Myelofibrosis (MF) is a chronic myeloproliferative neoplasm characterized by progressive bone marrow fibrosis, splenomegaly, debilitating constitutional symptoms, and cytopenias. Despite the benefits of ruxolitinib in controlling symptoms and spleen volume, challenges such as myelosuppression and limited impact on underlying fibrosis persist, particularly in cytopenic patients. Flonoltinib maleate (FM), a novel JAK2/FLT3/CDK6 inhibitor, shows preliminary potential in improving hematologic parameters and reducing fibrosis.

To evaluate the efficacy of low-/high-dose FM compared with RUX (primary objective), along with safety and the pharmacokinetic profile of FM (secondary objectives), in patients with intermediate- to high-risk MF (Trial registration: NCT06457425).

FMF-02 is a multicenter, randomized, open-label, active-controlled, phase IIb clinical trial.

Approximately 75 adults with primary or secondary MF will be randomized in a 1:1:1 ratio to receive low-dose FM (50 mg once daily), high-dose FM (100 mg once daily), or RUX (5, 15, or 20 mg twice daily, based on platelet count), with randomization stratified by the Dynamic International Prognostic Scoring System risk category. The primary endpoint is the proportion of patients achieving ⩾35% spleen volume reduction (SVR35) at week 24, as assessed by a blinded Independent Review Committee. Key secondary endpoints include the proportion with ⩾50% reduction in Total Symptom Score (TSS50), changes in myelofibrosis grade, objective remission rate [International Working Group for Myelofibrosis Research and Treatment (IWG-MRT) criteria], and safety. Subjects in the RUX group who complete the 24-week treatment or experience disease progression due to splenomegaly will crossover to receive FM. All subjects will continue long-term therapy until meeting discontinuation criteria, followed by survival follow-up.

The study commenced in June 2024 and is currently ongoing. The results will provide comparative data on the efficacy and safety profiles of FM versus RUX, including analyses of spleen response, symptom burden, hematologic parameters, and bone marrow fibrosis.

The FMF-02 trial is the first randomized phase IIb study directly comparing the novel inhibitor FM against RUX. Its findings are expected to generate pivotal evidence regarding whether FM offers superior or differentiated clinical benefits, thereby informing its potential as a frontline therapy for intermediate- to high-risk MF and guiding the design of future phase III studies.

Prefibrotic primary myelofibrosis (pre-PMF) is a subtype of primary myelofibrosis, having only been formally defined as a distinct entity since 2016. Diagnosis, using clinical assessment, peripheral blood analysis, genetic and molecular analysis, and bone marrow biopsy, is needed to distinguish pre-PMF from other myeloproliferative neoplasms, in particular essential thrombocythemia. While the 2022 International Consensus Criteria and World Health Organization diagnostic criteria are used in current clinical practice to aid diagnosis, prognostication for pre-PMF remains challenging. Advances in molecular testing and cytogenetics may enable new risk stratification and prognostic tools to inform treatment decisions for pre-MF. In this review, we aim to give an overview on pre-PMF including the latest updates on diagnostics and prognostic indicators. Furthermore, due to limited reviews on pre-PMF, there still remains no standardized treatment pathway; thus, we summarize the current management advice as well as suggest further trials and areas of research that may improve care in pre-PMF patients.

Hypereosinophilic syndrome (HES) is an assemblage of disorders leading to marked eosinophilic tissue infiltration resulting in organ dysfunction. This case report describes a challenging diagnosis of HES identified in the postpartum period, a rare presentation of this disease process.

A 32-year-old active-duty service member with allergic rhinitis and childhood eczema developed a progressive pruritic rash and severe, recurrent epigastric pain with vomiting and weight loss 3 months following the birth of her first child. The patient gradually developed intermittent facial swelling, night sweats, and dyspnea, resulting in hospitalization. Two absolute eosinophil counts (AECs) taken more than a month apart ranged from 1600 to 4787 cells/μL. Mature eosinophils were found on skin, bone marrow, and duodenal biopsies. Radiography revealed no detectable neoplasm, and there was no clinical evidence of cardiac involvement. Testing revealed no mutations indicative of familial, myeloproliferative, or lymphocytic variants. The patient was started on empiric treatment with symptom improvement, which was gradually discontinued due to a second pregnancy.

