen] (2025). Targeting proteostasis in multiple myeloma through inhibition of LTK. Leukemia. ISSN 0887-6924. 39(9), s. 2237–2245. doi: 10.1038/s41375-025-02682-8. Fulltekst i vitenarkiv Vis sammendrag

  Multiple myeloma (MM) cells secrete high levels of immunoglobulin and are therefore addicted to mechanisms that maintain proteome homeostasis (proteostasis). While proteasome inhibitors that target the degradative aspect of proteostasis have proven effective, only limited attempts have been made to target protein secretion. Here we show that the receptor tyrosine kinase LTK is a regulatory node in the proteostasis network that responds to secretory load and helps cells maintain a high secretory output. LTK is a highly similar paralog to ALK and by repurposing existing ALK inhibitors, we demonstrate that targeting LTK causes immunoglobulin retention, ER stress and subsequent apoptosis of primary MM cells, even in patients refractory to proteasome inhibitors. Thus, LTK is a novel therapeutic target in the biosynthetic pathway of proteostasis, with significant potential for MM treatment.

• Tasken, Kjetil & Mahon, Piers (2025). Accelerating precision oncology by converging pragmatic trials and real-world evidence. Nature Reviews Drug Discovery. ISSN 1474-1776. 24, s. 809–810. doi: 10.1038/d41573-025-00047-5. Fulltekst i vitenarkiv
• Wei, Qian; Foyn, Håvard; Landskron, Johannes; Wang, Shixiong; Rye, Inga Hansine & Skånland, Sigrid S [Vis alle 10 forfattere av denne artikkelen] (2025). Identification of a group of 9-amino-acridines that selectively downregulate regulatory T cell functions through FoxP3. iScience. 28(3). doi: 10.1016/j.isci.2025.111931. Fulltekst i vitenarkiv Vis sammendrag

  FoxP3+ regulatory T cells (Tregs) are responsible for immune homeostasis by suppressing excessive anti-self-immunity. Tregs facilitate tumor growth by inhibiting anti-tumor immunity. Here, we explored the targeting of FoxP3 as a basis for new immunotherapies. In a high-throughput phenotypic screening of a drug repurposing library using human primary T cells, we identified quinacrine as a FoxP3 downregulator. In silico searches based on the structure of quinacrine, testing of sub-libraries of analogs in vitro, and validation identified a subset of 9-amino-acridines that selectively abrogated Treg suppressive functions. Mechanistically, these acridines interfered with the DNA-binding activity of FoxP3 and inhibited FoxP3-regulated downstream gene regulation. Release from Treg suppression by 9-amino-acridines increased anti-tumor immune responses both in cancer patient samples and in mice in a syngeneic tumor model. Our study highlights the feasibility of screening for small molecular inhibitors of FoxP3 as an approach to pursuing Treg-based immunotherapy.

• Kelly, Michy P.; Nikolaev, Viacheslav O.; Gobejishvili, Leila; Lugnier, Claire; Hesslinger, Christian & Nickolaus, Peter [Vis alle 29 forfattere av denne artikkelen] (2025). Cyclic nucleotide phosphodiesterases as drug targets. Pharmacological Reviews. ISSN 0031-6997. 77(3). doi: 10.1016/j.pharmr.2025.100042. Fulltekst i vitenarkiv
• Diaz, Nuria Garcia; Solli, Elise; Hajjar, Ehsan; Cornillot‐Clément, Selma; Landskron, Johannes & Ahmad, Rafi [Vis alle 8 forfattere av denne artikkelen] (2025). MAPK and STAT3 Inhibitors Modulate FoxP3 Expression and Regulatory T Cell Function. European Journal of Immunology. ISSN 0014-2980. 55(2). doi: 10.1002/eji.202451225. Fulltekst i vitenarkiv Vis sammendrag

