Department of Hematology and Central Hematological Laboratory

Inselspital Bern

Hematology includes the diagnosis, treatment, and prevention of benign and malignant diseases of the hematopoietic and lymphatic system, blood coagulation, and thrombosis. The Department covers this entire field, offers comprehensive diagnostics and treatment at the highest level, and is also committed to teaching and research.

To the Inselspital website

Director

Prof. Anne Angelillo-Scherrer

Profile

  • Teaching students of medicine, dental medicine, pharmacy, biomedical sciences as well as graduate students at the Graduate School of Cellular and Biomedical Sciences (GCB) of the University of Bern
  • 9 research groups; research focus: investigation of epidemiological and pathophysiological processes as well as diagnosis, prognosis, and therapeutic approaches of blood-related disorders, pathophysiological processes that contribute to inflammation and tumor diseases
  • Clinical Study Management Unit (currently 19 ongoing studies)/ Biobanking
  • Largest clinical cell therapy program in Switzerland

External Partners

Steering committee and Advisory Board of Hereditary TTP Registry (www.ttpregistry.net); University of Oklahoma Health Sciences Center, Norman, OK, US; American Society for Transplantation and Cellular Therapy – Survivorship Special Interest Group, EBMT Chronic Malignancies Working Party (CMWP); DKFZ Heidelberg, Heidelberg, Germany; Hematology, Basel University Hospital, Basel, Switzerland; MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, UK; University Hospital Zurich and ETH Zurich, Zurich, Switzerland; University of Ottawa, Ottawa, Canada; Lowy Cancer Research Centre, UNSW Sidney, NSW, Australia; Foundation MPN Research Switzerland (Co-founder); Swiss Mastocytosis SCNM (Co-founder); Memorial Sloan Kettering Cancer Center, New York, USA; NYU Langone Perlmutter Cancer Center, New York, USA; Ajax Therapeutics, Cambridge, MA, USA; Landmark BioVentures; Nandasi Pharma Advisors; BleednFire Therapeutics (spin-off UNIBE, co-founders); Silence Therapeutics Silence Therapeutics GmbH, Berlin, Germany & plc, London, UK; Department of Interdisciplinary Oncology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA; Synapse Research Institute, Maastricht, the Netherlands; Division of Angiology and Hemostasis, University Hospitals of Geneva and Faculty of Medicine, University of Geneva, Geneva, Switzerland; Department of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA; Department of Immunology and Inflammation, Centre for Haematology, Imperial College London, London, UK; Australian Centre for Blood Diseases, Monash University, Melbourne, Australia; University Medical Centre Hamburg-Eppendorf, Hamburg, Germany; Baylor College of Medicine, Texas, USA; CSL Behring; MD Anderson Cancer Center, Houston, Texas, USA; Albert Einstein College of Medicine, Bronx, NY, USA; University of Texas at Austin, Austin, Texas, NY; Institute of Hematology and Transfuson Medicine, warsaw, Poland; Max Planck Institute for Plant Breeding Research; Department of Internal Medicine, Cardiology Services, Sanford University of South Dakota Medical Center; Institute of Biochemistry of the Romanian Academy , Bucharest, Romania

Grants

  • SNSF Project Funding 219306, 10000274, 10003602, 10005120, 10006706, 10006789; SNSF Scientific Exchanges 238259
  • Innosuisse 114.430 IP-LS, Innobooster, Innogrant, Unitectra PoC, Venture kick
  • National Science Centre, Poland, Grant 2021/43/B/NZ5/03345
  • SPHN Demonstrator project Therapy-related myeloid neoplasms after cytotoxic treatment (consortium member); Helmut Horton Foundation Consortium Project for Clinical Translation 2024-CON-027 Safety and Efficacy of Intravenous Thrombolysis in Stroke Patients on Recent DOAC Therapy: DO-IT Switzerland Trial (co-applicant); Canadian Institutes of Health Research project grant 527424 Development of a risk stratification score for recurrent venous thromboembolism and clinically­relevant bleeding in patients with cancer­associated venous thromboembolism. CAN­CATCH Study (co-applicants)
  • Bernese Cancer League, Jacques und Gloria Gossweiler Stiftung, Fondazione San Salvatore, Stiftung für krebskranke Kinder (Basel); Foundation for the Fight against Cancer,Swiss Hemophilia Network