The patient described in this case met diagnostic criteria for HES; however, the complicated clinical and laboratory features made it challenging to characterize her disease as a specific HES variant, rendering it difficult to determine the optimal treatment regimen. Further therapy was complicated by a new pregnancy. It is important for clinicians to recognize an abnormally elevated AEC, promptly initiate systematic evaluation, and minimize delays in diagnosis and treatment of potential HES in order to avoid the extensive morbidity and mortality that can be associated with HES.

The aim of this study is to develop a prognostic model for evaluating radiotherapy response in patients diagnosed with rectal neoplasms by integrating genomic and clinical data. Publicly accessible datasets from The Cancer Genome Atlas and Gene Expression Omnibus were analyzed to identify differentially expressed genes associated with drug resistance and mitophagy. Functional enrichment analyses were conducted to investigate relevant biological pathways. A prognostic risk model was constructed using least absolute shrinkage and selection operator regression and validated via receiver operating characteristic (ROC) curve analysis and Kaplan-Meier survival analysis. The final model incorporated 15 genes selected from an initial set of 121 differentially expressed genes and demonstrated moderate to high predictive accuracy for 1-, 2-, and 3-year overall survival (area under the ROC curve: 0.70-0.90). Kaplan-Meier analysis revealed statistically significant differences in survival outcomes between high-risk and low-risk patient groups. Pathway enrichment analysis indicated that the selected genes were involved in actin cytoskeleton reorganization and antiviral immune responses. Differential expression of key genes within the model was confirmed through quantitative polymerase chain reaction assays. The resulting prognostic model enhances understanding of the molecular mechanisms underlying radiotherapy response in rectal neoplasms and may support individualized therapeutic decision-making in clinical oncology.

Paraneoplastic dermatoses are rare cutaneous manifestations that are secondary to an underlying neoplasm. They may precede the diagnosis of cancer by months or even years. Some clinical presentations are relatively specific, which allows for an early diagnosis and treatment of certain cancers. In this context, their recognition by both specialists and non-specialists is essential. The aim of this article is to highlight some of these clinical presentations.

Although telehealth is increasingly implemented in palliative oncology, the psychosocial effectiveness of nurse-led telehealth interventions remains unclear. Existing reviews are largely descriptive and do not isolate nurse-delivered interventions or synthesize psychosocial outcomes for both patients and family caregivers.

To evaluate the effectiveness of nurse-led telehealth interventions on psychosocial outcomes among patients with cancer receiving palliative care and their family caregivers.

Systematic review and meta-analysis.

Nine electronic databases were searched from inception to April 2025 for randomized controlled trials evaluating nurse-led telehealth interventions.

Nine trials (n = 3177 participants) were included. Among patients, nurse-led telehealth significantly reduced anxiety (Hedges' g = 0.46) and improved quality of life (Hedges' g = 0.33). Effects on depressive symptoms were not statistically significant. Among family caregivers, significant improvements were observed in anxiety (Hedges' g = 0.30), depression (Hedges' g = 0.42), quality of life (Hedges' g = 0.45), and stress burden (Hedges' g = 0.44). Interventions comprising more than six sessions demonstrated greater effectiveness for selected outcomes.

Nurse-led telehealth interventions improve psychosocial outcomes in palliative oncology for both patients and family caregivers. Structured and adequately intensive programs may enhance intervention impact and support evidence-based digital nursing practice.

In this study, we aimed to examine the effects of cancer stem cells (CSCs) on residual hepatocellular carcinoma (HCC) after radiofrequency ablation (RFA), and how to reduce the frequency of carcinoma cells with the CSCs phenotype in residual tumors after RFA.