  Regulatory T cells (Tregs) are a subset of T cells defined by the expression of Forkhead box protein P3 (FoxP3) playing a crucial role in regulating effector T cell activity. Tregs accumulate in the tumor microenvironment facilitating tumor growth. Thus, targeting FoxP3+ Tregs could improve cancer immunotherapies. Here, we conducted a high-throughput, phenotypic screening of a drug repurposing library to identify compounds downregulating FoxP3 expression in human primary T cells. We identified the tyrosine kinase inhibitor bosutinib and the STAT3 inhibitor nifuroxazide effectively downregulating FoxP3 expression. To identify more potent compounds, structural analogs of these two compounds were searched and validated. These analogs were found to reduce FoxP3 expression in a similar- or more potent manner than the original hits. All compounds inhibited Treg suppressive functions and reduced the expression of Treg activation markers. Importantly, bosutinib disrupted FAK and CaMKII signaling more potently in Tregs, whilst nifuroxazide and its analog NA16 targeted STAT3 protein levels more effectively in Tregs. Additionally, bosutinib and NA16 targeted effector Tregs more effectively than other Treg subsets. In summary, bosutinib, nifuroxazide, and their analogs inhibited FoxP3 expression, Treg suppressive abilities, and Treg activation effectively, which could serve as tools for the improvement of current cancer immunotherapies.

• Sveen, Anita; Johannessen, Bjarne; Klokkerud, Solveig Margrete Knoph; Kraggerud, Sigrid M.; Meza, Leonardo Zepeda & Bjørnslett, Merete Pauline [Vis alle 13 forfattere av denne artikkelen] (2024). Evolutionary mode and timing of dissemination of high-grade serous carcinomas. JCI Insight. 9:e170423(3), s. 1–19. doi: 10.1172/jci.insight.170423. Fulltekst i vitenarkiv Vis sammendrag

  Dissemination within the peritoneal cavity is a main determinant of poor patient outcomes from high-grade serous carcinomas (HGSCs). The dissemination process is poorly understood from a cancer evolutionary perspective. We reconstructed the evolutionary trajectories across a median of 5 tumor sites and regions from each of 23 patients based on deep whole-exome sequencing. Polyclonal cancer origin was detected in 1 patient. Ovarian tumors had more complex subclonal architectures than other intraperitoneal tumors in each patient, which indicated that tumors developed earlier in the ovaries. Three common modes of dissemination were identified, including monoclonal or polyclonal dissemination of monophyletic (linear) or polyphyletic (branched) subclones. Mutation profiles of initial or disseminated clones varied greatly among cancers, but recurrent mutations were found in 7 cancer-critical genes, including TP53, BRCA1, BRCA2, and DNMT3A, and in the PI3K/AKT1 pathway. Disseminated clones developed late in the evolutionary trajectory models of most cancers, in particular in cancers with DNA damage repair deficiency. Polyclonal dissemination was predicted to occur predominantly as a single and rapid wave, but chemotherapy exposure was associated with higher genomic diversity of disseminated clones. In conclusion, we described three common evolutionary dissemination modes across HGSCs and proposed factors associated with dissemination diversity.

Se alle arbeider i NVA

• Tasken, Kjetil & Fagereng, Gro Live (2026). Norge godt i gang med tilpasset kreftbehandling. [Journal]. Aftenposten. doi: https:/e-avis.aftenposten.no/p/aftenposten/2026-09-28/a/norge-godt-i-gang-med-tilpasset-kreftbehandling/611/2470350/76163084. Fulltekst i vitenarkiv
• Tasken, Kjetil & Fagereng, Gro Live (2026). Norge godt i gang med tilpasset kreftbehandling: Flere enn 500 behandlet. [Journal]. Teknisk Ukeblad. doi: https:/www.tu.no/nyhetsstudio/norge-godt-i-gang-med-tilpasset-kreftbehandling-flere-enn-500-behandlet/133181. Fulltekst i vitenarkiv
• Tasken, Kjetil & Fagereng, Gro Live (2026). Norge godt i gang med tilpasset kreftbehandling: Flere enn 500 behandlet. [Journal]. Finansavisen. doi: https:/www.finansavisen.no/helse/2026/09/26/8383528/norge-godt-i-gang-med-tilpasset-kreftbehandling-flere-enn-500-behandlet. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). Over 500 nordmenn behandlet med persontilpasset kreftbehandling. [Journal]. Adresseavisen. doi: https:/www.adressa.no/nyheter/innenriks/i/Gxddy9/dagens-viktigste-nyheter-saa-langt. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). Helse Fonna med i satsing på persontilpasset kreftbehandling. [Internet]. Radio Haugaland. doi: https:/radioh.no/helse-fonna-med-i-satsing-pa-persontilpasset-kreftbehandling/. Fulltekst i vitenarkiv
• Tasken, Kjetil & Fagereng, Gro Live (2026). Norge skiller seg ut: – Ligger veldig godt an. [Journal]. Nettavisen. doi: https:/www.nettavisen.no/nyheter/norge-styrker-seg-innen-kreftbehandling/s/80-95-111701. Fulltekst i vitenarkiv
• Tasken, Kjetil & Fagereng, Gro Live (2026). Kreftdiagnostikken har tatt store steg – nå møter Europa neste barriere. [Journal]. Dagens Medisin. doi: https:/www.dagensmedisin.no/impress-kreft-legemidler/kreftdiagnostikken-har-tatt-store-steg-na-moter-europa-neste-barriere/773300. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). Understanding cancer and importance of data exchange: data-driven tools for precision oncology. Fulltekst i vitenarkiv
• Skaara, Turid Rygh; Puco, Katarina; Dyvik, Ingrid; Slørdahl, Kathinka Schmidt; Falk, Ragnhild Sørum & Brabrand, Sigmund [Vis alle 32 forfattere av denne artikkelen] (2026). Alteration-matched therapy in advanced lung cancer: results from the IMPRESS-Norway study. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). Mye forskning – lite butikk: Hvordan få mer næring ut av forskningspengene? doi: https:/bit.ly/4xF4mzp. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). Precision Medicine Implementation in Europe: where do we want to go with the Joint Action on PCM (JA PCM) and SPARC. [Internet]. YouTube. doi: https:/www.youtube.com/watch?v=hVec7ovJiCQ. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). Pharmaceutical partnerships (off-label use, risk-sharing agreements). Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). Tumor immune evasion mechanisms and immune regulation. Fulltekst i vitenarkiv Vis sammendrag

