Emerging evidence suggests that GRIP and coiled-coil domain-containing two enriched small extracellular vesicles (sEV-GCC2) may serve as diagnostic biomarkers of early-stage lung adenocarcinomas. However, the roles of these molecules remain unclear. This study evaluated the diagnostic and prognostic potential of sEV-GCC2 for detecting early-stage lung adenocarcinoma and its tumourigenic role in vitro and in vivo. This retrospective multicentre study analyzed 470 plasma samples (320 lung adenocarcinoma patients, 150 controls; mean follow-up: 34.7 ± 24.0 months) across five institutions. Size-exclusion chromatography and enzyme-linked immunosorbent assay were used to measure sEV-GCC2 levels, whereas immunohistochemistry was used to confirm GCC2 expression in tumour tissues. Functional studies were performed using the PC9 and H1650 lung adenocarcinoma cell lines in vitro and the corresponding PC9-based preclinical models in vivo to evaluate the tumour-related effects of sEV-GCC2. Patients exhibited significantly elevated sEV-GCC2 levels compared to controls (area under the receiver operating characteristic (ROC) curve [AUC]: 0.904, P < 0.001), with similar results in stage TisN0-T1miN0 disease (AUC: 0.781, P < 0.001). sEV-GCC2 levels were associated with the pathological TNM stage and tumour location. Higher sEV-GCC2 levels were correlated with poorer recurrence-free survival (RFS), overall survival and recurrence rates, even in patients with stage 0-IA1 disease. Functional studies have revealed that sEV-GCC2, but not GCC2-deficient sEVs, promote cancer cell proliferation, tumour growth and lymph node metastasis in vitro and in vivo. These findings highlight the diagnostic and prognostic potential of sEV-GCC2 and its tumourigenic role in early-stage lung adenocarcinoma. This study was registered at ClinicalTrials.gov (NCT04529915).

Micro-neurosurgery and minimally invasive neurosurgery have become more common in intracranial procedures for lesions such as Intraventricular tumors, intracranial hematomas, and Posterior fossa tumors. Deep seated lesions require bidirectional retraction of normal overlying brain tissue for better surgical access. For past many decades, conventional retractor systems are in use without any significant modification or innovation. Here we are introducing a novel retractor system suitable for ergonomics of neurosurgeons without disturbing microscopic and endoscopic vision.

A total of eighty (80) patients of deep-seated intracranial lesions were included in the study between January 1, 2024 and April 1, 2025. Forty patients were operated by the Conventional retractor system and rest 14 were operated by our novel retractor system. Surgical and radiological parameters of both the retractor system were calculated and compared along with outcome assessment. CT perfusion was conducted pre- and post-operatively in both the groups. A questionnaire regarding assistance, ergonomics, and instrument handling compared to the conventional retractor system was performed. All patients were followed up for 3 months to observe for any new neurological deficits.

In microsurgery for deep seated tumors, conventional retractor got replaced with our novel retractor system. The mean operative time with novel Saraj Retractor was similar as with conventional retractor. However, time of application and adjustment were reduced. The mean cerebral blood flow and mean transit time were similar in both the retractor groups without any ischemic changes on the surrounding brain parenchyma. There were no intra-operative complications directly related to the use of the device.

Our Novel retractor system is facilitating safe separation of brain parenchyma bilaterally with minimal retraction pressure. It effectively reduces the time for assembly and attachment as compared to conventional retractor system. It reduces the surgeon's fatigue and minimizes the dependency on assistant surgeon.

Glioblastoma (GBM) is the most frequent primary malignant brain tumor characterized by aggressive growth and poor prognosis, frequently accompanied by cognitive and affective deficits that severely impair quality of life (QoL). However, the short-term course of these cognitive and emotional functions after surgical resection remains insufficiently understood.

This study aimed to investigate changes in cognitive performance and affective symptoms before and 3 months after GBM resection and to explore the influence of tumor characteristics such as lateralization and location. We hypothesized that cognitive function and affective symptoms would improve or remain stable postoperatively and that tumor-related factors would modulate these trajectories.

