{"title":"Platelet Dysfunction in Liver and Kidney Disease.","authors":"Fynn L Elvers, Ton Lisman","doi":"10.1016/j.hoc.2026.09.012","DOIUrl":"https://doi.org/10.1016/j.hoc.2026.09.012","url":null,"abstract":"<p><p>Patients with liver or kidney disease exhibit complex hemostatic changes, including abnormalities in platelet count and function. Although patients frequently bleed, bleeding is often unrelated to and not predicted by platelet abnormalities. Likewise, routine platelet transfusion to correct platelet abnormalities does not appear to prevent bleeding. Patients also exhibit prohemostatic abnormalities such as increased von Willebrand factor levels and platelet activation, which may compensate for antihemostatic changes. Notably, thrombosis is a frequent complication in these patients. Here, we narratively review platelet abnormalities and their relation to clinical practice for bleeding and thrombosis in liver and kidney disease.</p>","PeriodicalId":55060,"journal":{"name":"Hematology-Oncology Clinics of North America","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149208401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Approach to Thrombocytopenia.","authors":"Tarinee Rungjirajittranon, Adam Cuker","doi":"10.1016/j.hoc.2026.09.010","DOIUrl":"https://doi.org/10.1016/j.hoc.2026.09.010","url":null,"abstract":"<p><p>Thrombocytopenia ranges from benign to life-threatening, requiring a systematic evaluation including history, physical examination, peripheral blood smear review, and targeted laboratory testing. Pseudothrombocytopenia must be excluded. Mechanisms of thrombocytopenia include decreased platelet production, decreased survival, and splenic sequestration. In the inpatient setting, clinicians should consider postoperative thrombocytopenia, heparin-induced thrombocytopenia (HIT), other drug-induced thrombocytopenias, extracorporeal device-related causes, infection, and disseminated intravascular coagulation (DIC). In the outpatient setting, selected causes of thrombocytopenia include immune thrombocytopenia, chronic DIC, thrombotic thrombocytopenic purpura (TTP), and myelodysplastic syndrome, among others. Early recognition and prompt management of life-threatening conditions such as HIT and TTP is critical.</p>","PeriodicalId":55060,"journal":{"name":"Hematology-Oncology Clinics of North America","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149197854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Platelet Clearance: Mechanisms, Disorders, and Therapeutic Implications.","authors":"Emily Diaz, Karin M Hoffmeister","doi":"10.1016/j.hoc.2026.09.007","DOIUrl":"https://doi.org/10.1016/j.hoc.2026.09.007","url":null,"abstract":"<p><p>Platelets are a critical, cellular component of thrombosis and hemostasis. Too few platelets can lead to increased bleeding events, seen in conditions like immune thrombocytopenia. Therefore, understanding the mechanisms by which platelets are cleared from the body leads to strategies to maintain platelets in circulation, supplement patients with platelets through transfusions, or induce platelet production in vivo. Here, we discuss 2 major platelet clearance mechanisms, glycan recognition by hepatocytes and apoptosis, and how they can be modulated to improve patient outcomes.</p>","PeriodicalId":55060,"journal":{"name":"Hematology-Oncology Clinics of North America","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149185894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Connor J Liu, Graeme F Woodworth, Chetan Bettegowda
{"title":"Converging Focused Ultrasound and Liquid Biopsy for Glioma Management: Next Steps.","authors":"Connor J Liu, Graeme F Woodworth, Chetan Bettegowda","doi":"10.1016/j.hoc.2026.08.003","DOIUrl":"https://doi.org/10.1016/j.hoc.2026.08.003","url":null,"abstract":"<p><p>Gliomas represent one of the most formidable challenges in oncology due to their diffuse infiltrative growth in the brain, marked molecular heterogeneity, immune evasion, and the restrictive nature of the blood-brain barrier (BBB), which collectively undermine effective therapy. This review examines the rationale, current evidence, and translational hurdles for integrating focused ultrasound (FUS)-mediated BBB opening and liquid biopsy strategies in gliomas. In this context, FUS may serve as both a therapeutic adjunct and a tool to improve biomarker accessibility and imaging integration, while artificial intelligence-driven analytics synthesize complex datasets into actionable insights.</p>","PeriodicalId":55060,"journal":{"name":"Hematology-Oncology Clinics of North America","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149149766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Noah B Drewes, Yiting Xu, Priya U Kumthekar, Atique U Ahmed