  Invited speaker

• Tasken, Kjetil (2026). Bridging Clinical Trials and Real-World Practice in Europe: A Collaborative Approach. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). EU Joint Action for Personalised Cancer Medicine - Data collection at European-wide scale. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). PRIME-ROSE. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). Collaboration Between Nordic University Hospitals. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). The Need for Artificial Intelligence in Future Health Research and in Healthcare Services. Fulltekst i vitenarkiv
• Tasken, Kjetil (2026). Transforming Cancer Research and Care– Changing Lives. Fulltekst i vitenarkiv Vis sammendrag

  Keynote speaker

• Tasken, Kjetil (2026). Prostaglandin E2 regulation of cAMP-signaling complexes implicated in tumor immune evasion. Fulltekst i vitenarkiv Vis sammendrag

  Invited speaker

• Bjørgo, Elisa; Ånensen, Nina; Fagereng, Gro Live; Russnes, Hege Elisabeth Giercksky; Smeland, Sigbjørn & Tasken, Kjetil [Vis alle 7 forfattere av denne artikkelen] (2026). Merging clinical research and standard healthcare – Nordic Precision Cancer Medicine Symposium 2025. Acta Oncologica. ISSN 0284-186X. 65, s. 185–185. doi: 10.2340/1651-226x.2026.45168. Fulltekst i vitenarkiv
• Brabrand, Sigmund; Steinskog, Eli Sihn Samdal; Blix, Egil Støre; Flobak, Åsmund; Puco, Katarina & Fagereng, Gro Live [Vis alle 20 forfattere av denne artikkelen] (2025). 3137O IMPRESS-Norway: A nationwide precision-oncology study for off-label targeted therapies - Results from the first 1,740 patients. doi: 10.1016/j.annonc.2025.08.1609. Fulltekst i vitenarkiv
• Helland, Åslaug; Tasken, Kjetil; Lindemann, Kristina Yvonne Kathe; Blix, Egil Støre & Haakensen, Vilde Drageset (2025). ESMO-kongressen 2025 – dette ser de norske onkologene frem til. [Journal]. Dagens Medisin. doi: https:/www.dagensmedisin.no/esmo-esmo-2025-forskning/esmo-kongressen-2025-dette-ser-de-norske-onkologene-frem-til/710408. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). A delicate balance between defense and self-harm. [Journal]. Nordic Life Science Magazine. doi: https:/nordiclifescience.org/a-delicate-balance-between-defense-and-self-harm/. Fulltekst i vitenarkiv
• Tasken, Kjetil & Flobak, Åsmund (2025). Presisjonsmedisin mot kreft - Åsmund Flobak og Kjetil Taskén - HealthTalk TV Onkologisk Forum. [Internet]. HealthTalk TV (YouTube). doi: https:/www.youtube.com/watch?v=alY8ruBcvFk. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Immune regulation and regulatory T cells. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Advancing Precision Cancer Medicine by Building National Initiatives and via International Collaboration. Fulltekst i vitenarkiv Vis sammendrag

