A decision-support tool for management of advanced epithelial ovarian cancer in a single centre in India (CT PAUSE Nomogram): a prospective Study (2022-2024).

Despite recent progress, advanced non-small cell lung cancer (NSCLC) has poor survival outcomes, necessitating the development of novel therapies. TNF-related apoptosis-inducing ligand (TRAIL) selectively induces cancer cell death and can be delivered to tumors by mesenchymal stromal cells (MSCs) due to the cells' migratory properties. This first-in-human phase I trial assessed safety and dose of umbilical cord-derived MSCs expressing TRAIL (UC-MSCTRAIL) alongside standard NSCLC therapy. Participants performance status 0-1 with treatment-naïve, inoperable stage IIIB/IV NSCLC received UC-MSCTRAIL infusions with each cycle of chemotherapy and immunotherapy, up to 3 cycles. A dose de-escalation design was used. Exploratory in vitro and in vivo studies further characterized UC-MSCTRAIL properties. Six participants enrolled; four received 4 × 10⁸ cells/infusion (median 5.4 × 106 cells/kg), and two received 2 × 10⁸ cells/infusion (median 2.4 × 106 cells/kg). Early termination occurred due to asymptomatic pulmonary emboli (N = 5), which included two patients that were anticoagulated as a protocol amendment with prophylactic low molecular weight heparin (enoxaparin 40 mg) and rivaroxaban 20 mg, respectively. Exploratory analyses found no clear pro-coagulant or immunogenic mechanisms, though participants receiving UC-MSCTRAIL had elevated inflammatory markers. This first-in-human study of UC-MSCTRAIL in advanced lung cancer was terminated early due to high prevelance of pulmonary embolism. THough exact mechanism remains unclear, UC-MSCTRAIL may have contributed to a pro-inflammatory environment in participants already at elevated risk of thrombosis due to malignancy. Future MSC-based therapies should incorporate close monitoring for asymptomatic thrombosis and follow a dose escalation design for safety. Safety concerns underscore the need for further research.

Association between diarrhea and survival in patients with HER2-positive advanced breast cancer treated with pyrotinib-based therapy: A landmark analysis from the real-world PRETTY study.

To develop and validate deep leaning-based machine learning models using longitudinal multi-sequence MRI for predicting treatment response of patients with locally advanced rectal cancer (LARC) to neoadjuvant chemotherapy (NCT). This retrospective study included 169 LARC patients who received 2-4 cycles of CAPOX chemotherapy before surgery. Patients were randomly divided into a training cohort (n = 118) and a test cohort (n = 51). High-resolution paired MRI sequences (CE-T1WI, T2WI, DWI) were acquired before and after NCT. These sequences were then independently input into a DenseNet121 network to generate predictive probability scores, which served as deep leaning (DL) signatures. Prediction models were built using an SVM classifier. These models were built either by integrating the deep learning signatures alone or by combining them with clinical and radiological features. Model performance was assessed using AUC, accuracy, sensitivity, and specificity. Calibration was evaluated with calibration plots and Brier scores, and clinical utility was analyzed via decision curve analysis (DCA). In the test cohort, the fusion DL model, integrating pre- and post-NCT multi-sequence DL signatures, achieved an AUC of 0.846. The combined clinical-radiological-deep learning (CRD) model, which added clinical-radiological features to the fusion DL model, reached the highest AUC of 0.851, but the improvement was not statistically significant. The fusion DL model showed strong performance in predicting pathological response in LARC. The post_DWI signature was the main contributor to the model.

MRI features and chemotherapy response score-based nomogram for post-neoadjuvant recurrence prediction in advanced ovarian cancer.

Dosimetric evaluation of proportion-based hybrid IMRT/RapidArc planning for neoadjuvant radiotherapy in locally advanced rectal cancer

