Although physical activity is associated with improved survival in lung cancer, most patients remain inactive. This study examined the impact of an oncologist's recommendation on exercise quantity, sedentary behavior, and quality of life (QoL) in patients with lung cancer.

In this single-blind, 3-arm randomized controlled trial, patients with lung cancer (stages I-IV) were assigned to: (1) usual care, (2) the oncologist's verbal and written exercise recommendation, or (3) the recommendation plus a printed exercise guidebook. Exercise, sedentary behaviors, and QoL were assessed at baseline, 4, and 8 weeks. Descriptive statistics, analysis of variance, and a generalized linear regression model were used to analyze data.

Overall, 91 patients (n = 31 recommendation group, n = 31 recommendation + guidebook group, n = 29 controls) were randomized. At 8 weeks, the recommendation group showed a significant increase in total (+270 min/week, p = 0.03) and light-intensity physical activity (+236 min/week, p = 0.01) versus controls. The recommendation plus guidebook group demonstrated a near-significant increase in total (+251 min/week, p = 0.05) and moderate-intensity physical activity (+145 min/week, p = 0.05). No significant changes were observed for sedentary behaviors. Regarding QoL, at 4 weeks, the recommendation plus guidebook group demonstrated an enhancement in cognitive function and the recommendation group in social function compared to controls. At 8 weeks, the recommendation + guidebook group reported improved constipation compared to the controls.

A brief oncologist-delivered recommendation effectively increased the total physical exercise in patients with lung cancer. Combining the oncologist's recommendation with a dedicated guidebook may be more effective in promoting moderate- and vigorous-intensity exercise, although the short follow-up limits conclusions regarding long-term effects.

ClinicalTrial.gov identifier: NCT05497544.

India accounts for one-third of the global incidence and mortality of oral cancer. The national oral cancer screening program uses Conventional Oral Examination by Primary Healthcare (PHC) workers. This subjective assessment leads to unnecessary referrals to higher centers for biopsy and false negatives due to inappropriate biopsy site selection. Angiogenesis is one of the steps in early carcinogenesis, as solid tumors, such as oral cancers, cannot grow beyond 2-3 mm in diameter without inducing their own blood supply. The increased vascular supply and metabolic rate in malignant cells lead to a rise in temperature, which can be detected by sensitive digital infrared (IR) cameras. An Artificial Intelligence-enabled automatic analysis of intraoral IR images of oral lesions can be used for screening, early detection of Stage I and II oral cancers, and biopsy site selection as an objective Point-of-Care (POC) adjunct. A standardized protocol for passive and active IR imaging of intraoral lesions (index test) with a smartphone-based IR camera will be prepared to train a Medical Scientist and Technician. IR images of already diagnosed normal, Inflammatory, potentially malignant disorders, and malignant oral lesions (N = 100 each) will be used in Phase I to train an AI model to classify images as malignant or non-malignant. A second set of IR images of these oral lesions will be used in Phase II (N = 100 each) for evaluating the performance of the AI model. The reference test for malignancy will be histopathology (Gold standard). The intra/inter observer reliability will be assessed using the kappa statistics A clinical trial and validation of the proof of concept are proposed for IR imaging of intraoral lesions as a noninvasive POC adjunct for early detection and screening of oral cancer by PHC workers, and for the selection of biopsy sites by surgeons. © 2026 Wiley Periodicals LLC.

Ubiquitin D, a ubiquitin-like protein, functions as a potential tumor promoter in various cancers. However, its biological role and clinical significance in breast cancer remain unclear. In this study, we evaluated UBD expression in malignant and normal breast tissues using bioinformatics databases. Analysis of clinical specimens showed that UBD expression was significantly higher in primary breast cancer tissues than in normal breast tissues and was closely associated with key clinicopathological features in affected patients. Subsequently, breast cancer cell line models were established to assess the impact of UBD on malignant properties in vitro. KEGG pathway analysis indicated that differentially expressed genes were significantly enriched in the PI3K/AKT signaling pathway. Western blot analysis was performed to examine changes in EMT-related markers and key signaling molecules involved in the PI3K/AKT pathway in breast cancer cells. The PI3K/AKT agonist 740Y-P and inhibitor LY294002 were employed to determine the contribution of this pathway to EMT regulation in breast cancer cells. The results demonstrated that EMT signature-derived ssGSEA scores indicated UBD had the strongest positive correlation with the EMT process, and that UBD enhanced the expression of EMT-related markers in breast cancer cells. The pathway inhibitor LY294002 suppressed UBD-induced increases in migration and invasion, as well as the expression of EMT-related markers. In contrast, the agonist 740Y-P restored the decreased migration, invasion, and EMT phenotypes induced by UBD knockdown. Collectively, our data demonstrated that UBD plays a critical role in the malignant progression of breast cancer, highlighting its potential as a novel therapeutic target for breast cancer patients.