Two HCC cell lines were exposed to 43 °C for 30 min in vitro using a water bath. Cell cycle, EdU assays and plate colony assays were performed to evaluate the proliferation of HCC cells. Cell migration was determined using wound healing and Transwell assays. Sphere formation and in vivo limiting dilution assays were performed to evaluate stemness. In vivo, two tumor-bearing mice were used to evaluate residual tumor growth, and treatments included an extracellular signal-regulated kinase (ERK) inhibitor U0126 and salinomycin (Sal).

In vitro, sublethal heat accelerated cancer cell proliferation, migration, and stemness, and induced molecular changes of epithelial-mesenchymal transition (EMT), ERK, and the β-catenin pathway. ERK inhibitor and Sal inhibited the proliferation, migration, and stemness of heat-treated HCC cells. The results showed that, in vivo, the ERK inhibitor + Sal significantly inhibited the growth of residual tumors after incomplete RFA. Compared with incomplete RFA alone, EMT markers, ERK, and the β-catenin pathway were also significantly inhibited after treatment with ERK inhibitor + Sal.

Incomplete RFA can accelerate cell proliferation, migration, and stemness in residual tumors. ERK inhibitor combined with Sal could inhibit cancer cell proliferation, migration, and stemness to synergically inhibit the progression of residual tumor.

Colorectal cancer (CRC) remains a significant global health burden, being the third most diagnosed cancer and second leading cause of cancer-related mortality. While there have been advances in early detection and treatment of CRC, outcomes for patients with advanced or metastatic disease remain poor due to high rates of therapy resistance and disease recurrence. Cancer-associated fibroblasts (CAFs) play a crucial role in the progression of CRC by actively modulating the tumor microenvironment (TME). CAFs differ from normal fibroblasts in that they remain persistently activated and acquire a myofibroblast-type behavior due to various signaling pathways, including transforming growth factor-beta (TGF-β), platelet-derived growth factor (PDGF), and interleukins in CRC. One of the most important ways that CAFs mediate their pro-tumorigenic effect is through the release of exosomes. Exosomes are small extracellular vesicles that carry a broad range of cargo, including proteins, lipids, microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and metabolites. These CAF-derived exosomes contribute to robust intercellular communication within the tumor microenvironment (TME), reprogramming both cancer cells and the remaining stromal elements. Also, particular emphasis is placed on how CAF-derived exosomes modulate cellular responses to cytotoxic agents, containing 5-fluorouracil, oxaliplatin, irinotecan, and radiotherapy. These exosomes alter DNA damage responses, ferroptosis, apoptosis, oxidative stress, and survival signaling, thereby reshaping the toxicity profile of anticancer treatments. Understanding these exosome-mediated mechanisms is critical for overcoming chemoresistance and radiosurvival in CRC.

M2-like macrophages and CD8+T cells are key immune components that influence tumor behavior and treatment response. Ubiquitin-specific protease 32 (USP32) is established as a key oncogenic factor in gastric cancer (GC). This study aimed to investigate the role of USP32 in regulating M2 macrophage polarization and CD8+T cell dysfunction in GC. Macrophages derived from THP1 cells (THP1-M0) or CD8+T cells were co-cultured with transfected AGS and HGC-27 GC cells. The proportion of CD206⁺ M2 macrophages and the apoptosis of CD8+T cells were assessed by flow cytometry. Cell invasion was analyzed by transwell assay. The interaction between USP32 and death-associated protein kinase 1 (DAPK1) was verified by GST pull down and Co-immunoprecipitation (Co-IP) experiments. The effect on tumor growth was tested by subcutaneous xenograft studies. USP32 and DAPK1 were overexpressed in GC tissues and cell lines. Mechanistically, USP32 stabilized DAPK1 protein through deubiquitination. DAPK1 downregulation reversed USP32-mediated enhancement in GC cell invasion, macrophage M2 polarization, and CD8+T cell apoptosis in vitro. USP32 depletion exhibited an in vivo anti-growth effect on AGS subcutaneous xenografts. This study identifies the USP32/DAPK1 cascade as a crucial regulator of M2 macrophage polarization and CD8+T cell apoptosis in GC, providing a novel mechanistic link between post-translational regulation and tumor immune evasion.