Intratumoral microbiota is being investigated as a potential biomarker in cancer. In this study, we investigated tissue microbiota in advanced non-small cell lung cancer (NSCLC) to evaluate response to immune checkpoint inhibitors (ICIs). We performed a retrospective study in 41 tumor tissues from patients with advanced NSCLC treated with ICI +/- chemotherapy. Microbial profiling was analyzed through 16S rRNA amplicon sequencing using Ion Torrent technology. Bioinformatic analysis was performed with the QIIME2 pipeline. Cox and logistic regression identified two bacterial consortia with prognostic relevance in terms of overall survival (OS), progression-free survival (PFS) and treatment response: the KBUBe score, which included four genera (Klebsiella, Brevundimonas, Undibacterium and Beijerinckiaceae), and the OSAA score, which comprised Olsenella, Salinarimonas, Actinobacillus and Lachnospiraceae genus A2. KBUBe and OSAA scores were significant predictors of OS (hazard ratio [HR]=0.501, p=0.009 and HR=0.491, p<0.001, respectively) and PFS (HR=0.579, p=0.040 and HR=0.133, p<0.001, respectively), outperforming PD-L1 expression, ECOG performance status or neutrophil-to-lymphocyte ratio. All patients with the highest KBUBe score were responders, compared with 50% in the lowest-score group (p=0.035). Similarly, 83.8% of patients with the highest OSAA score were responders, whereas no responders were observed in the lowest-score group (p=0.001). These findings were confirmed by internal validation and were not confounded by tobacco smoking status, type of therapy and histology. Intratumoral microbial communities are associated with survival and treatment response in ICI-treated NSCLC. The KBUBe and OSAA scores represent novel, independent prognostic biomarkers, warranting validation in larger cohorts.

Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors have become a cornerstone in the first-line management of hormone receptor-positive, human epidermal growth factor receptor 2-negative (HR+/HER2-) advanced breast cancer. Despite their clinical efficacy, most patients eventually experience disease progression, and optimal treatment strategies following CDK4/6 inhibitor resistance remain unclear. Emerging evidence suggests that switching endocrine therapy (ET) while continuing cyclin inhibition may provide additional clinical benefit. Dalpiciclib, a selective CDK4/6 inhibitor, in combination with physician-selected ET, represents a potential option in this setting. Concurrently, 16α-[18F]fluoro-17β-estradiol ([18F]FES) PET/CT, a novel imaging modality targeting estrogen receptors (ER), enables non-invasive, whole-body assessment of ER expression in metastatic lesions, offering a personalized approach to treatment selection. This is a prospective, single-center, single-arm Phase II clinical trial evaluating the efficacy and safety of dalpiciclib plus ET in HR+/HER2- advanced breast cancer patients who progressed on prior CDK4/6 inhibitor therapy. Forty eligible patients with confirmed metastases and at least one [18F]FES-positive lesion will be enrolled. Participants will receive dalpiciclib combined with ET as determined by the treating physician. The primary endpoint is progression-free survival (PFS). Secondary endpoints include objective response rate (ORR), disease control rate (DCR), and overall survival (OS). Beyond evaluating efficacy, this single-center phase II trial will provide practical insight into the feasibility of [18F]FES PET/CT-guided patient selection, including standardized imaging workflows and multidisciplinary implementation in routine clinical research. Positive outcomes may support a personalized, imaging-guided strategy to prolong disease control after prior CDK4/6 inhibitor progression. Approved by the Ethics Committee of Peking Union Medical College Hospital (Approval number: K3629); registered at ClinicalTrials. gov (NCT05613270).

Outcomes of folded submental flap reconstruction for full-thickness cheek defects in advanced oral cavity cancer.

Acute Toxicity From Short-Course Radiation Therapy for Rectal Cancer: A Single-Institution Experience.

The therapeutic landscape of metastatic castration-resistant prostate cancer (mCRPC) has evolved substantially over the past decade, with androgen receptor pathway inhibitors, taxanes, poly (ADP-ribose) polymerase (PARP) inhibitors, radioisotopes, bone-protecting agents, and emerging targeted therapies improving survival for patients. At the same time, earlier treatment intensification in the hormone-sensitive setting has resulted in heterogeneous clinical presentations at the onset of castration resistance, adding complexity to treatment sequencing and clinical decision making. Here, we propose a pragmatic, patient-centered framework to help guide the management of mCRPC by integrating clinical features, molecular profiling, imaging findings, and supportive care considerations. Confirmation of castration resistance remains a critical first step and requires documented biochemical or radiographic progression in the setting of castrate testosterone levels. Treatment selection should consider prior systemic therapies, disease burden and tempo, symptom profile, comorbidities, and frailty. Molecular characterization, including evaluation for homologous recombination repair alterations and mismatch repair deficiency, is highly important for identifying candidates for PARP inhibitors or immune checkpoint blockade and other emerging biomarker-driven targeted strategies. Prostate-specific membrane antigen (PSMA)-targeted radioligand therapy has emerged as a key treatment. PSMA-positron emission tomography-based selection, incorporating assessment of uptake intensity, tumor heterogeneity, and total tumor volume, may help identify patients who are most likely to benefit from this treatment. Clinical factors such as liver metastases and limited prior response to androgen receptor-directed therapy have been associated with less favorable outcomes. Early on-treatment assessment using prostate-specific antigen response and PSMA-based imaging may support adaptive treatment strategies and earlier recognition of resistance. Given the high prevalence of bone metastases, bone-protecting agents should be considered to reduce skeletal-related events. Early palliative care (EPC) is now widely recognized as a concurrent, patient-centered intervention that improves quality of life, symptom burden, coping, and satisfaction across advanced cancers. Prostate cancer represents an especially compelling setting for EPC because of prolonged advanced disease courses, cumulative symptom burden, repeated treatment transitions, and persistent unmet supportive needs.