  Ernst Knobil Distinguished Lecture 2026

• Tasken, Kjetil (2025). EU Cancer Mission Conference. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Immune regulation and regulatory T cells. Fulltekst i vitenarkiv Vis sammendrag

  Invited speaker

• Tasken, Kjetil (2025). Funksjonell profilering i onkologi. Fulltekst i vitenarkiv Vis sammendrag

  Invited speaker

• Tasken, Kjetil (2025). The role of pragmatic clinical trials (PRIME-ROSE). Fulltekst i vitenarkiv Vis sammendrag

  Keynote Speaker EU Health Policy Platform Webinar on Cancer Mission Diagnosis and Treatment

• Tasken, Kjetil (2025). Drug repurposing trials: What are they and where are they going? Fulltekst i vitenarkiv Vis sammendrag

  Invited Speaker: Young Oncologist session

• Tasken, Kjetil (2025). EU Joint Action on Personalised Cancer Medicine (JA-PCM) Round Table Discussion. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Europe’s Edge: Competitiveness, Collaboration & Cancer Care Readiness. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Status on PRIME-ROSE. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). European data sharing between precision medicine cancer trials - Status of the Cancer Mission project PRIME-ROSE and the starting Joint Action on Precision Cancer Medicine. Fulltekst i vitenarkiv
• Grødeland, Gunnveig; Pettersen, Frank O. & Tasken, Kjetil (2025). Vaksinepodden - Episode 38 - Regulatoriske T-celler. Fulltekst i vitenarkiv Vis sammendrag

  I år ble Nobelprisen i medisin tildelt Shimon Sakaguchi, Mary E. Brunkow og Fred Ramsdell for deres arbeid med regulatoriske T-celler og perifer immuntoleranse. De illustrerer hvordan immunsystemet ideelt sett er i balanse. i denne episoden av Vaksinepodden diskuterer vi hvorfor regulatoriske T-celler og demping av immunresponser er viktig for et sunt immunsystem. Vi ser også på de oppdagelsene nobelprisvinnerne gjorde som endret vår forståelse av immunsystemet. Som gjest i studio har vi Kjetil Taskén. Han er instituttleder for Institutt for Kreftforskning ved Oslo Universitetssykehus, og forskningsgruppeleder på Universitetet i Oslo ved Seksjon for kreftimmunologi ved Institutt for klinisk medisin. I tillegg deltar overlege Frank Olav Pettersen fra Infeksjonsmedisinsk avdeling ved Ullevål, og Gunnveig Grødeland som er professor i immunologi og leder for Senter for pandemi- og en-helseforskning ved Universitetet i Oslo.