{"title":"Purine Metabolism as a Therapeutic Target in Glioblastoma.","authors":"Noah B Drewes, Yiting Xu, Priya U Kumthekar, Atique U Ahmed","doi":"10.1016/j.hoc.2026.09.002","DOIUrl":"https://doi.org/10.1016/j.hoc.2026.09.002","url":null,"abstract":"<p><p>The most frequent primary malignant brain tumor in adults is glioblastoma, and recurrence with subsequent mortality is a significant issue in nearly all patients. Glioblastoma features such as rapid proliferation, chemotherapy resistance, and plasticity rely on the maintenance of adequate nucleotide pools. In this review, we investigate the role of purine metabolism in glioblastoma biology. Purine pathways promote stemness and plasticity, increase stress adaptation, and shape tumor microenvironments. The main vulnerabilities causing these malignant phenotypes include de novo purine synthesis, guanine synthesis via inosine monophosphate dehydrogenase, synthetic lethality secondary to methylthioadenosine phosphorylase loss, and extracellular adenosine signaling.</p>","PeriodicalId":55060,"journal":{"name":"Hematology-Oncology Clinics of North America","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149149554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Consulting Editor Farewell.","authors":"George P Canellos","doi":"10.1016/j.hoc.2026.09.017","DOIUrl":"https://doi.org/10.1016/j.hoc.2026.09.017","url":null,"abstract":"","PeriodicalId":55060,"journal":{"name":"Hematology-Oncology Clinics of North America","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149148598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Novel and Diverse Therapeutic Approaches to Glioma Management.","authors":"Debraj Mukherjee, Henry Brem","doi":"10.1016/j.hoc.2026.09.005","DOIUrl":"https://doi.org/10.1016/j.hoc.2026.09.005","url":null,"abstract":"","PeriodicalId":55060,"journal":{"name":"Hematology-Oncology Clinics of North America","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149129282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cancer Neuroscience: Next Steps.","authors":"Youssef E Sibih, Shawn L Hervey-Jumper","doi":"10.1016/j.hoc.2026.09.003","DOIUrl":"https://doi.org/10.1016/j.hoc.2026.09.003","url":null,"abstract":"<p><p>Cancer neuroscience has established that diffuse gliomas do not merely occupy neural tissue but, rather, malignant cells infiltrate and integrate within neuronal networks, actively remodeling neural circuit function. This relationship is bidirectional in that neuronal activity promotes tumor growth and progression, while glioma infiltration and expansion alter neuronal excitability and network dynamics, with clinically relevant consequences for seizure burden, cognitive function, and patient survival. This article focuses on the next steps required to translate our understanding of the cellular mechanisms of glioma-neuron cross-talk into patient benefit.</p>","PeriodicalId":55060,"journal":{"name":"Hematology-Oncology Clinics of North America","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149118531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Histone-modifying Enzymes as Therapeutic Targets in Glioma: Biological Rationale and Translational Findings.","authors":"Briana A Santo, A Karim Ahmed, Samuel Emerson","doi":"10.1016/j.hoc.2026.08.008","DOIUrl":"https://doi.org/10.1016/j.hoc.2026.08.008","url":null,"abstract":"<p><p>Histone-modifying enzymes have emerged as therapeutic targets in glioma, particularly H3K27M-altered diffuse midline glioma. This article reviews the biological rationale for targeting these enzymes and summarizes the current preclinical and clinical evidence for histone deacetylase, methyltransferase, and demethylase inhibitors. It also discusses the utility of nonenzymatic agents, including bromodomain and extraterminal inhibitors and dordaviprone, that have achieved similar epigenetic effects in this disease.</p>","PeriodicalId":55060,"journal":{"name":"Hematology-Oncology Clinics of North America","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149118629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Brain Tumor Vaccines: Next Steps.","authors":"Andres Santos, E Antonio Chiocca","doi":"10.1016/j.hoc.2026.08.005","DOIUrl":"https://doi.org/10.1016/j.hoc.2026.08.005","url":null,"abstract":"<p><p>High-grade gliomas remain among the most challenging malignancies despite extensive advances in molecular characterization and immunotherapy. This review highlights that while cancer vaccines consistently induce robust systemic immune responses, their clinical efficacy is limited by profound tumor heterogeneity and a highly immunosuppressive tumor microenvironment. Across peptide, dendritic cell, and mRNA-based platforms, outcomes are more strongly influenced by tumor biology than vaccine design. Emerging evidence supports a shift toward combinatorial strategies. Future progress will depend on spatially resolved tumor-immune analyses, biomarker-driven patient selection, and rational combination therapies to overcome immune resistance and achieve durable clinical benefit.</p>","PeriodicalId":55060,"journal":{"name":"Hematology-Oncology Clinics of North America","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149118552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}