In histoplasmosis-endemic regions, pulmonary nodules often raise concern for malignancy. Distinguishing benign infectious granulomas from neoplastic lesions while limiting invasiveness is a major diagnostic challenge.

We report a case series of 11 patients diagnosed with nodular pulmonary histoplasmosis at the University Hospital of Guadeloupe, a French West Indies institution located in an endemic area. Clinical, radiologic, microbiologic, and histopathologic data were retrospectively reviewed.

All 11 patients presented with solid pulmonary nodules associated with mediastinal and/or hilar lymphadenopathy, mimicking locally advanced lung cancer. Among the nine patients who underwent 18F-FDG PET/CT, all but one showed hypermetabolic activity in the nodule. Five patients were immunocompromised, and notably, four of the eleven patients were treated for rheumatoid arthritis. Diagnosis was established through surgical resection in five cases, percutaneous or lymph node biopsy in another five, and bronchoalveolar lavage (BAL) alone in one patient. Serologic testing was positive in all five patients tested, and H. capsulatum PCR on BAL was positive in two of the four cases tested. Exposure history and clinical context supported the diagnosis in several cases, but noninvasive tests alone were generally insufficient to exclude malignancy.

This series illustrates the diagnostic difficulty of pulmonary nodules in histoplasmosis-endemic areas and the frequent need for invasive procedures. The development of improved, noninvasive diagnostic strategies is essential to avoid unnecessary surgery while ensuring timely cancer diagnosis.

Uterine sarcomas are rare heterogeneous neoplasms, comprising only a small percentage of uterine malignancies. There is a diverse array of uterine sarcoma sub-types, each with distinct molecular, clinical, and behavioral features. In recent years, there has been significant advancement in all facets of the multi-disciplinary management of uterine sarcomas. Despite this, several challenges regarding optimization of treatment remain. Pre-operative diagnosis can be difficult, as imaging and biopsy may not reproducibly distinguish uterine sarcomas from benign entities. Early-stage uterine sarcomas are potentially curable with surgery; however, there remains a high risk of recurrence, and the use of adjuvant treatment is controversial. There is also a lack of high-quality data to guide best practices for fertility-sparing surgery in younger patients. Optimal management requires multi-disciplinary discussion by clinicians experienced in sarcoma management at specialized sarcoma centers, as initial management may have a profound impact on patient outcomes. In this review, we summarize and address many of these challenges facing patients with early-stage uterine sarcoma, and provide a comprehensive update on the clinical features, the molecular and genomic pathogenesis, and the current diagnostic and treatment landscape for these patients.

Antibody-drug conjugates (ADC) have emerged as an important part of systemic treatment across disease sites. To date, there is no robust pooled prevalence estimate of nausea and vomiting induced by ADCs. Establishing such estimates is essential to determine if ADC-induced nausea and vomiting (ADCINV) represents a clinically significant problem warranting further research into antiemetic prophylaxis. Our aim is to report the prevalence of reported ADCINV across literature.

A systematic search of Medline, Embase, Cochrane CENTRAL and Web of Science was conducted from database inception until September 24, 2025. Articles were included if they reported nausea and/or vomiting due to ADCs used in cancer treatment, in the abstract. Pooled prevalence was reported. Subgroup analysis was conducted by ADC. Meta-regression was conducted by age and sex. Quality assessment was conducted. Type I error was set at 0.05.

A total of 209 studies with 15,493 patients were included. Thirty-nine percent (95%CI, 36-42%) of patients experience any nausea, and 26% (95%CI, 23-29%) experience any vomiting. Younger patients are more likely to experience nausea; each 10-year increase in age is associated with a 12% decrease in nausea rates. Higher emetogenic ADCs include trastuzumab deruxtecan, sacituzumab govitecan, brentuximabvedotin and patritumab deruxtecan. Lower emetogenic agents include disitimab vedotin, telisotuzumab vedotin and rovalpituzumab tesirine.

