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The aerosol foam formulation of calcipotriol/betamethasone dipropionate (Cal/BD) is an efficacious topical treatment for psoriasis. This study evaluated the efficacy of Cal/BD foam versus ointment in Chinese patients, on the basis of investigator-assessed and patient-reported outcomes (PROs) from a 4-week clinical trial, including post hoc analyses after 2 weeks of treatment. A randomized, investigator-blind, active-controlled, parallel-group phase 3 trial was conducted in China. Native Chinese adults (≥ 18 years) with plaque psoriasis involving 2-30% of the body surface area (BSA), with at least mild disease severity according to the Physician's Global Assessment (PGA), and modified Psoriasis Area and Severity Index (mPASI) ≥ 2 were randomized 1:1 to receive either Cal/BD foam or ointment once daily for a 4-week treatment period. Efficacy was assessed at weeks 0, 2, and 4 using mPASI, PGA, BSA, Dermatology Life Quality Index (DLQI), Psoriasis Symptom Inventory (PSI), and Subject's Global Assessment of disease severity (SGA). A total of 302 patients were randomized to each treatment. Both groups had clinically meaningful improvements across all outcome measures from baseline to week 2, with sustained or further improvements at week 4. For Cal/BD foam-treated patients, mean change from baseline in mPASI was -59.87% at week 2 (versus ointment: -54.59%; P = 0.010) and -74.69% at week 4 (versus ointment: -70.22%; P = 0.043). Other investigator-assessed outcomes based on mPASI and PGA showed statistically significant treatment differences favoring Cal/BD foam at week 4. Improvements in PROs (DLQI, PSI, and SGA) were numerically slightly greater with Cal/BD foam than ointment, though not statistically significant. For Cal/BD foam-treated patients, mean change from baseline in DLQI was -3.9 at week 2 (versus ointment: -3.7; P = 0.5012) and -5.5 at week 4 (versus ointment: -5.3; P = 0.5119). Cal/BD foam showed rapid onset of action with clinically meaningful improvements in signs, symptoms, and quality of life in Chinese patients with plaque psoriasis. ClinicalTrials.gov: NCT05919082. Plaque psoriasis is the most common type of psoriasis, a chronic disease affecting the skin and other body systems. Plaques are thick, scaly patches of skin that can be itchy and painful, limiting patients' everyday activities. Plaque psoriasis has a major impact on quality of life, comparable with the impact of other chronic diseases such as cancer and heart disease. Many treatments, such as creams, tablets, and injections, can improve plaque psoriasis, but they do not always work well for everyone. In a clinical trial in China, we tested two treatments-a foam and an ointment-that have the same amount of two active ingredients: calcipotriol (Cal) and betamethasone dipropionate (BD). The goal was to find out if Cal/BD foam, which is the newer treatment, worked as well as Cal/BD ointment in Chinese men and women with plaque psoriasis. The trial participants were randomly distributed into two groups, each with 302 participants. One group applied Cal/BD foam on their plaques and the other group applied Cal/BD ointment, both once daily for 4 weeks. Both groups had meaningful improvements in psoriasis signs and symptoms as well as quality of life already after 2 weeks, with sustained or further improvements after 4 weeks. Overall, the improvements were slightly greater with Cal/BD foam than with Cal/BD ointment.

Ankle fractures are common orthopaedic injuries with wide variability in recovery duration and outcome. While long-term outcomes are well documented, less is known about the short-term recovery period. An updated analysis using claims data would provide greater clarity on short-term recovery patterns. The study aimed to characterise recovery duration after treatment for ankle fracture and to evaluate associations between comorbidities, perioperative complications, additional procedures and healthcare costs. Healthcare claims from the IBM MarketScan database (2015-2018) were analysed to determine recovery costs for the index treatment and subsequent events including revision surgery, motion restoring surgery (MRS), rehospitalizations, and complication-related interventions. Recovery duration was defined as the interval between the initial surgery/treatment and the final physical/occupational therapy claim. Outcomes were summarised using medians and interquartile ranges (IQR). Among 7,112 patients, the median index treatment cost was $5163 (IQR: $994-$12,444), and the recovery duration was 88 days (IQR: 36-492). Thirty-eight percent of patients required more than 6 months to complete recovery. Post-treatment complications were associated with markedly longer and more expensive recovery. Patients who required a complication-related surgery had a recovery duration that was 4 times longer and incurred costs that were 8 times greater than those without such events. Joint contracture and MRS were strongly associated with prolonged and costly recoveries. This claims‑based analysis identified wide variation in short‑term recovery after ankle fracture. Strong associations were demonstrated between complications, including joint contracture, MRS and rehospitalizations, and extended recovery duration and higher costs. These findings may help clinicians identify patients at risk for delayed recovery and support more informed decision‑making in early post‑treatment care.