Whole genome sequencing of locally advanced and metastatic breast carcinoma unravels relevant molecular signatures and novel events.

Chemotherapy (CT) remains the standard first-line treatment for advanced triple-negative breast cancer (aTNBC), despite the emergence of innovative therapies, including targeted therapies (TT) and immune checkpoint inhibitors (ICI). Studies have shown that the treatment strategies for aTNBC vary widely, with inconsistent efficacy acrossdifferent treatment modalities. A comprehensive search was carried out in electronic databases, such as PubMed and Embase, for systematic reviews and randomized clinical trials (RCTs) that investigated the efficacy of TT, ICI, and CT to treat aTNBC until June 2025. Seventeen published meta-analyses and 52 RCTs reporting the prognosis of the disease treated with TT, ICI, and CT in aTNBC patients were analyzed. It showed that in terms of prolonging PFS, both the TT group and the ICI group were superior to the CT group [ICI: HR = 0.81 (0.69, 0.94); TT: HR = 0.68 (0.62, 0.74)]. In terms of OS, the TT group was superior to the CT group [HR = 0.77 (0.68, 0.88)]. In the subgroup analysis of TT, compared with CT alone, both sacituzumab govitecan (SG) monotherapy and trilaciclib combined with chemotherapy (TRI_CT) significantly improved the time of PFS [SG: HR = 0.41 (0.30, 0.56); TRI_CT: HR = 0.62 (0.46, 0.86)] and OS [SG: HR = 0.48 (0.33, 0.70); TRI_CT: HR = 0.41 (0.28, 0.59)]. This umbrella review supports SG monotherapy and TRI_CT as the first choice for patients with aTNBC. Additionally, the review was rated as high-quality evidence using AMSTAR 2, the credibility classification standard, and GRADE rating. The study is reported following the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guideline and is registered with PROSPERO: CRD420251034666.

Are patient factors associated with real-world antibody-drug conjugate outcomes in gynecologic cancers?

To assess interobserver agreement of computed tomography (CT) features in colon cancer, their association with pathological staging, and the influence of baseline characteristics on clinical-pathological agreement. CT scans of patients with locally advanced colon cancer treated between 2011 and 2020 at two Dutch hospitals were analyzed. Eleven radiologists independently reviewed the scans in pairs using a structured template. Interobserver agreement was evaluated using Krippendorff's alpha (α) and intraclass correlation coefficients (ICC). Associations between CT features and pathological stages, and the impact of baseline characteristics on clinical-pathological agreement, were assessed using mixed-effects logistic regression. Interobserver agreement was α = 0.55 (95% CI: 0.51-0.60) for T stage, α = 0.57 (95% CI: 0.52-0.61) for N stage, α = 0.44 (95% CI: 0.36-0.51) for retroperitoneal surgical margin, α = 0.59 (95% CI: 0.52-0.65) for bowel obstruction, α = 0.27 (95% CI: 0.22-0.33) for extramural vascular invasion, α = 0.22 (95% CI: 0.14-0.31) for tumor deposits, ICC = 0.72 (95% CI: 0.70-0.75) for tumor length, and ICC = 0.62 (95% CI: 0.58-0.65) for largest node diameter. Significant associations (P < 0.05) were observed between clinical cT, cN, tumor length, and cEMVI with pT, and between cN, node diameter, and node heterogeneity with pN. Age, tumor location, and differentiation grade significantly influenced agreement. Several CT features were significantly associated with pathological stage, but their inconsistent interpretation across observers, indicates limited reliability for individualized treatment decisions. Interpretation should therefore focus on features with proven reproducibility, namely tumor length and largest node diameter, applied within standardized protocols, and integrated with the broader clinical and pathological context.

