Jon Riise

• Ladetto, Marco; Gutmair, Katja; Tavarozzi, Rita; Pawlikowski, Alexandra; Schomaker, Michael & Doorduijn, Jeanette [Vis alle 41 forfattere av denne artikkelen] (2026). Rituximab Maintenance Added to Ibrutinib-Containing Therapy in Younger, Untreated Patients With Mantle Cell Lymphoma: Results From the TRIANGLE Trial. Journal of Clinical Oncology. ISSN 0732-183X. 44(27), s. 2582–2589. doi: 10.1200/JCO-26-00705.
• Lewis, David J.; Jerkeman, Mats; Sorrell, Lexy; Wright, David; Glimelius, Ingrid & Poulsen, Christian B. [Vis alle 95 forfattere av denne artikkelen] (2025). Ibrutinib and rituximab versus immunochemotherapy in patients with previously untreated mantle cell lymphoma (ENRICH): a randomised, open-label, phase 2/3 superiority trial. The Lancet. ISSN 0140-6736. 406(10514), s. 1953–1968. doi: 10.1016/S0140-6736(25)01432-1. Fulltekst i vitenarkiv
• Meriranta, Leo; Jørgensen, Rasmus Rask Kragh; Pasanen, Annika; Kolstad, Arne; Hutchings, Martin & Niemann, Carsten Utoft [Vis alle 15 forfattere av denne artikkelen] (2025). Circulating tumor DNA determinants of response and outcome in relapsed/refractory mantle cell lymphoma. Blood Advances. ISSN 2473-9529. 9(17), s. 4528–4541. doi: 10.1182/bloodadvances.2025015791. Fulltekst i vitenarkiv Vis sammendrag

  Clinical tools to guide treatment decisions in relapsed/refractory mantle cell lymphoma (R/R MCL) are limited. Moreover, the translational potential of circulating tumor DNA (ctDNA) remains largely unproven. We designed and applied panel-based duplex sequencing of ctDNA to study molecular determinants of response and outcome in 58 patients with R/R MCL treated with venetoclax, lenalidomide, and rituximab. Genetic analysis revealed molecular predictors of response that were independent of clinical prognostic factors, with SMARCA4-mutated R/R MCLs responding to therapy, whereas TP53 mutations conferred resistance. Pretreatment ctDNA captured spatial heterogeneity, and its concentration was associated with multiple clinicopathological disease features and survival, independently of molecular predictors. Dynamic ctDNA assessment for minimal residual disease complemented clinical response evaluation and uncovered refractoriness in patients with molecular remission according to contemporary real-time quantitative polymerase chain reaction assay. Features of clonal hematopoiesis (CH) at baseline were associated with hematologic toxicity during treatment and poor outcomes on follow-up. Positive selection of TP53-related CH during treatment did not compromise the specificity of ctDNA response analysis, and fragmentation signatures allowed distinction between MCL ctDNA and CH-bearing cell-free DNA. Taken together, we report novel features in MCL ctDNA that reveal new minimally invasive tools that could potentially transform clinical decision-making in R/R MCL.

• Forsgren, Elin; Jørgensen, Rasmus R. K.; Bentzen, Hans; Riise, Jon; Haaber, Jacob & Pasanen, Annika [Vis alle 12 forfattere av denne artikkelen] (2025). Ibrutinib, lenalidomide, and rituximab in relapsed mantle cell lymphoma: Long-term follow-up of the Nordic Lymphoma Group MCL6 Philemon trial. HemaSphere. 9(3). doi: 10.1002/hem3.70101. Fulltekst i vitenarkiv
• Dreyling, Martin; Doorduijn, Jeanette; Giné, Eva; Jerkeman, Mats; Walewski, Jan & Hutchings, Martin [Vis alle 38 forfattere av denne artikkelen] (2024). Ibrutinib combined with immunochemotherapy with or without autologous stem-cell transplantation versus immunochemotherapy and autologous stem-cell transplantation in previously untreated patients with mantle cell lymphoma (TRIANGLE): a three-arm, randomised, open-label, phase 3 superiority trial of the European Mantle Cell Lymphoma Network. The Lancet. ISSN 0140-6736. 403(10441), s. 2293–2306. doi: 10.1016/S0140-6736(24)00184-3. Fulltekst i vitenarkiv
• Jerkeman, Mats; Kolstad, Arne; Hutchings, Martin; Pasanen, Annika; Meriranta, Leo & Niemann, Carsten Utoft [Vis alle 15 forfattere av denne artikkelen] (2024). MRD-driven treatment with venetoclax-R2 in mantle cell lymphoma: the Nordic Lymphoma Group MCL7 VALERIA trial. Blood Advances. ISSN 2473-9529. 8(2), s. 407–415. doi: 10.1182/bloodadvances.2023011920. Fulltekst i vitenarkiv Vis sammendrag