Cancer therapy-related cardiac dysfunction (CTRCD) is among the most important adverse effects of treatment of childhood cancer. In the EARLY study (Early detection of acute and early-onset cARdiovascuLar toxicity in children with cancer using a multiparametric approach), cardiac function in children treated for cancer was monitored during and shortly after treatment, using advanced echocardiography, electrocardiography, and cardiac magnetic resonance (CMR) techniques. In this prospective pilot study, 100 children newly diagnosed with childhood cancer receiving anthracyclines as part of their cancer treatment were included. A subgroup of 30 children was included in the CMR sub-study. Echocardiography, electrocardiography, and CMR were performed before (T0), three and a half months after (T1), and one year after (T2) start of anthracycline treatment. In this article, we focus on the methodological aspects of the EARLY study, including patient enrollment and characteristics of the study cohort, as well as the feasibility of advanced echocardiography. The last patient was included in August 2022. Follow-up for the last patient was finalized in August 2023. Follow-up was completed by 92% of the total study population and 97% of the CMR sub-study. Protocol adherence was high (92%-97%) and a full collection of data on each included individual was achieved. Advanced echocardiography, i.e., 4D ejection fraction and global longitudinal strain, was feasible in 76% and 69% of measurements, respectively. Cardiac outcomes during and shortly after treatment, as well as associations with known risk factors for CTRCD, such as anthracycline dose, dose of radiotherapy involving the heart, childhood cancer disease profile, age at diagnosis and sex will be reported in a future publication. The feasibility of the study allows for future insight into the correlation between early-onset CTRCD and heart failure during long-term follow-up of childhood cancer patients. ClinicalTrials.gov identifier: NL-OMON22737.

Local recurrence after definitive radiotherapy for prostate cancer (PCa) remains a challenging clinical problem. Salvage irreversible electroporation (sIRE) is a non-thermal focal ablation approach with limited published evidence in the radiorecurrent setting. We report safety and early oncologic outcomes of sIRE for these patients. We performed a retrospective review of consecutive patients undergoing sIRE at a single institution (December 2023 to June 2025). Inclusion required biopsy-confirmed intraprostatic recurrence and PSMA PET demonstrating no metastatic disease. Outcomes included perioperative morbidity, early PSA response, and post-treatment prostate MRI findings. Eighteen patients underwent sIRE. Mean age was 73.78 ± 7.0 years. Seventeen patients were discharged on the day of surgery. Postoperative urinary morbidity included urinary tract infection in 3 patients (16.7%), urinary retention requiring limited TURP in 2 (11.1%), and new bothersome storage lower urinary tract symptoms requiring treatment in 2 (11.1%). Mean PSA decreased from 5.37 ± 2.09 ng/mL pre-IRE to 1.61 ± 1.57 ng/mL at approximately 3 months, and 2.17 ± 1.92 ng/mL at approximately 6 months. Twelve patients underwent post-IRE prostate MRI; results included post-treatment change, or ablation defect, or susceptibility artifact in most patients. One patient underwent repeat PSMA PET for a rising PSA and was found to have a PSMA-avid lung lesion consistent with metastatic disease. Salvage IRE for radiorecurrent prostate cancer has generally manageable short-term urinary morbidity and encouraging early PSA responses, with limited utility of post-treatment MRI. A longer follow-up is needed to define durability and optimal selection.

This study was needed because traditional patient-reported outcome questionnaires are often too long and impractical for use in busy colorectal cancer clinics, even though understanding patients’ quality of life and function during and after treatment is essential.The key problem we addressed was how to design and implement a brief, user-friendly tool that could reliably capture patients’ quality of life and functional outcomes and their key priorities, and be seamlessly integrated into routine colorectal surgery practice without adding burden to patients or clinicians.We developed a concise electronic “Colorectal Scorecard,” covering key quality-of-life and functional domains and including questions about patient priorities, displayed in a one-page, color-coded report integrated into the electronic health record. The Scorecard was implemented with training, automated reminders, and both at-home and in-clinic completion options.Our main results show that approximately 13,400 patients used the Scorecard between 2019 and 2024, with completion rates rising from about 33% to over 70%. The median time to finish was only 4 min, and fewer than 4% of patients who started failed to complete it. We also found that patients’ priorities evolve over the treatment journey: before surgery, patients most often emphasized cancer control and treatment planning, while after surgery their priorities shifted toward recovery and functional concerns, particularly bowel function.Postoperative priorities differed by cancer type—rectal cancer patients were nearly twice as likely as colon cancer patients to prioritize bowel function and more often highlighted urinary and sexual function—underscoring the need to align supportive care with patients’ changing quality-of-life priorities. Because this project evaluated feasibility and workflow integration, further research is needed to determine whether Scorecard use improves clinical outcomes (e.g., symptom control, satisfaction, utilization).

