The dural venous sinus system (DVSS) plays a central role in cerebral venous drainage and cerebrospinal fluid (CSF) reabsorption. Compromise of the DVSS is traditionally thought to predispose patients to elevated intracranial pressure and hydrocephalus. However, research evaluating this relationship is often scarce.

To determine whether compromise of the DVSS system, especially the superior sagittal sinus, is associated with an increased risk of hydrocephalus in pediatric and young adult patients.

We performed a retrospective cohort study (n = 62) of pediatric and young adult patients (≤23 years of age) with radiologically confirmed dural venous sinus compromise (sinus thrombosis or stenosis) who were treated within the Montefiore Hospital system from 2016 to 2025. DVSS compromise etiologies included infection, congenital malformations, hypercoagulability/neoplasm, and other causes. Patients were categorized based on the presence or absence of hydrocephalus. Baseline demographics, DVSS sinus involvement, etiology, and clinical outcomes including herniation were analyzed. Group comparisons were performed using appropriate univariate tests. A multivariable logistic regression model evaluated predictors of hydrocephalus, adjusting for age, sex, ethnicity, etiology, number of compromised sinus categories, specific sinus involvement, and herniation.

Sixty-two patients with radiologically confirmed dural venous sinus compromise were identified, of whom 8 (13%) developed hydrocephalus. Patients who developed hydrocephalus were significantly younger than those who did not (mean age 7 vs. 13 years, P = 0.024) and were more frequently male (88% vs. 41%, P = 0.036). There were no significant differences between groups in the distribution of specific sinus involvement (P = 0.418), number of compromised sinus categories (P = 0.520), pattern of sinus involvement (P = 0.454), or etiology (P = 0.966). Herniation occurred more frequently in patients who developed hydrocephalus (38% vs. 9%), though this did not reach statistical significance on univariate analysis (P = 0.097). On multivariable logistic regression adjusting for age, sex, and herniation, only herniation was independently associated with hydrocephalus OR 18.22 (95% CI 1.61-374.76; P = 0.029). Age demonstrated a protective trend OR 0.99 (95% CI 0.97-1.00; P = 0.073), while male sex was not independently associated with hydrocephalus OR 5.77 (95% CI 0.67-129.3; P = 0.155).

In this cohort, hydrocephalus development was not independently associated with compromise of any dural venous sinus, nor was it associated with the total number of affected dural venous sinuses. Instead, the presence of brain herniation was the only predictor associated with hydrocephalus. Patients with younger age and male sex were associated with hydrocephalus on univariate analysis but did not remain independently significant after adjustment. These findings suggest that compensatory venous and CSF drainage pathways may mitigate the impact of dural venous sinus compromise on hydrocephalus formation in children and young adults. Further, important clinical factors such as age, sex, and brain herniation may play a more critical role in the surgical management of these patients than previously considered. These findings suggest that further investigation with larger studies should be performed to further evaluate the relationship between DVSS compromise and hydrocephalus development.

Solitary fibrous tumors (SFTs) are rare mesenchymal neoplasms with variable clinical behavior, ranging from indolent to aggressive. Immunohistochemical data regarding p16 and ß-catenin are conflicting, a direct comparative analysis of both makers has not been carried out and a correlation with the Demicco grading system is missing. A cohort of 30 surgically resected SFTs was analyzed by 11 immunohistochemical markers (p16, p53, Ki-67, PHH3, Cyclin E1, STAT6, ß-catenin, CD34, Vimentin, BCL2, CD99). Results (with a focus on p16 and ß-catenin) were statistically compared with the Demicco grading and available clinicopathological parameters. Three immunophenotypic subgroups were identified: p16+/ β-catenin- (12/30, 40%), p16-/ β-catenin+ (10/30, 33.3%) and double-negative (8/30, 26.7%); co-expression was not observed. The p16+ subtype showed higher Demicco scores, heterogeneous but often increased proliferative activity, frequent p53 alterations and the highest rate of metastases. In contrast, the β-catenin+ subtype occurred exclusively in pleuropulmonary SFTs and was associated with intermediate Demicco scores. Double-negative tumors clustered within the low-risk Demicco category and showed uniformly low proliferation indices. Overall, the three subtypes correlated significantly with Demicco risk classification (p = 0.0088). We identified three SFT subgroups based on p16 and β-catenin expression, which correlate with established Demicco risk categories and tumor localization. These markers may complement existing risk stratification and highlight biologically distinct subsets of SFT. Further studies are warranted to validate their clinical utility, particularly given their reproducibility and ease of implementation in routine diagnostic practice.

Patients undergoing cancer-related scans often experience scan-associated anxiety, which can significantly impact their mental well-being. So far, this so-called scanxiety has not been clearly defined, even though it has gained more attention. This study investigated features of scanxiety in cancer patients.

Two nominal group technique (NGT) sessions were conducted with curatively treated and advanced cancer patients. In the first round, participants took turns sharing features of scanxiety, followed by a group discussion to clarify unclear or overlapping features. Finally, participants rated the extent to which they thought features applied to scanxiety. Additional to the NGT sessions, interviews were conducted with patients and healthcare professionals to provide further insights. Findings from the NGT sessions and interviews were collated and reviewed by the research team using a qualitative content analysis.