In this multicenter pre-post observational study, 37 adults with histopathologically confirmed GBM (World Health Organization [WHO] 2021) were assessed using the Montreal Cognitive Assessment (MoCA) and the Hospital Anxiety and Depression Scale (HADS). Paired t-tests, Wilcoxon tests, ANOVA, and linear regression were conducted to evaluate pre- to postoperative changes and correlations with tumor characteristics.

Cognitive performance remained stable after resection. Although the HADS total score showed no significant pre- to postoperative change, patients with preoperative anxiety or depressive symptoms demonstrated significant postoperative improvement (HADS-A p = 0.010; HADS-D p = 0.012). Higher preoperative HADS scores predicted greater symptom reduction. Higher affective burden was shown in patients with right-hemispheric and parieto-occipital tumors, while temporal lobe tumors were associated with anxiety that decreased after resection (p = 0.009).

GBM resection maintained cognitive function while improving affective symptoms in patients with elevated preoperative distress. Systematic psychological screening and tailored psychosocial interventions may enhance emotional resilience and QoL in GBM care.

Amelanotic melanoma lacks melanin and is more challenging to diagnose than pigmented melanoma, often leading to delayed detection and worse outcomes. We conducted a retrospective cohort study of 322 patients (28 with amelanotic melanoma and 294 with melanotic melanoma) treated at Sheba Medical Center between 2017 and 2023. Clinical features, treatment modalities, and 1-year outcomes were analyzed. Tumor stage at diagnosis was the strongest predictor of remission, disease progression, and mortality in both groups. Pigmentation was associated with a higher likelihood of treatment modification (p = 0.02) and showed a borderline association with progression (p = 0.08). Subgroup analysis by stage revealed no significant outcome differences except for increased therapy change in stage 2 melanotic melanoma. The findings reinforce the importance of early detection, especially in amelanotic melanoma.

Plant Homeodomain Finger Protein 6 (PHF6) gene mutations are rare in acute myeloid leukemia (AML), with unclear mechanisms and uncertain prognostic value. They may compromise risk stratification and treatment decisions. This study analyzed clinical features and survival outcomes in PHF6-mutated AML patients, evaluating the impact of allogeneic hematopoietic stem cell transplantation (HSCT) and co-mutations on prognosis. Precise stratification helps optimize prognostic models and guide individualized therapy.

This study retrospectively analyzed 45 AML patients with PHF6 gene alterations at our institution. Clinical features, treatment approaches, therapeutic outcomes, and gene co-mutation profiles were comprehensively assessed to determine their prognostic significance. Overall survival (OS), disease-free survival (DFS), and event-free survival (EFS) among different groups were compared using the Kaplan-Meier method and log-rank test. A multivariate Cox regression model identified independent prognostic predictors.

PHF6-mutated AML was associated with shorter OS compared with wild-type (p = 0.003), but PHF6 mutation was not an independent predictor of OS in multivariate Cox analysis. HSCT improved OS, DFS, and EFS compared with no transplantation (all p < 0.05). Median WBC at diagnosis was 2.04 × 10⁹/L; WBC ≥ 9.70 × 10⁹/L independently predicted poor prognosis. RUNX1 co-mutation correlated with shorter OS; IDH1/IDH2 co-mutation with longer OS. Neither affected DFS or EFS.

This study provides clinical evidence for prognosis assessment in PHF6-mutated AML, enabling more precise risk stratification, individualized treatment, and further pathogenesis research.