• Myklebust, June Helen; Sollid, Ludvig Magne & Tasken, Kjetil (2025). Oppdagelser om immunsystemet kan gi gjennombrudd i behandling av kreft og betennelsessykdommer. Aftenposten. Fulltekst i vitenarkiv
• Myklebust, June Helen & Tasken, Kjetil (2025). Nobelpris for regulatoriske T-celler og immuntoleranse. Tidsskrift for Den norske legeforening (Tidsskriftet). ISSN 0029-2001. 145(15). doi: 10.4045/tidsskr.25.0649. Fulltekst i vitenarkiv
• Eriksen, Annelin; Westergaard, Marit; Tasken, Kjetil & Lohndal, Terje (2025). Vitenskapsakademiet vil bruke utestemmen, også om Palestina. doi: https:/www.khrono.no/vitenskapsakademiet-vil-bruke-utestemmen-ogsa-om-palestina/988353. Fulltekst i vitenarkiv
• Yaqub, Sheraz & Tasken, Kjetil (2025). Adjuvant Aspirin Fails in Phase 3 Trial of Patients With Colorectal Cancer Liver Metastases. [Internet]. Oncology News Central. doi: https:/www.oncologynewscentral.com/colorectal-cancer/adjuvant-aspirin-fails-in-phase-3-trial-of-patients-with-colorectal-cancer-liver-metasases. Fulltekst i vitenarkiv
• Yaqub, Sheraz & Tasken, Kjetil (2025). Studie med KLINBEFORSK-finansiering presentert ved ASCO. [Internet]. Helse Sør-øst. doi: https:/www.helse-sorost.no/klinbeforsk/asac-studien-asco/. Fulltekst i vitenarkiv
• Yaqub, Sheraz & Tasken, Kjetil (2025). Aspirin beskytter ikke mot tilbakefall for tarmkreftpasienter med spredning til lever. [Internet]. Oslo universitetssykehus. doi: https:/www.oslo-universitetssykehus.no/om-oss/nyheter/aspirin-beskytter-ikke-mot-tilbakefall-for-tarmkreftpasienter-med-spredning-til-lever/. Fulltekst i vitenarkiv
• Isachsen, Henriette Bertheussen; Yaqub, Sheraz & Tasken, Kjetil (2025). Vi kan ikke anbefale denne pasientgruppen å begynne med aspirin. [Journal]. Dagens medisin. doi: https:/www.dagensmedisin.no/asco-2025-kirurgi-kreft/norsk-kirurg-pa-asco-vi-kan-ikke-anbefale-denne-pasientgruppen-a-begynne-med-aspirin/688581. Fulltekst i vitenarkiv
• Eriksen, Annelin; Westergaard, Marit; Tasken, Kjetil & Lohndal, Terje (2025). Fem Tiltak for å sikre tillit til vitenskap - Et forslag fra Det Norske Videnskaps-Akademi. doi: https:/www.morgenbladet.no/ideer/fem-tiltak-for-a-sikre-tillit-til-vitenskap/9613882. Fulltekst i vitenarkiv
• Eriksen, Annelin; Westergaard, Marit; Tasken, Kjetil & Lohndal, Terje (2025). Under Trump er akademisk frihet under angrep. s. 42–43. doi: https:/www.aftenposten.no/meninger/kronikk/i/OoBEJ1/under-trump-er-akademisk-frihet-under-angrep. Fulltekst i vitenarkiv
• Litvinova, Yulia; Tasken, Kjetil; Hansen, Torben Frøstrup; Steffensen, Karina Dahl; Pajusalu, Sander & Sharma, Tarang [Vis alle 8 forfattere av denne artikkelen] (2025). Transforming cancer care with precision oncology. Eurohealth. ISSN 1356-1030. 31(1), s. 37–42. doi: https:/eurohealthobservatory.who.int/publications/i/transforming-cancer-care-with-precision-oncology. Fulltekst i vitenarkiv
• Eriksen, Annelin; Westergaard, Marit; Tasken, Kjetil & Lohndal, Terje (2025). Støtter forskere og forskning under press. [Internet]. Det norske videnskaps-akademi. doi: https:/dnva.no/detskjer/2025/02/stotter-forskere-og-forskning-under-press. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). National Cancer Strategy – Want to double the number of cancer patients in clinical trials. [Journal]. Dagens medisin. doi: https:/www.dagensmedisin.no/jan-christian-vestre-kliniske-studier-kreft/vil-doble-antall-deltagere-i-kreftstudier/674483. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Bridging Clinical Trials and Real-World Practice: A Collaborative Approach. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Advancing Precision Cancer Medicine by Building National Initiatives and via European Collaboration. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Democratizing Trials – Blueprint for Inclusive Innovation. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Advancing Precision Cancer Medicine by Building National Initiatives and via European Collaboration. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Functional Precision Medicine and Precision Immune Oncology Strategies. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Oppsummering av høydepunktene fra ASCO. doi: https:/www.dagensmedisin.no/dmarena/dagens-medisin-inviterte-til-dm-arena-post-asco-12-juni-se-opptaket-her/669612. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Update on DRUP-like trials and data aggregation in PCM4EU & PRIME-ROSE. How can we Improve Access and What are the Roads to Reimbursement? Fulltekst i vitenarkiv
