Masson's tumor, also known as intravascular papillary endothelial hyperplasia, is a rare condition characterized by nonspecific clinical manifestations, which frequently lead to its misidentification as malignant neoplasms such as sarcoma. A definitive diagnosis is established through histopathological examination. This report describes a case of a patient presenting with a mass in the left thigh accompanied by intermittent claudication of the ipsilateral lower limb, who was subsequently diagnosed with Masson's tumour​ following surgical intervention.

Diffuse large B-cell lymphoma (DLBCL) is characterized by profound heterogeneity that underpins varied clinical outcomes. To decipher this complexity, we performed an integrated single-cell and genomic analysis. Using scRNA-seq data (GSE182434), we identified six distinct malignant B-cell subclusters (MB1-MB6) within the DLBCL ecosystem. Cell-cell communication analysis revealed intricate interaction networks, particularly involving the MIF and Complement pathways. Prognostic analysis of bulk transcriptomic data (GSE32918) identified the MB5-related gene signature as the most critical factor associated with poor overall survival. This MB5 subgroup was associated with enhanced proliferative processes, a higher tumor mutational burden, and specific comutations. Leveraging MB5 marker genes, we developed and validated a robust CoxBoost-RSF machine-learning model that effectively stratified patient risk in independent cohorts. Our study defines the MB5 malignant B-cell subgroup as a key driver of DLBCL aggressiveness and provides both a novel prognostic biomarker and a framework for personalized therapeutic targeting.

Gynecological malignancies are characterized by profound cellular heterogeneity, dynamic immune remodeling, and frequent therapeutic resistance, which together limit durable clinical responses. Single-cell sequencing has emerged as a powerful approach for dissecting tumor ecosystems at unprecedented resolution, enabling the identification of malignant subclones, immune cell states, stromal subsets, lineage trajectories, and intercellular communication networks. In cervical cancer, single-cell studies have revealed epithelial diversity, HPV-associated immune suppression, exhausted T/NK-cell populations, macrophage polarization, and genomic alterations linked to chemoradiotherapy resistance. In ovarian cancer, single-cell analyses have refined the understanding of fallopian tube origin, molecular subtypes, metastatic dissemination, ascites-associated immune suppression, platinum resistance, and tertiary lymphoid structure-related immune phenotypes. In endometrial cancer, single-cell profiling has uncovered heterogeneous cancer-associated fibroblast populations, epithelial biomarkers, and stromal-immune interactions with prognostic relevance. This review summarizes recent advances in single-cell sequencing across cervical, ovarian, and endometrial cancers, with particular emphasis on immune heterogeneity, tumor-microenvironment crosstalk, therapeutic resistance, and emerging opportunities for precision immunotherapy.

Inducible nitric oxide synthase (iNOS) and its product nitric oxide (NO) were historically linked to poor melanoma outcomes, yet recent evidence shows NO supports anti-tumor immunity. This study examines how iNOS shapes anti-PD-1 efficacy, particularly through interferon signaling.

B16-D5 melanoma tumors were implanted in wild-type (WT) and iNOS knockout (KO) mice to compare tumor growth and response to anti-PD-1 therapy. Flow cytometry, apoptosis assays, and RNA sequencing assessed NO production, PD-L1 expression, and interferon-related gene activation. In vitro, melanoma cells were treated with NO donors (DETA NONOate, SNAP) to assess proliferation and apoptosis. Peripheral blood mononuclear cells from 27 melanoma patients receiving anti-PD-1 therapy were analyzed with multiparameter flow cytometry to correlate NO-associated immune subsets with progression-free survival (PFS).

Tumors grew significantly faster in iNOS KO mice, and anti-PD-1 therapy had no effect, demonstrating that iNOS-derived NO contributes to treatment efficacy. NO donors inhibited melanoma proliferation and induced apoptosis in vitro. Transcriptomic analysis showed anti-PD-1 upregulated interferon pathway genes (STAT1, IRF1, IFNB1) in WT but not iNOS KO mice. In patients, a NO-producing dendritic-cell subset (DAF-FM⁺CD11c⁺) was associated with improved PFS (hazard ratio 0.453; 95% CI = 0.270-0.992; p=0.048), indicating a NO-dependent enhancement of interferon-driven immune activity.

iNOS-derived NO is necessary for effective anti-PD-1 immunotherapy in melanoma, promoting interferon signaling and immune activation. Loss of iNOS impairs tumor control and immune responsiveness, supporting NO as a potential biomarker and therapeutic adjunct to be explored while challenging assumptions about its deleterious role in melanoma.

The goal is to design and validate a noninvasive screening model for advanced colorectal neoplasia(ACN) utilizing routine blood tumor markers and inflammatory indices, and to develop an online calculator for assessing individual risk.