BACKGROUND Splenic marginal zone lymphoma (SMZL) is a low-grade B-cell lymphoma associated with chronic hepatitis C infection. It typically presents with diffuse splenomegaly rather than a focal splenic mass. Focal splenic lesions with vascular enhancement patterns are usually due to vascular tumors which may be benign or malignant, examples of which include sclerosing angiomatoid nodular transformation, hemangiomas, or angiosarcomas. CASE REPORT A 60-year-old man with newly diagnosed hepatitis C-related Child-Pugh A cirrhosis was incidentally found to have a splenic lesion during index abdominal imaging. He was initiated on hepatitis C treatment and successfully achieved a sustained virologic response. Despite viral eradication, serial imaging over 3 years demonstrated a sudden increase in size from 3.3 cm to 5.7 cm. Multiphasic computed tomography (CT) of the abdomen demonstrated a progressive peripheral-to-central enhancement pattern, mimicking a vascular splenic tumor. A review by a multidisciplinary tumor board recommended splenectomy due to progressive enlargement, rupture risk, and inability to exclude a malignant lesion. Histopathological examination revealed SMZL with extensive central infarction and granulomatous reaction, confirming the diagnosis with characteristic biphasic architecture and CD20-positive B-cell populations. No features of aggressive transformation were identified. CONCLUSIONS Our case highlights an unusual presentation of SMZL as a focal splenic mass, rather than diffuse splenomegaly, which grew despite hepatitis C eradication. Tumor infarction and slow organization can produce radiologic features that mimic vascular splenic lesions. This demonstrates the importance of clinicoradiological-pathological correlation and the necessity of histological confirmation in indeterminate splenic masses to avoid delays in management.

Sarcopenia has emerged as a potential prognostic factor in patients with advanced prostate cancer (PCa), requiring interventions for its prevention and treatment.

We aimed to systematically identify, critically assess and synthesize the available evidence on the effectiveness and safety of interventions for preventing or treating sarcopenia in advanced PCa patients.

MEDLINE, Embase and Web of Science were searched. Randomized and non-randomized controlled trials or longitudinal observational studies with a control group focusing on PCa patients aged 60 years and older were considered. Study selection, data extraction and risk-of-bias assessment of the included studies were performed in duplicate. When possible, pooled effect estimates were calculated.

Twenty studies (n = 1275) were included. Resistance training (RT) (MD = 3.22 kg; 95% CI 0.69, 5.75) and the use of antimyostatin peptibody (MD = 2.2 kg; SE 0.8%) demonstrated statistically significant prevention of lean body mass loss in men undergoing androgen deprivation therapy (ADT). Exercise improved leg press (MD = 25.17 kg; 95% CI [8.71, 41.62]), leg extension (MD = 9.63 kg; 95% CI [4.83, 14.42]), seated row (MD = 4.38 kg; 95% CI [1.54, 7.22]) and chest press strength (MD = 1.70 kg; 95% CI [-1.48, 4.88]) and enhanced patients' physical functioning in chair sit-to-stand tests (MD = -1.02 kg; 95% CI [-1.70, -0.34]). RT improved health-related quality of life (HRQoL) in both general and specific domains and also reduced somatization (MD = -0.69 kg; 95% CI [-1.32, -0.07]) and psychological distress (MD = -1.63 kg; 95% CI [-3.10, -0.15]).

The findings highlight the potential benefits of RT and selected pharmacological interventions on muscle-related and functional outcomes. However, the significant heterogeneity and lack of comprehensive outcome reporting underscore the need for more standardized and long-term research through larger, well-designed randomized controlled trials with standardized measurement methods to draw conclusive evidence and enhance the reliability and applicability of findings in clinical practice.