• Tasken, Kjetil & Bulcke, Marc Van den (2025). Showcase and future outlooks: CAN.HEAL, PCM4EU, PRIME-ROSE and upcoming Joint Action on Personalised cancer medicine. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Future in Precision Medicine beyond 2030. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). How to advance implementation on the EU4Health Joint Action on PCM? Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). How Do We Secure Sustainable, Cost-Effective and Equitable Precision Medicine at a National Level? Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). The National Norwegian Model: Best Practices in Innovative Molecular Diagnostics and Tailored Therapies. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Aggregering av data fra kliniske studier i EU Cancer Mission prosjektet www.prime-rose.no  og i EU4Health Joint Action for presisjonsmedisin i kreft som skal starte. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Health data and AI. Fulltekst i vitenarkiv
• Tasken, Kjetil (2025). Precision Medicine. Fulltekst i vitenarkiv
• Subbiah, Vivek; Curigliano, Giuseppe; Sicklick, Jason K.; Kato, Shumei; Tasken, Kjetil & Medford, Arielle [Vis alle 12 forfattere av denne artikkelen] (2025). Cancer treatment paradigms in the precision medicine era. Nature Medicine. ISSN 1078-8956. doi: 10.1038/s41591-025-03711-w. Fulltekst i vitenarkiv
• Guren, Marianne; Malinen, Eirik; Smeland, Sigbjørn; Straume, Oddbjørn; Waldeland, Einar & Tasken, Kjetil (2024). Kreftbehandling: Nå er det mulig å tilby mer skånsom stråleterapi for kreftpasienter. s. 34–35. doi: https:/e-avis.aftenposten.no/p/aftenposten/2024-12-27/a/na-er-det-mulig-a-tilby-mer-skansom-straleterapi-for-kreftpasienter/611/1797967/59577861. Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). Ny strategi: KI og sikkerhet - nye satsingsområder for Akademiet. [Internet]. Det Norske Videnskaps-Akademi. doi: https:/dnva.no/detskjer/2024/12/ki-og-sikkerhet-nye-satsingsomrader-akademiet. Fulltekst i vitenarkiv
• Hestdal, Kjetil & Tasken, Kjetil (2024). Interview with Kjetil Hestdal about SERCA Pharmaceuticals, ischemia reperfusion injury. [Internet]. Finansavisen. doi: https:/tv.finansavisen.no/nb/watch/1493?zephr_sso_ott=LEhNU4. Fulltekst i vitenarkiv
• Tasken, Kjetil; Nygård, Mari Kiens & Widerberg, Ketil (2024). Pionersamarbeid om deling av data gir raskere utvikling av medisin. [Internet]. Khrono. doi: https:/www.khrono.no/pionersamarbeid-om-deling-av-data-gir-raskere-utvikling-av-medisin/922790. Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). Institutt for Kreftforskning 70 år - og sprekere enn noensinne. doi: https:/soundcloud.com/user-972208711/episode-314?si=7bca6686ee6e43fb8c9578a494105276&utm_source=clipboard&utm_medium=text&utm_campaign=social_sharing. Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). PRIME-ROSE and PCM4EU: Capitalizing on and Increasing Effectiveness of Industry Collaboration with DRUP-Like Clinical Trials. Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). Public-private collaboration in the EU: PRIME-ROSE and PCM4EU. Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). Cross-country collaboration in PRIME-ROSE. Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). Value of the DRUP-like clinical trials (DLCT) network for personalized oncology in Europe. Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). The Institute for Cancer Research is a hub in the cancer clinic for development of advanced diagnostics and complex clinical trials. Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). Research and innovation in the diagnostic pathway - Development of functional precision medicine strategies. Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). Prostaglandin E2 and beta-adrenergic regulation of cAMP-signaling complexes implicated in tumor immune evasion and ischemia-reperfusion injury. Fulltekst i vitenarkiv
• Fagereng, Gro Live; Russnes, Hege Elisabeth Giercksky; Tasken, Kjetil; Smeland, Sigbjørn & Helland, Åslaug (2024). Presisjonsmedisin innen kreft. [Journal]. Aftenposten (Persontilpasset Behandling – Addendum to AP). Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). ASCO24 Updates: How PRIME-ROSE is Expanding Access to Precision Cancer Medicine. [Internet]. OncoDaily. Fulltekst i vitenarkiv
• Dyvik, Ingrid; Fagereng, Gro Live; Lien, Tonje; Nygaard, Vigdis; Silwal-Pandit, Laxmi & Noon, J Christopher [Vis alle 20 forfattere av denne artikkelen] (2024). Comprehensive genomic profiling of circulating tumor DNA for treatment recommendation: A sub-project of the IMPRESS-Norway trial. Fulltekst i vitenarkiv
• Tasken, Kjetil (2024). Introduction to the Clinical Trial & Design Drug Trial Protocols. Fulltekst i vitenarkiv

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