Hypofractionated salvage radiotherapy is increasingly used for biochemical recurrence of prostate cancer post-prostatectomy, yet its toxicity profile remains underexplored. This study evaluates the incidence, timing, and resolution of treatment-related toxicities in this setting. A retrospective cohort study of 403 men receiving hypofractionated salvage radiotherapy (62.5 Gy in 25 fractions) from 2017 to 2024 was conducted. Toxicities, categorized as genitourinary (hematuria, urinary incontinence, frequency, dysuria) or gastrointestinal (rectal bleeding, diarrhea, proctitis, nausea), were graded (1-3) using CTCAE-based criteria. Outcomes included any-time incidence, Kaplan-Meier time-to-first-event estimates (12- and 24-month cumulative incidence), and first-onset timing. Episode-level analyses merged events ≤ 30 days apart, assessing resolution and intervention. Median follow-up was 18.2 months. Any-grade genitourinary and gastrointestinal toxicities occurred in 34.2% and 24.6% of patients, respectively (24-month incidence: genitourinary 40.4%; gastrointestinal 28.9%). Grade 2+ toxicities were less frequent (genitourinary 9.7%; gastrointestinal 7.7%), with Grade 3+ rare (genitourinary 1.7%; gastrointestinal 0.7%). In terms of patient-level ever-event incidences, common symptoms included urinary incontinence (20.3%), rectal bleeding (19.9%), and hematuria (13.9%). Urinary toxicities predominantly onset at 6-12 months, whereas rectal bleeding and hematuria emerged later (≥ 12 months). Approximately two-thirds of Grade 2+ episodes resolved (e.g., urinary incontinence, 66.7%; rectal bleeding, 69.2%), with median resolution times of 3.0-8.4 months. With a median follow-up of 18.2 months, hypofractionated salvage radiotherapy demonstrates favorable short-to-intermediate term tolerability, with infrequent severe toxicities. Vigilant monitoring for late-onset rectal bleeding and hematuria is recommended during the 6-24 months after treatment to optimize patient management. Longer follow-up is required to confirm long-term safety.

Oral dysbiosis can accelerate the progression of head and neck squamous cell carcinoma (HNSCC) by fostering a pro-inflammatory, immunosuppressive, and metabolically altered environment. This narrative review examines the relationships between periodontitis-associated bacteria and HNSCC, focusing on their impact on oncogenic pathways, immune modulation, and epigenetic alterations. A comprehensive search of PubMed and Google Scholar was conducted up to January 28, 2026, without time limitations, using all relevant keywords related to HNSCC, head and neck cancers, periodontitis, and the oral microbiome. Key periodontitis-associated bacteria, including Fusobacterium nucleatum, Porphyromonas gingivalis, Capnocytophaga gingivalis, and Prevotella intermedia, may play a vital role in HNSCC. These bacteria stimulate several oncogenic pathways, including Wnt/β-catenin, NF-κB, and PI3K/Akt, enabling HNSCC to evade immune responses, trigger epithelial-to-mesenchymal transition and angiogenesis, and encourage cell proliferation and stemness. Furthermore, microbial interactions within the tumor microenvironment significantly impact treatment resistance, particularly in the context of immune checkpoint inhibitor therapy. Incorporating periodontal screening, microbiome profiling, and bacterial-targeted therapies into oncology could enhance treatment outcomes for HNSCC. Future research should investigate CRISPR-based microbial interventions, targeted epigenetic therapies, and microbiome-driven precision oncology strategies.