In this retrospective analysis, 1,290 patients who underwent colonoscopy and had full preoperative blood test results were included. Based on pathology, patients were categorized into a group with advanced colorectal neoplasms and another with non-advanced neoplasms. Patients were randomly assigned to a training set, making up 70%, and a test set, making up 30%.Candidate variables were initially screened using univariate logistic regression, and those with statistical significance were then included in a multivariate logistic regression model to determine independent predictors. To assess potential nonlinear relationships between continuous variables and the risk of advanced neoplasms, restricted cubic splines were employed. Prediction models were constructed using five machine learning algorithms and evaluated using the area under the receiver operating characteristic curve. The robustness of key predictors was further assessed through sensitivity and stratified analyses. SHAP was applied to interpret the final model, which was subsequently implemented as an online calculator.

Among the 1,290 patients, 210 were diagnosed with advanced colorectal neoplasms. CEA, SII, NLR, ALB, and PLR were identified as independent predictors, and their associations remained stable across sensitivity and stratified analyses. Among the models, XGBoost achieved the best performance, with an AUC of 0.956 (95% CI 0.936-0.976). SHAP analysis identified SII as the most influential predictor.

A machine learning model based on key blood markers such as CEA, SII, and NLR can effectively support noninvasive screening for advanced colorectal neoplasms. This online calculator is a convenient and practical resource for evaluating risk on an individual basis in clinical practice.

Myeloid/lymphoid neoplasms with PDGFRB rearrangements are rare hematologic malignancies usually associated with eosinophilia and sensitivity to tyrosine kinase inhibitors, whereas atypical presentations remain poorly defined. We report a 60-year-old man with persistent leukocytosis and thrombocytopenia detected during a routine health examination. Bone marrow examination revealed marked granulocytic proliferation without increased blasts, and peripheral blood showed predominant neutrophilia with only mild eosinophilia. Cytogenetic analysis identified a t(5;14) translocation. RNA sequencing detected an in-frame CCDC88C exon 12::PDGFRB exon 11 fusion, and targeted sequencing additionally identified an ATM frameshift mutation. Treatment with low-dose imatinib (200 mg daily) led to rapid normalization of leukocyte counts within one week and sustained hematologic remission during follow-up. This case broadens the clinicopathologic spectrum of CCDC88C::PDGFRB-rearranged neoplasms and highlights the value of RNA sequencing in identifying actionable kinase fusions in atypical myeloproliferative presentations.

Several RET-targeted agents, including highly selective RET inhibitors (SRIs) and multi-kinase inhibitors (MKIs), have been approved for the treatment of advanced medullary thyroid cancer (MTC). Despite these agents targeting the same pathway, direct comparative data is lacking. This study aims to evaluate the relative efficacy and safety of these agents via network meta-analysis (NMA).

We systematically searched PubMed, Embase, Cochrane Library, Web of Science, and CNKI (up to March 2026) for RCTs evaluating RET-targeted therapies for advanced MTC. The primary outcome was progression-free survival (PFS); secondary outcomes included objective response rate (ORR) and ≥Grade 3 adverse events (AEs). A frequentist random-effects model was employed, and treatments were ranked using P-scores. The study was registered in PROSPERO (CRD420261342793).

Five RCTs (n = 1,076) were included. Selpercatinib demonstrated the most significant PFS benefit (HR = 0.10, 95% CI: 0.05-0.18; P-score = 0.999), outperforming cabozantinib (HR = 0.28) and vandetanib (HR = 0.46). It also ranked first for ORR (OR = 122.6, 95% CI: 34.5-435.6). Regarding safety, selpercatinib showed no significant difference in ≥Grade 3 AEs compared to placebo (OR = 1.34), whereas anlotinib exhibited the highest toxicity (OR = 12.00). Although selpercatinib was associated with hepatotoxicity (OR = 4.20), it avoided the off-target toxicities typical of MKIs, such as hypertension and diarrhea.

This network meta-analysis demonstrates that selpercatinib exhibits superior efficacy (PFS and ORR) and a more favorable safety profile compared to MKIs for advanced MTC. These results support its role as a recommended first-line option for advanced MTC. However, due to the heterogeneity of included populations (mixed RET mutation status and therapy lines), clinicians should interpret these findings with caution regarding the generalizability to strictly defined RET-mutant populations. Clinical decisions should be individualized.Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420261342793, identifier CRD420261342793.

Breast cancer (BC) is the most common cancer among women worldwide, and age significantly influences prognosis. In July 2024, Luxembourg expanded BC screening programme (Programme Mammographie, PM), changing the eligible age from 50-69 to 45-74 years. This study assessed age-related BC prognosis before expansion.