BRAF kinases are involved in cancer cell survival and metastasis. Mutations in BRAF are frequent in several types of cancer, occurring in more than 50% of melanomas, 50-70% of thyroid cancers, 15% of colorectal cancers, and 5-8% of non-small-cell lung cancers. The most prevalent mutation is V600E. Vemurafenib and dabrafenib are two selective BRAF inhibitors approved by the FDA for clinical use. However, due to the increasing resistance to current kinase inhibitors, there is an urgent need to identify new molecular scaffolds with potential BRAF inhibitory activity. In this work, molecular docking, molecular dynamics, and metadynamics simulations were performed on twelve triterpenes to identify the best ligands with potential binding to BRAFWT and BRAFV600E. The interaction profiles of the selected triterpenes revealed key contacts with residues ILE463, THR529, GLN530, TRP531, CYS532, and PHE583, which contribute to stabilizing the conformation of both inhibitors and triterpenes within the catalytic binding site of the proteins. The ΔG of betulinic acid (-57.46 kcal/mol) in complex with BRAFWT is comparable to the BRAF inhibitors vemurafenib-OMe and dabrafenib reported in previous work, the ΔG of β-amyrin (-51.83 kcal/mol) showed a ΔG comparable to the inhibitors with BRAFV600E; moreover, the ΔG of lupeol (-62.43 kcal/mol) and moronic acid (-61.05 kcal/mol) are more favorable with BRAFV600E than vemurafenib-OMe and dabrafenib. These computational calculations allow us to consider these triterpenes as potential candidates for drug design cycles and to optimize the binding profile for the development of new selective inhibitors for BRAFV600E to cancer treatments.

Molecular docking calculations using AutoGrid 4.2.6, AutoDockGPU 1.5.3, and AutoDockTools 1.5.6 were performed. Molecular dynamics and metadynamics simulations were performed in the Desmond module of the academic version of the Schrödinger-Maestro 2021-4 program, utilizing the OPLS-2005 force field. Finally, all the protein figures presented in this article were made in the PyMOL program and the RMSD graphics were made in the statistical package R and RStudio 2025.05.1.

Follicular dendritic cell sarcoma (FDCS) is a rare neoplasm with morphologic and phenotypic features resembling those of normal follicular dendritic cells (FDCs). FDCS has been classified into two distinct entities based on their association with Epstein-Barr Virus (EBV): classic FDCS (cFDCS) and EBV-positive inflammatory FDCS (EBV + IFDCS). Diagnosis relies on characteristic histopathology and immunohistochemistry using FDC markers and EBV in situ hybridization (EBER). This study aimed to compare the clinical presentations, histologic features, and immunoprofiles between these two entities in a Taiwanese cohort. We retrospectively reviewed histological features of in-house and consultation cases of FDCS. Immunohistochemistry with novel markers including serglycin (SRGN), FDC-secreted protein (FDCSP) was applied, together with conventional FDC markers (CD21, CD23, CD35) and EBER. Programmed death ligand-1 (PD-L1), a potential therapeutic marker, was additionally evaluated and scored. Clinical and histological parameters, inflammatory cell infiltration, mitotic rate, and PD-L1 tumor proportion score (TPS) were compared statistically. We identified 30 patients including 16 cFDCS and 14 EBV + IFDCS. The median age was 56 years old (range, 22-80), with a female preponderance in EBV + IFDCS. EBV + IFDCS occurred exclusively in extra-nodal sites, while cFDCS more commonly involved lymph nodes. EBV + IFDCS showed significantly higher PD-L1 TPS (p = 0.012), more prominent inflammatory cell infiltration (90.0% vs. 12.5%, p < 0.001) in the presence of germinal centers (50% vs. 6%, p = 0.012), and lower mitotic activity (0.5 vs. 2.5/10 HPFs, p = 0.002). We identified distinct clinical and histologic features, as well as differential PD-Ll expression between cFDCS and EBV + IFDCS, supporting their classification as separate entities. Further molecular studies are needed to investigate their pathogenesis.