This is the first study to report prevalence of ADCINV across ADCs. It is a prevalent adverse effect akin to chemotherapy-induced nausea and vomiting that should be viewed as clinically relevant and further investigated to help develop optimal strategies related to antiemetics.

Breast cancer is a common malignant tumor with limited treatment options and poor prognosis. SNRPB2, a core spliceosomal component involved in pre-mRNA splicing, is dysregulated in multiple cancers, but its role in breast cancer remains incompletely understood.

We analyzed SNRPB2 expression in breast cancer using TCGA, CPTAC, and HPA databases, and assessed its prognostic value via Kaplan-Meier plotter. The biological function of SNRPB2 was evaluated through in vitro cell line assay, and the underlying molecular mechanisms were determined via RNA-seq, RT-qPCR, and additional GEO datasets. Our findings demonstrated that SNRPB2 was significantly overexpressed in breast cancer tissues and correlated with malignant progression and poor prognosis. Knockdown of SNRPB2 induced G2/M cell cycle arrest in cancer cells, decreased expression of numerous genes related to cell cycle and immune modulation, and triggered alterations in multiple alternative splicing events. Mechanistically, SNRPB2 knockdown might promote cancer cell cycle arrest by regulating HMGA2 splicing and expression, while simultaneously suppressing the expression of immune-related genes such as CSF1, CSF1R, IL6, and CX3CL1. Immune infiltration analysis revealed that SNRPB2 expression correlated with increased infiltration of activated inflammatory cells and myeloid-derived suppressor cells.

SNRPB2 potentially plays a dual role in promoting breast cancer progression and shaping the immunosuppressive microenvironment, partly through HMGA2 splicing modulation and immune-regulatory gene suppression. These findings suggest that SNRPB2 may represent a promising therapeutic target for breast cancer.

Tumor is a major disease that seriously threatens human health, and its occurrence and progression involve complex interactions between the genome, epigenome, and environmental factors. Epigenetic modifications-such as DNA methylation, histone modifications, non-coding RNA regulation, and mRNA modifications-play key roles in tumor progression, metastasis, and drug resistance. Natural medicines offer multi-target and holistic regulatory effects, showing unique advantages in cancer therapy. Emerging evidence suggests that natural medicines and its active components can exert anti-tumor activities by modulating epigenetic mechanisms. This review summarizes natural medicines-mediated epigenetic regulation against tumors. It details how natural medicines influences DNA methylation by suppressing DNA methyltransferases (DNMTs) and altering tumor suppressor gene promoter methylation. The modulation of histone modifications through targeting histone deacetylases (HDACs), histone lysine methyltransferases (HKMTs), and histone lysine demethylases (HKDMs) is also discussed. Furthermore, the review covers natural medicines's regulation of non-coding RNAs (e.g., lncRNAs, miRNAs, circRNAs) and their downstream pathways, as well as its role in mRNA modifications, notably N6-methyladenosine (m6A). Overall, this work highlights the epigenetic potential of natural medicines in tumor therapy, enhancing the mechanistic understanding of its anti-tumor effects and supporting natural medicines modernization and precision oncology. However, challenges remain due to natural medicines complexity and tumor epigenetic heterogeneity, calling for deeper investigation and clinical validation.

Phakomatoses, also known as neurocutaneous syndromes are rare disorders characterized by multisystem involvement with variable neurological manifestations in children, including intracranial vascular malformations. Cavernous malformations may present with acute haemorrhage and stroke-like symptoms. Diagnostic difficulty arises when radiologic findings suggest a benign lesion, yet histopathology reveals discordant malignant pathology.