  Despite improvements in treatment of mantle cell lymphoma (MCL), most patients eventually relapse. In this multicenter phase 1b/2 trial, we evaluated safety and efficacy of minimal residual disease (MRD)-driven venetoclax, lenalidomide, and rituximab (venetoclax-R2) in relapsed/refractory (R/R) MCL and explored the feasibility of stopping treatment in molecular remission. The primary end point was overall response rate (ORR) at 6 months. After dose escalation, the recommended phase 2 dose was lenalidomide 20 mg daily, days 1 to 21; venetoclax 600 mg daily after ramp-up; and rituximab 375 mg/m2 weekly for 4 weeks, then every 8 weeks. MRD monitoring by RQ-PCR was performed every 3 months. When MRD-negativity in the blood was reached, treatment was continued for another 3 months; if MRD-negativity was then confirmed, treatment was stopped. In total, 59 patients were enrolled, with a median age of 73 years. At 6 months, the ORR was 63% (29 complete remission [CR], 8 partial remission [PR]), and 40% (4 CR, 2 PR) for patients previously failing a Bruton tyrosine kinase (BTK) inhibitor. Median progression-free survival (PFS) was 21 months, with median overall survival of 31 months. TP53 mutation was associated with inferior PFS (P < .01). Overall, 28 patients (48%) discontinued treatment in molecular remission, and 25 remain MRD negative after a median of 17.4 months. Hematological toxicity was frequent, with 52 of 59 (88%) patients with G3-4 neutropenia and 21 of 59 (36%) patients with G3-4 thrombocytopenia. To conclude, MRD-driven venetoclax-R2 is feasible and tolerable and shows efficacy in R/R MCL, also after BTK inhibitor failure. This trial was registered at www.ClinicalTrials.gov as #NCT03505944.

• Vistnes, Maria; Erusappan, Pugazendhi Murugan; Sasi, Athiramol; Nordén, Einar Sjaastad; Bergo, Kaja Knudsen & Romaine, Andreas [Vis alle 22 forfattere av denne artikkelen] (2023). Inhibition of the extracellular enzyme A disintegrin and metalloprotease with thrombospondin motif 4 prevents cardiac fibrosis and dysfunction. Cardiovascular Research (CVR). ISSN 0008-6363. 119(10), s. 1915–1927. doi: 10.1093/cvr/cvad078. Fulltekst i vitenarkiv Vis sammendrag

  Abstract Aims Heart failure is a condition with high mortality rates, and there is a lack of therapies that directly target maladaptive changes in the extracellular matrix (ECM), such as fibrosis. We investigated whether the ECM enzyme known as A disintegrin and metalloprotease with thrombospondin motif (ADAMTS) 4 might serve as a therapeutic target in treatment of heart failure and cardiac fibrosis. Methods and results The effects of pharmacological ADAMTS4 inhibition on cardiac function and fibrosis were examined in rats exposed to cardiac pressure overload. Disease mechanisms affected by the treatment were identified based on changes in the myocardial transcriptome. Following aortic banding, rats receiving an ADAMTS inhibitor, with high inhibitory capacity for ADAMTS4, showed substantially better cardiac function than vehicle-treated rats, including ∼30% reduction in E/e′ and left atrial diameter, indicating an improvement in diastolic function. ADAMTS inhibition also resulted in a marked reduction in myocardial collagen content and a down-regulation of transforming growth factor (TGF)-β target genes. The mechanism for the beneficial effects of ADAMTS inhibition was further studied in cultured human cardiac fibroblasts producing mature ECM. ADAMTS4 caused a 50% increase in the TGF-β levels in the medium. Simultaneously, ADAMTS4 elicited a not previously known cleavage of TGF-β-binding proteins, i.e. latent-binding protein of TGF-β and extra domain A-fibronectin. These effects were abolished by the ADAMTS inhibitor. In failing human hearts, we observed a marked increase in ADAMTS4 expression and cleavage activity. Conclusion Inhibition of ADAMTS4 improves cardiac function and reduces collagen accumulation in rats with cardiac pressure overload, possibly through a not previously known cleavage of molecules that control TGF-β availability. Targeting ADAMTS4 may serve as a novel strategy in heart failure treatment, in particular, in heart failure with fibrosis and diastolic dysfunction.