While atherosclerosis is a disease of vascular hypercholesterolemia, reports have also shown the presence of intracellular hypercholesterolemia in cancer tumor cells. Since the dietary cholesterol in the blood vessel is the major source of intracellular cholesterol, a low blood cholesterol level is maintained in people having carcinogenesis. Because of the variance found in blood cholesterol level, the carotid artery intimal media thickness (CIMT) was considered as a confirmation marker to distinguish these two diseases. 50 patients of each category and 25 disease-free healthy subjects were included in a single-center study. Subjects were classified into two groups viz., normoglycemic and hyperglycemic. Since both atherosclerosis and carcinogenesis are inflammatory, stressful diseases; the relative variations of plasma or serum concentrations of different characteristic discriminating markers related to inflammation and stress were evaluated in this study to compare the severity of stress between these two dreadful diseases. The respective inflammatory and stress markers were Ox-LDL, TNF-α, IL-10, Cortisol, PERK, and NF-kB. ELISA-based commercial kits were used for the assay of the respective parameters. Based on the relative severity of the bio-marker values, subjects were also divided into risk liable sub-groups. Linear regression analysis against serum low density lipoprotein (LDL) concentration for each of the inflammation (Ox-LDL, TNF-α, and IL-10) and stress (Cortisol, PERK, and NF-kB) factors was carried out for a clear outcome of the absolute severity of each component in the pathogenicity of these two disease processes. Calculated fold alarming severity earmarked hyperglycemic carcinogenesis as the most stressful alarming disease over the others.

Fibrotic interstitial lung diseases (F-ILDs) are increasingly complicated by early-stage non-small cell lung cancer. For many of these patients, stereotactic ablative body radiotherapy (SABR) is the only feasible curative-intent option. However, pre-existing fibrosis markedly increases the risk of severe, sometimes fatal, post-treatment respiratory events. These episodes are usually labelled radiation pneumonitis (RP), yet their timing, distribution and lethality often resemble acute exacerbations (AEs) of the underlying interstitial lung disease (ILD) rather than classical, field-confined RP. In this narrative review, we synthesise observational data from the SABR series enriched for ILD, focusing on acute respiratory deterioration within weeks to months after treatment. We examine how inconsistent terminology and heterogeneous case definitions obscure the distinction between RP and radiation-triggered AE (RT-AE)-ILD, and we summarise clinical, radiological, physiological, dosimetric and biomarker risk factors. Mechanistic models suggest that radiation may amplify a primed fibrotic lung via convergent epithelial, endothelial and immune pathways, with potential modulation by antifibrotic therapy, corticosteroid exposure and infection. We argue that in patients with progressive F-ILD, at least a subset of post-SABR 'pneumonitis' episodes are better conceptualised as RT-AE, with implications for corticosteroid stewardship, infection prophylaxis and continuation of antifibrotics. Given the absence of trial-level evidence and the high baseline mortality of F-ILD, management must prioritise multidisciplinary evaluation, explicit shared decision-making and cautious individualisation rather than reflexive transplantation of RP algorithms. Prospective registries, standardised ILD phenotyping and translational studies are urgently needed to define risk boundaries and test whether antifibrotic-radiation strategies or particle therapies can safely deliver curative-intent treatment to this highly vulnerable population.

Physical performance strongly influences peri-treatment outcomes in gastric cancer (GC), yet simple molecular markers reflecting functional status are lacking. Lipidomics may help identify circulating biomarkers linked to physical fitness.

To assess whether physical performance is associated with distinct plasma lipidomic profiles in GC patients.

Nineteen male GC patients (60-75 years) from the PROTECT trial were classified as high- (HighP) or low-performance (LowP) based on the 6-min walk test. Plasma lipidomics (LC-MS/MS) quantified 232 lipid species and a total of 25 fatty acids were quantified by gas chromatography-MS. Multivariate and univariate analyses, group comparisons, and correlations examined associations with clinical, anthropometric, and fitness parameters.

Lipid profiles differed by performance status. HighP patients showed higher phosphatidylinositol (PI 36:2) and trends toward increased plasmalogen phosphatidylethanolamines (PE), whereas sphingomyelin (SM 43:2) was higher in LowP patients. Plasmenyl-PE species correlated positively with functional tests, muscle mass, body mass index, and nutritional status; SM 43:2 correlated negatively. Acylcarnitines showed minimal associations.

GC patients with different physical performance status display distinct circulating lipid signatures. PI 36:2, PE plasmalogens, and SM 43:2 species appear linked to physical fitness, suggesting potential value as preoperative biomarkers. Validation in larger cohorts is warranted.