Highlights 2025

Enhancing hemostasis potency in hemophilia with a small interfering ribonucleic acid targeting protein S

This study evaluated whether inhibition of protein S (PS) enhances thrombin generation in hemophilia A and B and explored a liver-targeted PS–siRNA therapeutic strategy to improve hemostasis while minimizing thrombotic risk. In plasma from patients with hemophilia A and B, PS inhibition significantly increased thrombin generation. A hepatocyte-specific PS–siRNA conjugated with N-acetylgalactosamine was developed to selectively reduce hepatic PS production while preserving PS function in other tissues. In preclinical hemophilia models, subcutaneous PS–siRNA treatment reduced PS levels, improved clot formation, and prevented bleeding in multiple injury models without inducing pathological thrombosis. These findings support PS reduction as a promising therapeutic approach for hemophilia and justify further clinical development.

The PS-siRNA technology has been further developed and is now referred to as BnF-001. Its continued development is being pursued by BLEEDnFIRE Therapeutics, a spin-off company from the University of Bern. The principal authors of this publication are also co-founders of the spin-off founded in 2025.

Eladnani et al., J Thromb Haemost. 2025

Specific inhibition effect on AML cells in MTS assay. THP-1 (B7-H3+) and RAJI (B7-H3-) cells were treated with Aff-MAG2 for 6 h. (A) Inhibitory dose-response curves. The points on the curves represent, in order from left to right, mean percentage cell viability, normalized to untreated cells, at the following concentrations of cytotoxic compound: 0 μM, 1.56 µM, 3.12 µM, 6.25 µM, 12.5 µM, 25 μM, 50 μM and 100 µM. (B) MTS assay-derived pairwise comparison analysis between mean percent viability of RAJI and THP-1 cells, respectively, normalized to untreated cells, for treatment with 25 μM, 50 μM and 100 µM of Aff-MAG2, respectively. Triton X-100 0.02% - positive control for membrane permeabilization. Error bars represent ±SD, n = 3. Unpaired one-tailed t-test, ns–not significant (p ≥ 0.05), **p < 0.01, ***p < 0.001. Data show results from a representative experiment out of three performed.

A novel cytotoxic anti-B7-H3 affibody with therapeutic potential in acute myeloid leukemia

Acute myeloid leukemia (AML) remains a highly aggressive malignancy with limited effective therapies. This study focused on B7-H3, an immune checkpoint ligand associated with poor prognosis and therapeutic resistance in AML, as a targeted treatment strategy. We designed and produced a novel recombinant anti–B7-H3 affibody conjugated to the cytotoxic peptide Magainin-2. The conjugate was expressed and purified in E. coli and evaluated in vitro using B7-H3–positive AML cells and B7-H3–negative control cells. The affibody–drug conjugate demonstrated potent, B7-H3–specific antiproliferative and cell death–inducing activity in AML cells, with significantly greater efficacy than Magainin-2 alone. These results support further preclinical development of this targeted therapeutic approach for AML.

Vasilescu et al., Front Pharmacol. 2025

Safety and efficiency of D-dimer testing in combination with clinical decision rules to exclude pulmonary embolism in patients with cancer: individual patient data meta-analysis

This study evaluated the safety and diagnostic yield of commonly used clinical decision rules (CDRs) for suspected pulmonary embolism (PE) in patients with cancer. Using individual patient–level data from 17 prospective diagnostic studies, we compared failure rates and imaging avoidance among patients managed with the Wells score, revised Geneva score, and YEARS algorithm versus those undergoing standard imaging. Among 2,258 patients with cancer, the 3-month incidence of venous thromboembolism after PE exclusion was low and comparable across all management strategies. The revised Geneva score with age-adjusted D-dimer and the YEARS algorithm achieved the highest diagnostic yield, safely avoiding imaging in up to 26% of patients. These findings demonstrate that current PE diagnostic algorithms are safe and effective in patients with cancer and can be applied without increased risk when imaging is withheld.