A total of 16 patients (9 men and 7 women) participated in the NGT sessions and an additional 14 people were interviewed (3 patients and 11 healthcare professionals). The NGT sessions and interviews initially generated 72 and 67 features, respectively. After merging and removing duplicates, the final list of features included 63 features. Following discussions in the multidisciplinary research team informed by predefined decision rules, 23 features were identified as unique to scanxiety. These features reflect emotional, cognitive, behavioural, physiological and physical reactions, social and interpersonal characteristics, and care- and process-related characteristics associated with scanxiety.

This study provides a first comprehensive characterisation of scanxiety by identifying features that are unique to anxiety associated with cancer-related scans and lays the groundwork for improved assessment and targeted support in cancer care.

IntroductionDysregulated epidermal growth factor receptor (EGFR) signaling is a key mechanism driving cancer progression and metastasis. Owing to its frequent overexpression in pancreatic cancer (PCa), EGFR has become a desirable molecular target for targeted therapies. XYZ-I-73 (N-(5-fluoro-2-oxo-1-(tetrahydrofuran-2-yl)-1,2-dihydropyrimidin-4-yl) dodecanamide), a structural analog of 5-fluorouracil (5-FU), has been previously synthesized and shown to exhibit cytotoxicity against PCa cells.MethodsXYZ-I-73 was entrapped in liposomes via thin-film hydration and subsequently conjugated to EGFR antibodies to produce an immunoliposome formulation- Ab-XYZ-I-73LnP (where 'Ab' denotes antibody-conjugated and 'LnP' denotes liposomal nanoparticle). In vitro efficacy was assessed by measuring cell viability and apoptosis in MiaPaCa-2 and PANC-1 cells, while pharmacokinetics and antitumor efficacy were determined in a cell line-derived xenograft (CDX) mouse model.ResultsAb-XYZ-I-73LnP exhibited a mean particle size of 143nm ± 2.3, PDI (0.37), and zeta potential -46.2 ± 1.3mV. In MiaPaCa-2 cells, Ab-XYZ-I-73LnP showed remarkably higher cytotoxicity than 5-FU in both 2D (IC₅₀ = 2.5 ± 0.9μM vs 13.2 ± 1.1μM) and 3D cultures (IC₅₀ = 8.1 ± 1.1μM vs 26.7 ± 1.1 μM). Similarly, in PANC-1 cells, Ab-XYZ-I-73LnP showed lower IC₅₀ values compared to 5-FU;2D (IC₅₀ = 2.9 ±1.1 μM vs 20.4±1.2 μM), 3D (IC₅₀ = 12.9 ± 0.6μΜ vs 37.1±0.9 μM). Pharmacokinetic analysis revealed a prolonged half-life for Ab-XYZ-I-73LnP compared with free 5-FU (t1/2 = 1.62 ± 0.03 h vs 0.49 ± 0.01 h, p < 0.001). There was about a 2-fold increase in the area under the curve (AUC) for Ab-XYZ-I-73LnP compared to 5-FU (AUC= 0.32 ± 0.04µg/(L*hr) vs 0.15 ± 0.02µg/(L*hr), p<0.01).ConclusionOverall, the study supports the formulation of an immunoliposome of modified 5-FU, which may significantly enhance drug bioavailability and therapeutic potential for the treatment of PCa.

The mechanisms underlying the interactions between disseminated tumor cells (DTCs) and their tissue microenvironment during metastatic colonization are currently poorly understood. We integrated multimodal single-cell and spatial profiling from liver cancer mouse models and human metastases to track the spatiotemporal dynamics of DTCs and their microenvironments from single-cell seeding to overt lung metastasis. We identified a residual population of quiescent Phgdh^high DTCs that survived initial innate immune clearance and became transiently enriched in micrometastases. These cells shaped an immune-scarce microenvironment through PHGDH-dependent, H3K27me3-mediated epigenetic silencing of chemokine transcription, thereby promoting metastatic expansion. Cx3cr1^high interstitial macrophages were also transiently enriched before DTC expansion, creating an immune-privileged niche for metastatic outgrowth by recruiting immunosuppressive cells. Inactivating the PHGDH-H3K27me3 axis in DTCs or depleting interstitial macrophages restored immune surveillance and inhibited metastatic colonization. These findings provide insights into the development of micrometastasis-targeting regimens.

Lymphangioleiomyomatosis (LAM) is a rare disease of unknown etiology that occurs almost exclusively in women, primarily of reproductive age. This disease is characterized by smooth muscle cell proliferation, most commonly in the lungs. However, cases of extrapulmonary LAM have been reported, such as in the lymph nodes of mediastinum, abdominal cavity, and retroperitoneum. The clinical manifestations of pelvic lymph node LAM are subtle manifesting as symptoms of compression due to a large tumor mass but more often diagnosed incidentally in lymph node specimens removed during gynecologic oncology surgeries. This article provides literature data and our own observation of lymph node LAM in a patient with metastatic endometrial cancer.