Urological cancers exhibit significant sex differences in incidence, treatment response, and prognosis, with males generally showing higher morbidity and mortality. This review systematically summarizes the underlying molecular and clinical mechanisms of these disparities, focusing on sex hormones, chromosome biology, tumor immune microenvironment, and microbiota. Sex hormones modulate key tumor processes including proliferation, apoptosis, non-apoptotic cell death, and DNA repair. Genetic factors such as X chromosome inactivation escape genes and Y chromosome loss also contribute to sex-biased cancer susceptibility. Furthermore, sex-specific differences in the urinary system and gut microbiota influence local immunity and inflammation, thereby affecting tumor progression and therapeutic response. Lifestyle and environmental factors, including smoking, alcohol consumption, and occupational exposures, further exacerbate these disparities. Clinically, sex differences impact the efficacy of immunotherapy and targeted therapies, underscoring the need for sex-informed treatment strategies. Integrating sex as a biological variable in research, clinical practice, and public health policies is essential for advancing precision oncology in urologic cancers.

Approximately 75% of the ovarian cancer (OC) patients are diagnosed in advanced stages and platinum-based chemotherapy presents severe side effects and high recurrence rates. This narrative review consolidates current knowledge and describes the pathophysiological characteristics of OC and how molecular aspects influence clinical outcomes of traditional and antibody-drug chemotherapies. Subsequently, a comprehensive picture regarding the current benefits identifies gaps and potential adverse risks of ADCs to treat OC. High-grade serous carcinomas, the most frequently diagnosed OCs, present TP53 and BRCA1/2 mutations, hypermethylation, and deregulation of retinoblastoma 1 and phosphatidylinositol 3-kinase (PI3K)/Akt/Ras pathways. After conventional treatment (surgery with or without systemic chemotherapy) and follow-up by CA125 levels, poly(ADP-ribose) polymerase inhibitors and hormone therapies were included. Unfortunately, approximately half of advanced patients who achieved a complete response following chemotherapy exhibit residual tumor(s). In this context, ADCs displayed marked cytotoxicity and incorporated a hypothesis-driven target identification strategy to recognize specific/tumor overexpressing-proteins. Independent clinical studies bibliographic searches in the PubMed database conducted between January 2020 and May 2025 revealed some ADCs have expanded progression-free survival and displayed partial/complete remission in OC patients at small doses if compared to traditional chemotherapies, suggesting acceptable safety profiles and potential synergism among cisplatin/carboplatin/paclitaxel/doxorubicin and ADC-based immunotherapies. A total of 18 clinical trials selected indicate (i) mild-to-moderate severity of side/adverse effects up to grade 2, (ii) low intervention or drug discontinuation, (iii) few drug-related deaths, and/or (iv) reversible toxicity. Thus, therapeutic performance of ADCs demonstrated that personalized treatment maximizes clinical benefits and improves efficacy for heterogeneous populations and polyclonal tumors.

Neutrophil extracellular traps (NETs) play a critical role in amplifying intestinal inflammation in ulcerative colitis (UC). Clostridium butyricum (CB) has shown anti-inflammatory effects in gastrointestinal diseases; however, its impact on NETs formation and related molecular mechanisms remains unclear. UC was induced in C57BL/6 mice by DSS, followed by CB and/or PMA administration. Colonic injury was assessed by colon length measurement, histopathology, and histological scoring. NETs formation was determined by immunofluorescence staining of Ly6G and citrullinated histone H3 (Cit-H3), and serum myeloperoxidase (MPO)/Cit-H3 levels were quantified by ELISA. In vitro, NETs release was induced in neutrophils by PMA with or without CB supernatant (CBS) administration. RNA-seq and qRT-PCR/Western blot analyses were used to explore underlying signaling pathways. IL-17A knockdown via siRNA was conducted to validate mechanistic involvement. CB significantly alleviated DSS-induced colitis, evidenced by reduced colon shortening, lower colon mass, and improved mucosal architecture. CB markedly suppressed NETs formation in both colonic tissue and serum. Comparative transcriptomics indicated that CBS suppresses NETs formation primarily through modulation of the IL-17 signaling pathway. DSS-induced colitis and PMA stimulation markedly increased the expression of IL-17A, IL-17RA, and p-p65 and elevated pro-inflammatory cytokines (IL-1β and TNF-α), while reducing the anti-inflammatory cytokine IL-10. CB or CBS treatment significantly reversed these pathological changes in both colon tissues and neutrophils. Importantly, IL-17A knockdown significantly reduced PMA-induced activation of the IL-17A/IL-17RA/NF-κB, and CBS treatment further enhanced these inhibitory effects under IL-17A-deficient conditions. CB protects against DSS-induced colitis by suppressing IL-17A/IL-17RA/NF-κB-mediated NETs formation in neutrophils. IL-17A knockdown confirmed IL-17A as a critical upstream regulator of NETs, establishing the IL-17A-NETs axis as a central mechanistic target of CB.