New-onset sarcopenia may develop after gastrectomy even in patients with normal muscle mass, but its detection in routine practice remains challenging. This study evaluated body composition changes after gastrectomy and identified clinical parameters associated with sarcopenia development.

This retrospective study included gastric cancer patients who underwent gastrectomy between 2009 and 2023. Body composition, including body weight (BW), skeletal muscle index (SMI), visceral fat area (VFA), and subcutaneous fat area (SFA), was assessed using CT images obtained preoperatively and 1 year postoperatively. Postoperative sarcopenia was defined as new-onset sarcopenia in patients without preoperative sarcopenia.

Among 1932 patients, mean percent changes in BW, SMI, VFA, and SFA at 1 year after gastrectomy were - 9.8%, + 1.0%, - 52.8%, and - 34.3%, respectively. Of 1259 preoperative non-sarcopenic patients, 145 (11.5%) developed postoperative sarcopenia and had significantly worse overall survival than those who maintained non-sarcopenia (HR, 2.516; 95% CI, 1.560-4.058; P < 0.001). Among these patients, recurrence incidence in those with stage II or III disease did not differ (Gray's test, P = 0.294), whereas post-recurrence survival was significantly worse in those with postoperative sarcopenia (log-rank, P < 0.001). Four clinical parameters (sex, age ≥ 60, extent of gastrectomy, and BW loss ≥ 8 kg) showed acceptable discrimination for identifying postoperative sarcopenia (simplified risk model; AUROC, 0.792; 95% CI, 0.755-0.829; P < 0.001).

New-onset sarcopenia 1 year after gastrectomy was independently associated with poor survival, underscoring its oncologic relevance. Simple clinical parameters may help identify high-risk patients and guide nutritional or exercise interventions.

Sidedness influences colorectal cancer (CRC) prognosis and treatment response, yet the mechanism dictating differential EGFR inhibitor (EGFRI) sensitivity is unclear. This study investigated the tumor microenvironment (TME) in relation to EGFRI eligibility-clinically defined by factors such as tumor sidedness (e.g., left-sided), RAS/BRAF wild-type status, and microsatellite stability (MSS)-using integrated single-cell RNA sequencing (scRNA-seq), with bulk RNA-seq and spatial transcriptomics validation. We found cancer cell features reflected EGFRI eligibility more strongly than sidedness. EGFRI eligible tumors exhibited high Epiregulin (EREG) expression by cancer cells. Cell interaction analysis revealed a specific "EREG/EGFR/CSF axis" in EGFRI eligible CRC: EREG derived from cancer cell stimulates EGFR-expressing non-myCAF subtypes of cancer-associated fibroblasts (CAFs), which signal via CSF to M1/M2-like Tumor-Associated Macrophages/Monocytes (TAM/TAMo), potentially promoting M2 polarization. Spatial analysis confirmed the proximity of these interacting cell populations and localized EGFR pathway activation near cancer cells specifically in eligible tumors. This study provides a TME-centric view of EGFRI eligibility, identifying a key intercellular communication network driving differential responses. These findings suggest TME features could offer more precise patient stratification than sidedness alone, potentially improving CRC therapeutic strategies.

Detection of intraductal neoplasms of the bile duct (IN-Bs) remains suboptimal despite various diagnostic modalities. We evaluated the efficacy of digital single-operator cholangioscopy (D-SOC) for screening and surveillance of IN-Bs in patients with bile duct dilatation after stone removal.

In a prospective cohort of 181 patients with post-stone removal common bile duct dilatation (> 10 mm), screening D-SOC was followed by two rounds of surveillance at 1-year intervals. Outcomes included cumulative incidence of IN-Bs, technical success of D-SOC and D-SOC-guided biopsy, and number needed to screen (NNS) to identify a neoplastic lesion at each round.

Technical success of D-SOC was achieved in all patients. Among 181 patients who underwent D-SOC, nine were diagnosed with IN-Bs: cholangiocarcinoma (CCA) (n = 3), intraductal papillary neoplasms of the bile duct (n = 5), and adenoma with dysplasia (n = 1). Curative resection was performed in two patients with CCA. The cumulative incidence of IN-Bs was 6.3% (95% confidence interval, 2.4-10.7%). The NNS values to detect one neoplastic lesion were 29.4, 21.8, and 9.7 at initial screening and 1- and 2-year surveillance.

D-SOC can be useful for risk-enriched detection and surveillance of IN-Bs in patients with post-stone-removal biliary dilatation, warranting further evaluation in those with additional CCA risk factors (clinical trial registration number: NCT05600803).