Vrotniakaite-Bajerciene et al., J Thromb Haemost. 2025

Left to right: Prof. Andreas Wicky (President of the Swiss Society of Medical Oncology), Dr. Rim Diab (award recipient), Prof. Anne Angelillo-Scherrer (Past President of the Swiss Society of Hematology), Prof. Miklos Pless (President of the Swiss Group for Clinical Cancer Research, SAKK)

Swiss Society of Hematology award for the best abstract presented at the Swiss Oncology Hematology Congress 2025 in the field of hemostasis, transfusion medicine, vascular, laboratory medicine, benign hematology

Enhancing hemostasis in Glanzmann thrombasthenia via protein S inhibition
R. Diab, T. Knopp, M. Fiore, S. Avoue-Celerier, L. Schacher, R. Prince-Eladnani, A. Angelillo-Scherrer
Presented by: R. Diab

Glanzmann thrombasthenia (GT) is a rare inherited platelet disorder characterized by impaired aggregation and severe bleeding. This study evaluated whether partial inhibition of protein S (PS), a natural anticoagulant, could enhance thrombin generation (TG) and improve hemostasis in GT. A single subcutaneous dose of PS–siRNA in GT (Itgb3⁻/⁻) mice significantly reduced mucocutaneous and gastrointestinal bleeding, increased thrombin generation, and decreased splenomegaly, an indirect marker of chronic bleeding. Consistent with these findings, antibody-mediated PS reduction in platelet-rich plasma from GT patients significantly increased thrombin generation. Together, these results demonstrate that partial PS inhibition rebalances hemostasis in GT and support further preclinical evaluation of PS–siRNA as a novel prophylactic therapeutic strategy.

To the website of the Swiss Oncology and Hematology Congress (SOHC) - Awards

Stefanie Arunasalam, award recipient (left) and Prof. Sara Meyer (right)

Swiss Society of Medical Oncology/Swiss Society of Hematology award for the best abstract presented at the Swiss Oncology Hematology Congress 2025 in the field of experimental hematology/oncology

Loss of SHP2 reduces JAK2V617F hematopoietic stem cell clone size and corrects MPN phenotype in preclinical models and patient cells
C. Albrecht, S. Arunasalam, S. Hallenberger-Jungius, S. Mattei, M. Christen, A. Rovo, A. Angelillo-Scherrer, S. Dirnhofer, B. G. Neel, R. L. Levine, R. Koche, S. C. Meyer
Presented by: S. Arunasalam

Myeloproliferative neoplasms (MPNs) are driven by constitutive JAK2 signaling, with persistent MAPK activation limiting the disease-modifying effects of JAK2 inhibitors. This study investigated the role of SHP2, a key MAPK mediator, in sustaining malignant signaling and clonal persistence. Genetic depletion or pharmacologic inhibition of SHP2 suppressed MAPK signaling, sensitized JAK2V617F cells to ruxolitinib, and reduced malignant clone size in vitro and in mouse models. In competitive transplantation assays, SHP2 loss significantly decreased JAK2V617F stem/progenitor cell burden. Combined SHP2 and JAK2 inhibition produced the most robust correction of cytosis, splenomegaly, and progenitor expansion in multiple MPN models and in primary patient cells. These findings identify SHP2 as a critical driver of MPN persistence and support combined SHP2/JAK2 inhibition as a promising disease-modifying therapeutic strategy.

To the website of the Swiss Oncology and Hematology Congress (SOHC) - Awards