The paper presents a clinical case of appendiceal mucinous adenocarcinoma with invasion into the right ovary, imitating an ovarian tumor. The primary tumor was diagnosed only after a pathological evaluation of the surgical material with differential immunohistochemical assay after laparotomy and removal of the ovarian tumor and appendectomy. Difficulties in establishing an accurate diagnosis were caused by extensive invasion of the appendiceal tumor into the ovary. This disease requires increased oncological alertness and a clear algorithm for differential diagnosis of mucinous tumors of the appendix and ovary.

To determine the molecular genetic characteristics of the epithelial neoplasia of extrahepatic bile ducts (EHD) depending on the degree of epithelial dysplasia in order to identify mutations that facilitate their differential diagnosis.

The study included 44 EHD biopsies containing epithelial neoplasms and cholangiocarcinoma. All samples underwent massive parallel sequencing of DNA isolated from 10-μm-thick histological sections. Mutations of categories I-III of clinical significance were considered. Statistical analysis of the obtained data utilized a two-tailed Pearson χ² test with Holm's correction for multiple comparisons (p<0.045).

The most frequent mutations in epithelial neoplasia of the EHD were identified: MYC, KRAS, PIK3CA, CDKN2A, ERBB2, KIT 6, TP53 6, FBXW7, POLE and TERT. The highest proportion of mutations was in biliary intraepithelial neoplasia and cholangiocarcinoma. Among epithelial neoplasia and cholangiocarcinoma, mutations in KRAS, POLE and TERT differed significantly. KRAS (p<0.045) - BilIN LG and BilIN HG, IPNB HG and cholangiocarcinoma; POLE (p<0.045) - BilIN LG and cholangiocarcinoma; TERT (p<0.045) - BilIN LG and cholangiocarcinoma. Specificity and sensitivity indicators for KRAS were 28 and 50%; POLE - 35 and 100%; TERT - 100 and 100%.

Mutations have been identified that should be considered in the differential diagnosis of the degree of epithelial dysplasia and the types of epithelial neoplasia of the extrahepatic bile ducts.

To study the morphological patterns of immune-related cutaneous lesions (irCLs) that occur during antitumor immunotherapy in cancer patients.

The study included 48 patients with the following nosology: malignant neoplasms of the skin and soft tissues - 20 patients (41.7%), malignant neoplasms of the genitourinary system - 13 (27%), malignant neoplasms of the lungs and bronchi - 9 (18.8%), malignant neoplasms of the upper respiratory tract - 5 (10.4%), malignant neoplasms of the gastrointestinal tract - 1 (2.1%), with immune-mediated skin lesions during treatment with pembrolizumab - 25 (52.1%), nivolumab - 18 (37.5%), prolgolimab - 4 (8.3%), avelumab - 1 (2.1%).

Among the irCLs in the study cohort, lichenoid - 14 (29.2%) cases and psoriasiform - 11 cases (22.9%) were predominant, while other morphological variants were significantly less common. IrCL morphologically mimic classic dermatoses, but have distinctive features indicating their drug-induced, immune-related nature.

The study demonstrated that irCLs are clinically significant complications of PD-1/PD-L1 inhibitor therapy. Histological analysis confirmed their immunoinflammatory nature and revealed characteristic morphological changes, emphasizing the importance of routine skin biopsies for optimal patient management.

Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, driven by late-stage diagnosis, metastatic progression, and therapeutic resistance. Src homology region 2 domain-containing phosphatase 2 (SHP2) has emerged as a critical regulator of oncogenic signaling in gastric tumorigenesis, yet its therapeutic targeting remains underexplored. In this study, we evaluated the anti-cancer efficacy of NSC 57774, a novel SHP2 inhibitor, using integrated bioinformatics and functional assays in AGS gastric cancer cells. Analysis of The Cancer Genome Atlas (TCGA) and UALCAN datasets revealed marked upregulation of SHP2 and multiple receptor tyrosine kinases in gastric cancer tissues. NSC 57774 potently inhibited cell proliferation and migration, demonstrating selective cytotoxicity towards cancer cells over non-cancerous fibroblasts. Mechanistically, NSC 57774 disrupted key oncogenic pathways including MAPK/ERK, AKT and STAT3 in a concentration- and time-dependent manner, with higher doses achieving more sustained pathway suppression. NSC 57774 suppressed NF-κB inflammatory signaling at early timepoints and induced cleaved caspase-3 across all treatment groups at 72 hours, indicative of pro-apoptotic activity. A paradoxical late-phase increase in phospho-p38 was observed at 72 hours, consistent with a compensatory pro-apoptotic stress response. Comparative analysis revealed that NSC 57774 outperformed the commercial SHP2 inhibitor NSC 87877 and doxorubicin in reducing viability and migration of gastric cancer cells. Collectively, these findings position NSC 57774 as a promising candidate for targeted gastric cancer therapy, capable of disrupting multiple signaling pathways involved in tumor progression, metastasis, and inflammation, warranting further preclinical and clinical investigation.