Outcomes of consolidative surgery following enfortumab vedotin plus pembrolizumab for advanced urothelial cancer: A real-world experience.

Immobilization of Bacillus-derived protease onto carboxymethyl chitosan aerogel: A bioactive platform for bacterial inactivation, skin cancer therapy, and accelerated wound healing.

Docetaxel (DTX) remains the first-line chemotherapeutic for advanced prostate cancer, however, its therapeutic efficacy remains limited by poor aqueous solubility, rapid systemic clearance, and severe dose-dependent toxicity. To overcome these constraints, we developed a PEGylated, disulfide-bridged hierarchical mesoporous silica nanocarrier (PEG-HMS) as a redox-sensitive delivery system for DTX (PEG-HMS-DTX). The nanostructure was fabricated by integrating disulfide-containing organosilanes into the silica framework and conjugating thiol-reactive PEG chains, thereby combining long circulation stability with tumor-selective release. Comprehensive physicochemical characterization confirmed uniform spherical morphology, an optimal hydrodynamic size (∼40-50nm), attenuated surface charge following PEGylation, and high colloidal stability in physiological media, while disulfide linkages enabled responsive structural changes under reductive conditions. Drug release was minimal under physiological conditions (<30% at 72h) but markedly accelerated in the presence of glutathione (∼60% at 72h). Compared with free DTX or non-PEGylated carriers, PEG-HMS-DTX exhibited stronger cellular uptake and enhanced cytotoxicity in RM-1 prostate cancer cells. In tumor-bearing mice, PEG-HMS-DTX achieved superior tumor accumulation (peak at ∼12h), pronounced tumor growth inhibition (>70%), minimal systemic toxicity, and elevated apoptosis characterized by increased cleaved caspase-3 and reduced PCNA/Bcl-2 expression. Collectively, this "stable-in-circulation, trigger-in-tumor" platform substantially improves intratumoral DTX delivery and apoptosis-driven antitumor efficacy, while maintaining systemic safety. These findings highlight PEG-HMS-DTX as a promising and generalizable strategy for prostate cancer chemotherapy, warranting further pharmacokinetic, immunogenicity, and GLP toxicology studies to support translational advancement.

Cumulative gastrointestinal adverse events in EMBRACE-I: comparative evaluation of CTCAE vs. MOSES methods in predicting the impact of incident vs. persistent adverse events on quality of life.

Drug-drug interaction (DDI) management is critical for safe and effective use of oral anticancer drugs (OADs). Our study objectives were to (i) compile clinically relevant pharmacokinetic (PK) DDI mechanisms for OADs and (ii) assess the prevalence of PK potential DDIs (PDDIs) in patients with advanced solid cancers. OADs approved through January 2023 were assigned DDI mechanisms based on studies obtained from drug labels and primary literature showing ≥ 2-fold exposure change or significant adverse health outcomes during co-administration with interacting drugs. Electronic health records of 3,697 solid cancer patients were reviewed retrospectively to detect PDDIs, defined as overlapping prescriptions of OADs with relevant interacting drugs. FDA labels were reviewed for 99 OADs, and 239 studies were extracted from the primary literature, yielding a total of 748 drug-drug pairs for analysis. Eighty-five OADs (85.9%) had ≥ 1 DDI mechanism. The most common DDI mechanisms were victims with metabolic inducers (71.7%), CYP3A substrates (55.6%), CYP3A perpetrators (29.3%), and victims with acid reducers (17.2%). Our primary literature search detected clinically relevant DDI mechanisms without actionable recommendations in the drug labels for 14 drugs. Among patients prescribed ≥ 1 OADs (46.9%), 17.4% had ≥ 1 PDDI, most commonly involving OADs acting as CYP3A (58.9%) or CYP2D6 (32.5%) perpetrators. Most OADs (~86%) had ≥ 1 DDI mechanism, and ~17% of solid tumor board patients had a clinically relevant PDDI.