• Riise, Jon; Meyer, Saskia; Blaas, Isaac; Chopra, Adity; Tran, Trung & Delic-Sarac, Marina [Vis alle 22 forfattere av denne artikkelen] (2022). Rituximab-treated patients with lymphoma develop strong CD8 T-cell responses following COVID-19 vaccination. British Journal of Haematology. ISSN 0007-1048. 197(6), s. 697–708. doi: 10.1111/bjh.18149. Fulltekst i vitenarkiv Vis sammendrag

  B-cell depletion induced by anti-cluster of differentiation 20 (CD20) monoclonal antibody (mAb) therapy of patients with lymphoma is expected to impair humoral responses to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) vaccination, but effects on CD8 T-cell responses are unknown. Here, we investigated humoral and CD8 T-cell responses following two vaccinations in patients with lymphoma undergoing anti-CD20-mAb therapy as single agent or in combination with chemotherapy or other anti-neoplastic agents during the last 9 months prior to inclusion, and in healthy age-matched blood donors. Antibody measurements showed that seven of 110 patients had antibodies to the receptor-binding domain of the SARS-CoV-2 Spike protein 3–6 weeks after the second dose of vaccination. Peripheral blood CD8 T-cell responses against prevalent human leucocyte antigen (HLA) class I SARS-CoV-2 epitopes were determined by peptide-HLA multimer analysis. Strong CD8 T-cell responses were observed in samples from 20/29 patients (69%) and 12/16 (75%) controls, with similar median response magnitudes in the groups and some of the strongest responses observed in patients. We conclude that despite the absence of humoral immune responses in fully SARS-CoV-2-vaccinated, anti-CD20-treated patients with lymphoma, their CD8 T-cell responses reach similar frequencies and magnitudes as for controls. Patients with lymphoma on B-cell depleting therapies are thus likely to benefit from current coronavirus disease 2019 (COVID-19) vaccines, and development of vaccines aimed at eliciting T-cell responses to non-Spike epitopes might provide improved protection.

• Bach, Trond; Bergholtz, Stine Louise; Riise, Jon; Qvigstad, Eirik; Skomedal, Tor & Osnes, Jan-Bjørn [Vis alle 7 forfattere av denne artikkelen] (2014). Identification of small molecule NPR-B antagonists by high throughput screening - potential use in heart failure. Naunyn-Schmiedeberg's Archives of Pharmacology. ISSN 0028-1298. 387(1), s. 5–14. doi: 10.1007/s00210-013-0940-6. Fulltekst i vitenarkiv
• Ørstavik, Øivind; Ata, Salmana H; Riise, Jon; Dahl, Christen Peder; Andersen, Geir Øystein & Levy, Finn Olav [Vis alle 9 forfattere av denne artikkelen] (2014). Inhibition of phosphodiesterase-3 by levosimendan is sufficient to account for its inotropic effect in failing human heart. British Journal of Pharmacology. ISSN 0007-1188. 171(23), s. 5169–5181. doi: 10.1111/bph.12647. Fulltekst i vitenarkiv
• Riise, Jon; Ørstavik, Øivind; Qvigstad, Eirik; Dahl, Christen Peder; Osnes, Jan-Bjørn & Skomedal, Tor [Vis alle 8 forfattere av denne artikkelen] (2012). Prostaglandin E-1 facilitates inotropic effects of 5-HT4 serotonin receptors and beta-adrenoceptors in failing human heart. Basic Research in Cardiology. ISSN 0300-8428. 107(5). doi: 10.1007/s00395-012-0295-z. Fulltekst i vitenarkiv
• Riise, Jon; Nguyen, Hong Cam Thi; Hussain, Rizwan; Dahl, Christen Peder; Ege, Maren Stapnes & Osnes, Jan-Bjørn [Vis alle 10 forfattere av denne artikkelen] (2012). Prostanoid-mediated inotropic responses are attenuated in failing human and rat ventricular myocardium. European Journal of Pharmacology. ISSN 0014-2999. 686(1-3), s. 66–73. doi: 10.1016/j.ejphar.2012.04.022. Fulltekst i vitenarkiv

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• König, Marton; Holmøy, Trygve; Nygaard, Gro Owren; Riise, Jon; Midtvedt, Karsten & Goll, Guro Løvik [Vis alle 11 forfattere av denne artikkelen] (2026). Vaccination of immunosuppressed patients. Tidsskrift for Den norske legeforening (Tidsskriftet). ISSN 0029-2001. doi: 10.4045/tidsskr.25.0555. Fulltekst i vitenarkiv
• Røe, Åsmund Treu; Aronsen, Jan Magnus; Frisk, Michael; Lunde, Ida Gjervold; Riise, Jon & Sejersted, Ole M [Vis alle 10 forfattere av denne artikkelen] (2013). Compensatory alterations in cardiomyocytes Ca2+ homeostasis during aortic stenosis. Circulation. ISSN 0009-7322. 128. Fulltekst i vitenarkiv

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