Inflammation-induced thrombosis represents a severe complication in patients with myeloproliferative neoplasms (MPN) and in those with kidney dysfunction. Overlapping disease-specific attributes suggest common mechanisms involved in MPN pathogenesis, kidney dysfunction, and thrombosis. Data from 1420 patients with essential thrombocythemia (ET, 33.7%), polycythemia vera (PV, 38.5%), and myelofibrosis (MF, 27.9%) were extracted from the bioregistry of the German Study Group for MPN. The total cohort was subdivided according to the calculated estimated glomerular filtration rate (eGFR, (mL/min/1.73 m²)) into eGFR1 (≥90, 21%), eGFR2 (60–89, 56%), and eGFR3 (<60, 22%). A total of 29% of the patients had a history of thrombosis. A higher rate of thrombosis and longer MPN duration was observed in eGFR3 than in eGFR2 and eGFR1. Kidney dysfunction occurred earlier in ET than in PV or MF. Multiple logistic regression analysis identified arterial hypertension, MPN treatment, increased uric acid, and lactate dehydrogenase levels as risk factors for kidney dysfunction in MPN patients. Risk factors for thrombosis included arterial hypertension, non-excessive platelet counts, and antithrombotic therapy. The risk factors for kidney dysfunction and thrombosis varied between MPN subtypes. Physicians should be aware of the increased risk for kidney disease in MPN patients, which warrants closer monitoring and, possibly, early thromboprophylaxis.

Patients with cancer, both hematologic and solid malignancies, are at increased risk for thrombosis and thromboembolism. In addition to general risk factors such as immobility and major surgery, shared by non-cancer patients, cancer patients are exposed to specific thrombotic risk factors. These include, among other factors, cancer-induced hypercoagulation, and chemotherapy-mediated endothelial dysfunction as well as tumor-cell-derived microparticles. After an episode of thrombosis in a cancer patient, secondary thromboprophylaxis to prevent recurrent thromboembolism has long been established and is typically continued as long as the cancer is active or actively treated. On the other hand, primary prophylaxis, even though firmly established in hospitalized cancer patients, has only recently been studied in ambulatory patients. This recent change is mostly due to the emergence of direct oral anticoagulants (DOACs). DOACs have a shorter half-life than vitamin K antagonists (VKA), and they overcome the need for parenteral application, the latter of which is associated with low-molecular-weight heparins (LMWH) and can be difficult for the patient to endure in the long term. Here, first, we discuss the clinical trials of primary thromboprophylaxis in the population of cancer patients in general, including the use of VKA, LMWH, and DOACs, and the potential drug interactions with pre-existing medications that need to be taken into account. Second, we focus on special situations in cancer patients where primary prophylactic anticoagulation should be considered, including myeloma, major surgery, indwelling catheters, or immobilization, concomitant diseases such as renal insufficiency, liver disease, or thrombophilia, as well as situations with a high bleeding risk, particularly thrombocytopenia, and specific drugs that may require primary thromboprophylaxis. We provide a novel algorithm intended to aid specialists but also family practitioners and nurses who care for cancer patients in the decision process of primary thromboprophylaxis in the individual patient.

Active cancer by itself but also chemotherapy is associated with an increased risk of cardiovascular disease (CVD) and especially coronary artery disease (CAD) and atrial fibrillation (AF). The frequency of CVD, CAD, and AF varies depending on comorbidities (particularly in older patients), cancer type, and stage, as well as the anticancer therapeutic being taken. Many reports exist for anticancer drugs being associated with CVD, CAD, and AF, but robust data are often lacking. Because of this, each patient needs an individual structured approach concerning thromboembolic and bleeding risk, drug–drug interactions, as well as patient preferences to evaluate the need for anticoagulation therapy and targeting optimal symptom control. Interruption of specific cancer therapy should be avoided to reduce the potential risk of cancer progression. Nevertheless, additional factors like thrombocytopenia and anticoagulation in the elderly and frail patient with cancer cause additional challenges which need to be addressed in daily clinical management. Therefore, the aim of these recommendations is to summarize the available scientific data on antithrombotic therapy (both antiplatelet and anticoagulant therapy) in cancer patients with CVD and in cases of missing data providing guidance for optimal careful decision-making in daily routine.

Myelodysplastic syndromes/myelodysplastic neoplasms (MDS) are clonal hematopoietic stem cell disorders characterized by ineffective hematopoiesis, dysplasia of blood and bone marrow cells, and an elevated risk of progression to acute myeloid leukemia (AML). Patients with higher-risk MDS have a poorer prognosis, with up to 40% of them experiencing disease progression to AML within two years of diagnosis. Allogeneic stem cell transplantation (allo-SCT) remains the only potentially curative treatment for high-risk MDS. However, its use is limited by factors, such as patient age, comorbidities, cytogenetic profile, performance status, patient preference and donor availability. This article provides an overview of the therapeutic options for higher-risk MDS that are already established or in development, including hypomethylating agents, IDH1/IDH2 inhibitors, BCL2 inhibitors, RARA agonists, selective inhibitors of nuclear export, liposomal dual-drug chemotherapy and agents targeting aberrant inflammation. This review does not give detailed recommendations for single treatments. PEER REVIEWERED ARTICLE Peer reviewers: Prof. Ulrich Germing, Clinic for Hematology, Oncology and Clinical Immunology, Heinrich-Heine University, Dusseldorf, Germany One anonymous peer reviewer This article was received on May 10, 2025; accepted after peer review on May 30, 2025; published online on June 02, 2025.

A small proportion of patients with acute promyelocytic leukemia (APL) harbor variant chromosomal translocations that lead to fusion of *RARA* to one of several alternative partner genes. The most frequently reported of variant is the t(11;17)(q23;q21), which generates the fusion of the zinc finger gene *ZBTB16* (formerly PLZF) to the *RARA* locus (*ZBTB16::RARA* fusion). This APL subtype is typically resistant to standard APL-directed therapies and most patients with this translocation relapse within one year with limited subsequent treatment options. Here, we report on a patient with *ZBTB16::RARA* APL who achieved durable molecular complete remission lasting more than two years after high-dose chemotherapy with busulfan and cyclophosphamide followed by autologous stem cell transplantation. This therapeutic approach has not previously been described for this rare APL variant and may represent a promising consolidation strategy in selected patients. PEER REVIEWED ARTICLE **Peer reviewers:** Prof. Dr Stefan Balabanov, Department of Medical Oncology and Hematology, University Hospital Zurich, Zurich, Switzerland Prof. Dr Alicia Rovó, Department of Hematology and Central Hematology Laboratory, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland Received on January 19, 2026; accepted after peer review on February 19, 2026; published online on February 23, 2026.