An 8-year-old female presented with sudden-onset left hemiparesis and recurrent seizures. Physical examination revealed multiple cutaneous naevi, raising suspicion of a syndromic association. Brain magnetic resonance imaging demonstrated a well-circumscribed right parietal intra-axial lesion with a "popcorn" appearance and hypointense susceptibility blooming, highly suggestive of a cavernous malformation. Cranial computed tomography scan subsequently showed an associated large intracerebral haematoma. The patient underwent right parietal craniotomy with haematoma evacuation and excision of the lesion. The immediate postoperative course was initially satisfactory with neurological improvement. Histopathological examination of the excised specimen, however, revealed a malignant neoplasm, establishing a significant radiologic-histologic discordance which fundamentally altered the diagnostic interpretation. The patient had a relapse of symptoms two months after surgery, with repeat neuroimaging showing multicentric tumour recurrence, necessitating referral for adjuvant neuro-oncologic management.

This case illustrates a rare diagnostic pitfall and challenge in paediatric neurosurgery, where a malignant intracranial tumour mimicked a cavernous malformation in the context of cutaneous stigmata. The report emphasizes the limitations of neuroimaging alone and underscores the importance of careful clinicoradiologic correlation, histopathological confirmation, and multidisciplinary evaluation when managing presumed vascular lesions in children, particularly in resource-limited settings.

We present a case of a primary subcutaneous sarcoma harboring an ATXN1::DUX4 gene fusion in a 52-year-old female, representing to our knowledge the first documented occurrence of this molecular subtype arising in soft tissue. The tumor presented as a painless back mass, clinically mimicking a lipoma. Histologic examination revealed an aggressive neoplasm with round to epithelioid morphology, high mitotic activity (30/2 mm²), geographic necrosis, and focal myxoid stroma. Immunohistochemically, the tumor showed focal strong ALK (D5F3) expression, partial membranous CD99 positivity, and focal nuclear WT1 expression (with diffuse non-specific cytoplasmic staining). A broad panel of other lineage-specific markers was negative, while INI1 and BRG1 expression was retained. ALK and CIC break-apart fluorescence in situ hybridization (FISH) were negative. Targeted RNA sequencing identified an in-frame ATXN1::DUX4 fusion (exon 8 to exon 1), which retains the AXH domain of ATXN1. The fusion was validated by RT-PCR and Sanger sequencing, and an ATXN1 break-apart FISH assay confirmed rearrangement in 65% of tumor nuclei. DNA methylation analysis demonstrated that the tumor clustered with CIC-rearranged sarcomas.The patient experienced local recurrence five months after resection despite adjuvant chemotherapy. Recent functional studies have demonstrated that ATXN1::DUX4 activates CIC target genes in an AXH domain-dependent manner, supporting its classification within the emerging family of CIC/ATXN1 pathway-altered sarcomas. This case expands the anatomic spectrum of ATXN1::DUX4-fusion sarcomas and provides further epigenetic evidence supporting their inclusion within the CIC/ATXN1 pathway-altered sarcoma family.

Locoregional CAR-T delivery is increasingly explored for glioblastoma to improve intracranial tumor exposure; however, organ-level biodistribution kinetics after intracranial administration remain poorly quantified in vivo, limiting route-informed optimization and preclinical risk assessment. Here, we report a dual-modality cell labeling and tracking strategy based on indocyanine green-conjugated iron nanoparticles (ICG-NPs) for in vivo assessment of B7-H3-targeting CAR-T cell (TX103) biodistribution using second near-infrared window (NIR-II) fluorescence imaging and magnetic resonance imaging (MRI). Using a heparin-protamine-assisted protocol, TX103 cells were labeled with high efficiency (83.1%) without detectable changes in viability, CAR expression, immunophenotype (including activation/exhaustion marker profile and CXCR3 expression), or cytotoxic function. In vitro imaging demonstrated a linear correlation between NIR-II fluorescence intensity and labeled cell numbers (R² = 0.973, p < 0.001), while MRI provided complementary anatomical context at higher cell densities. In an orthotopic glioma mouse model, longitudinal MRI and NIR-II imaging captured route-dependent differences in tumor-associated localization and whole-body biodistribution following intracerebroventricular and intravenous administration. Furthermore, organ-level NIR-II exposure showed a positive association with CD3⁺ T-cell density across organs (R² = 0.552, p < 0.001), supported by multi-organ pathological validation. Collectively, we establish a biocompatible dual-modality workflow that links intracranial anatomical localization with longitudinal whole-body biodistribution readouts for preclinical CAR-T tracking in solid tumor models.