Endometrial cancer continues to be the most common gynecologic malignancy in the United States. Endometrial tumors frequently express hormonal receptors, making this pathway targeting an attractive anti-cancer treatment. Recent advances have broadened our understanding of the androgen receptor's role in solid tumors beyond prostate cancer. Understanding the significance of androgen receptor signaling and its effects on tumor behavior and therapeutic outcomes in endometrial cancer is important for further clinical development. This review presents inter-connected pathways involving sex hormone-binding globulin, androgens, and androgen receptor signaling in cellular processes related to tumor pathogenesis. Sex hormone-binding globulin regulates androgen levels, influencing aromatase activity and estrogen production, which in turn activates estrogen receptors involved in gene expression promoting cell growth. Concurrently, notch pathway transcription factor forkhead box A1 modulates androgen receptor activity, impacting androgen receptor target gene expression and cell proliferation. Lysin-specific histone demethylases lysine demethylase 4A and lysine demethylase 4B modify chromatin at c-Myc and p27 promoter regions, respectively, affecting gene expression critical for cell-cycle regulation and tumor progression, demonstrating complex regulation of cellular mechanisms by hormone signaling pathways. lysine demethylase 4A interacts with androgen receptor signaling through chromatin remodeling, influencing transcriptional regulation of key cell-cycle genes. The complexity of androgen receptor signaling in endometrial cancer, marked by its varied expression and influence, necessitates a deeper investigation to harness its full therapeutic potential. The exploration of androgen receptor-targeted therapies offers promising avenues for refining treatments and improving outcomes of patients with endometrial cancer. This narrative review synthesizes current evidence on androgen receptor signaling and its therapeutic implications in endometrial cancer. Several potential androgen receptor-targeted approaches are also discussed in the context of future therapeutic development. These possible candidates to call for further development include (1) triple hormonal targeting with androgen receptor inhibitor, aromatase inhibitor, gonadotropin-releasing hormone and agonism, (2) targeting androgen receptor and lysine-specific demethylase 1-dependent forkhead box A1 demethylation, (3) targeting lysine demethylase 4B, (4) gamma secretase inhibitor combination therapy, and (5) combined androgen receptor and immune checkpoint inhibition.

Microglia-mediated neuroinflammation is a key determinant of ischemic brain injury. Electroacupuncture (EA) is known to promote M2 polarization of microglia by upregulating Signal Transducer and Activator of Transcription 6 (STAT6) / Peroxisome Proliferator-Activated Receptor γ (PPARγ), however, the epigenetic mechanism governing the transcriptional stability and recruitment efficiency of this pathway remain poorly understood. We hypothesized that the transcriptional coactivator E1A-binding protein P300 (P300) may serve as a functional partner involved in facilitating this process. To test this, we established a middle cerebral artery occlusion (MCAO) model in mice and evaluated the neuroprotective effects of EA through laser speckle blood flow imaging, gait analysis, and triphenyl tetrazolium chloride (TTC) and Hematoxylin and Eosin (HE) staining. The effects of EA on microglial neuroinflammation were verified via transmission electron microscopy (TEM), immunofluorescence (IF), and Enzyme-Linked Immunosorbent Assay (ELISA). Furthermore, we utilized Western Blot (WB), co-Immunoprecipitation (Co-IP), chromatin immunoprecipitation followed by quantitative polymerase chain reaction (CHIP-qPCR), and CD68 promoter-driven adeno-associated virus (AAV) with P300 shRNA knockdown technology to deeply explore the core mechanism by which P300 regulates the assembly of the STAT6/PPARγ transcriptional complex during EA treatment. Results demonstrated that EA significantly restored cerebral blood flow, reduced infarct volume, and restore neurological function. Moreover, local knockdown of P300 in the ischemic penumbra via CD68 promoter driven AAV significantly attenuated the EA-induced M2 transition. Mechanistically, EA promoted the functional recruitment of P300 to STAT6, which was associated with the enhanced assembly of the STAT6/PPARγ complex on target promoters. In summary, EA promotes M2 polarization by enhancing the stability of the P300 associated STAT6/PPARγ transcriptional complex, providing a novel epigenetic intervention target for ischemic stroke treatment.