This retrospective cohort study analysed 3,003 women diagnosed with invasive BC in Luxembourg (2013-2018) using National Cancer Registry data. Patients were stratified into four age groups: <40, 40-49, 50-69, and ≥70 years. Tumour characteristics, treatment, and five-year overall survival (OS) were compared across groups using Kaplan-Meier and Cox proportional hazards models.

Younger patients (<40 years) showed higher triple-negative tumours (24%, P<0.001) and chemotherapy use (78%). Five-year OS varied by age group, with the highest rates in women aged 40-49 (95.3%) and 50-69 (92.3%), followed by those <40 (91.0%), and lower survival in women ≥70 (65.4%) (P<0.001), a finding that partly reflects competing causes of mortality in this age group rather than BC prognosis alone. Screen-detected cases had better survival (95.8%). Advanced stage (hazard ratio [HR]=2.92, 95% confidence interval [CI]: 2.05-4.17) and triple-negative subtype (HR = 2.39, 95% CI: 1.69-3.38) linked to worse prognosis. Mastectomy (HR = 2.04) and absence of surgery (HR = 8.58) were associated with poorer survival, likely reflecting disease complexity rather than causal treatment effects.

Age at diagnosis influences BC prognosis through distinct tumour characteristics, including molecular subtype, histology, clinical stage, and mode of detection, which collectively impact treatment and survival. Women aged 40-49 and 50-69 achieved the most favourable survival outcomes. Among women in the established screening target group (50-69 years), early detection through organised mammography was associated with particularly high survival, reinforcing the value of standardised early detection in this group. Younger patients presented with more aggressive tumour biology, while older patients showed lower OS, an estimate that substantially reflects competing causes of death, including cardiovascular disease and other malignancies, in addition to any BC-attributable mortality disadvantage. These findings establish a baseline for evaluating expanded PM and highlight the need for age-specific strategies.

Feline mammary carcinomas (FMCs) are heterogeneous neoplasms often comprising multiple histological patterns within a single case. The current practice of focusing on a prominent subtype hinders prognostic accuracy and potentially produces suboptimal therapeutic decisions. This retrospective study proposed criteria for grouping these mixed patterns and evaluated their prognostic significance in FMCs. The criteria were based on the tubular carcinoma composition and adopted from those of human breast cancer. Eighty-seven cats with FMCs were divided into groups according to tubular carcinoma composition: pure tubular carcinoma (PTC, n = 34), tubular carcinoma mixed with other subtypes (TMC, n = 16), and nontubular carcinoma (NTC, n = 37). Prognostic factors and overall survival (OS) were compared among the groups. The PTC and TMC groups were significantly associated with early-stage FMCs (P = .03) and low argyrophilic nucleolar organizer region values (P = .02). Conversely, NTCs had the poorest prognosis (P = .03) and were associated with incomplete surgical margins (P = .004), advanced clinical stage (P < .001), and high histological grade (P < .001) on multivariable analysis. Median OS for the PTC, TMC, and NTC groups was 221, 242, and 147 days, respectively. Considering individual histological subtypes, cats with adenosquamous carcinoma had a shorter OS (60 days) than those with comedocarcinoma (147 days) and tubular carcinoma (240 days, P < .001). These criteria were associated with FMC outcome in this cohort, providing a potentially useful framework for prognosis. However, further validation through prospective studies is needed to fully establish their clinical utility.

Adrenocortical oncocytomas are rare adrenal neoplasms and are most often reported as nonfunctioning adenomas. A minority, however, exhibit steroid hormone hypersecretion and may present with Cushing's syndrome, pheochromocytoma-like syndromes, feminization in males, or virilization in females. Adrenocortical oncocytoma presenting with primary aldosteronism is an exceptionally uncommon entity.Case presentation: We report a 44-year-old man with severe hypertension and hypokalaemia, accompanied by a right adrenal lesion on computed tomography. A comprehensive renin-angiotensin-aldosterone system evaluation and confirmatory testing supported primary aldosteronism. Adrenal venous sampling demonstrated right-sided aldosterone secretion dominance. The patient subsequently underwent laparoscopic right adrenalectomy. Postoperative histopathology identified an adrenocortical oncocytoma. Immunohistochemistry for aldosterone synthase (CYP11B2), together with biochemical findings and functional interpretation at the cellular level, supported the diagnosis of an aldosterone-secreting adrenocortical oncocytoma.

The patient achieved biochemical correction and clinical improvement, with favourable outcomes at 19-month follow-up. Although most oncocytomas behave benignly, this tumour type carries potential malignant risk. Once adrenocortical oncocytoma is diagnosed, surgical resection is recommended to reduce the risk of recurrence and metastasis.