Adaptive radiotherapy (ART) has been shown to improve geometric and dosimetric accuracy, with emerging evidence for clinical benefit, but it remains resource-intensive and lacks scalability. This limitation arises from multiple factors, including the complexity of current systems, the closed and proprietary nature of radiotherapy platforms, and the need for human oversight driven in part by clinical risk considerations. Historically, major advances in radiotherapy-from Intensity-Modulated Radiation Therapy (IMRT) and Image-Guided Radiation Therapy (IGRT) to Magnetic Resonance-guided Radiotherapy (MRgRT) and Deep Learning in Radiotherapy (DLinRT) (particularly for auto-contouring)-have thrived through open collaboration and transparency. The community can accelerate ART innovation by returning to this model. Open-source initiatives such as Computational Environment for Radiotherapy Research (CERR), Open Knowledge-based Planning (OpenKBP), and matRad demonstrate how shared tools and methods improve reproducibility and drive scientific progress. The next critical step is to develop collaborative, structured frameworks that enable safe, secure interaction between academic and vendor systems-safeguarding intellectual property while fostering co-development and validation. Through structured transparency and shared accountability, the radiotherapy field can transform automation from a closed, non-transparent architecture into a collective learning ecosystem, ultimately extending the life-saving benefits of ART to more patients worldwide through openness, trust, and collective innovation.

Despite the growing evidence of persistent cognitive dysfunction after COVID-19, the role of cognitive reserve as a modifying factor of post-infectious neurocognitive outcomes remains insufficiently explored, particularly in relation to disease severity and premorbid lifestyle characteristics.

To analyze the characteristics of cognitive reserve in patients after SARS-CoV-2 infection and to assess its impact on the structure and severity of post-COVID cognitive impairments.

The study included 247 patients aged 31-67 years who had recovered from COVID-19 (93 hospitalized and 154 treated on an outpatient basis) and 50 age-matched controls without a history of COVID-19. Cognitive reserve and related factors were assessed using the Cognitive Reserve Questionnaire (CRQ), Test of Premorbid Functioning (TOPF), Montreal Cognitive Assessment (MoCA), Trail Making Test A/B, Digit Span Backward, and semantic verbal fluency test. Premorbid lifestyle characteristics, occupational cognitive complexity, physical activity, disease severity, body mass index, and inflammatory markers (peak C-reactive protein) were recorded. Multivariate linear regression models were constructed with global cognitive performance (MoCA score at 12 months) as the dependent variable.

Post-COVID patients demonstrated significantly lower CRQ total scores compared with controls (7.82±0.12 vs 9.41±0.15; p<0.001), with the lowest values observed in hospitalized patients. Educational level and premorbid intelligence (TOPF) did not differ between groups, indicating preserved premorbid cognitive capacity. Reduced CRQ scores were primarily driven by lower occupational cognitive complexity and diminished cognitively active lifestyle, suggesting impaired utilization of cognitive reserve rather than loss of reserve capacity. MoCA scores were significantly lower in post-COVID patients (25.4±0.19 vs 27.8±0.22; p<0.001), with predominant impairment of executive functions, attention, and processing speed. In multivariate analysis, better cognitive outcomes were independently associated with higher CRQ scores, greater occupational complexity, and higher premorbid physical activity, while disease severity, elevated inflammatory markers, and older age were associated with poorer MoCA performance (Adjusted R²=0.521; p<0.001).

Post-COVID cognitive impairment occurs despite preserved premorbid cognitive reserve and is characterized by reduced utilization and engagement of reserve mechanisms, particularly following severe disease.