tbuckley/cabot-search huggingface dataset:
Research Progress on Antibacterial Applications of Bioactive Materials in Wound Infections: Design, Challenges, and Prospects
Authors: Wang Zheng, Yuanfang Cheng, Hui Shen, Litao Liu, Wei Hu, Haisheng Qian
Journal: Advanced Healthcare Materials (2025)

Bacterial wound infections pose a significant threat to global health, exacerbated by the increase in multidrug-resistant bacteria (MDRB) and the formation of elastic biofilms. This review explores the transformative potential of bioactive materials in addressing these challenges, focusing on their design, mechanisms of action, and therapeutic effects. In vivo, bioactive materials are designed to respond to unique bacterial microenvironment (BME), utilizing enzyme activity, controlled gas release, surface functionalization, and immune regulation to combat infections. In vitro, this review provides a comprehensive overview of the latest advances in the rational design of these materials, emphasizing the synergistic integration of structural modifications (such as size and morphology) with external physical stimuli (such as light, sound, electricity, magnetism, and force) to enhance antibacterial performance. Finally, the outstanding challenges and prospects in this rapidly evolving field are discussed.
Spectrum of cancer risk in Asian American and Pacific Islander solid organ transplant recipients
Authors: Jun Tao, Jaimie Z Shing, Kelly Yu, Aimée R Kreimer, Mei-Chin Hsieh, Karen S Pawlish, Jie Li, Baozhen Qiao, Judy R Rees, Kekoa Taparra, Jacqueline B Vo, Eric A Engels
Journal: JNCI Journal of the National Cancer Institute (2025)

Solid organ transplant recipients (SOTRs) have increased cancer risk, which may differ across racial groups. Cancer risk among Asian American and Pacific Islander SOTRs is ill-defined. We evaluated Asian, Pacific Islander, and White SOTRs from a linkage of the United States SOTR registry with 34 cancer registries (1990-2019). We calculated age-and-sex adjusted incidence rate ratios (aIRRs) to compare cancer risk between races and standardized incidence ratios (SIRs) to measure risk relative to race-matched general populations. Compared with Asian SOTRs, Pacific Islander SOTRs had notably higher incidence of pancreatic cancer (aIRR = 3.7, 95%CI = 1.6-8.6) and melanoma (aIRR = 6.7, 95%CI = 1.2-36). Compared with White SOTRs, Asian and Pacific Islander SOTRs had lower melanoma incidence but higher nasopharyngeal carcinoma incidence. Compared with the general population, Asian SOTRs had increased risk of cancers of the anus (SIR = 7.9, 95%CI = 3.6-15), penis (SIR = 8.9, 95%CI = 2.9-21), non-epithelial skin (SIR = 9.8, 95%CI = 5.4-17), kidney (SIR = 5.3, 95%CI = 4.3-6.5), and renal pelvis (SIR = 7.4, 95%CI = 3.7-13); non-Hodgkin lymphoma including chronic lymphocytic leukemia (NHL/CLL) (SIR = 6.4, 95%CI = 5.6-7.3); Hodgkin lymphoma (SIR = 6.1, 95%CI = 2.8-12); and Kaposi sarcoma (SIR = 15, 95%CI = 6.6-30). Compared with the general population, Pacific Islander SOTRs had increased risk of cancers of the anus (SIR:12, 95%CI = 1.5-45), pancreas (SIR = 3.3, 95%CI = 1.3-6.8), non-epithelial skin (SIR = 9.3, 95%CI = 1.1, 34), and thyroid (SIR = 3.4, 95%CI = 1.2-7.4); NHL/CLL (SIR = 4.5, 95%CI = 2.3-7.9); and Kaposi sarcoma (SIR = 71, 95%CI = 8.6-258). Asian, Pacific Islander and White SOTRs all experienced elevated cancer risk compared with their race-matched general population. Different cancer risks in these racial groups might be explained by differences in risk factors in the general population or unique features of SOTRs in these groups.
Rectal diclofenac versus indomethacin for prevention of post-ERCP pancreatitis (DIPPP): a multicentre, double-blind, randomised, controlled trial
Authors: Xiaoyu Kang, Mingxing Xia, Jun Wang, Xiangping Wang, Hui Luo, Wenhao Qin, Zirong Liang, Gang Zhao, Longbao Yang, Hao Sun, Jie Tao, Bo Ning, Li Zhong, Rongchun Zhang, Xuyuan Ma, Jianghai Zhao, Laifu Yue, Haifeng Jin, Chenxi Kang, Gui Ren, Shuhui Liang, Haiying Wang, Ling Wang, Yongzhan Nie, Kaichun Wu, Dai-Ming Fan, Yanglin Pan
Journal: Gut (2025)

Recent meta-analyses suggested diclofenac may be superior to indomethacin in preventing post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP). The aim of our study was to compare the efficacy of 100 mg rectal indomethacin versus diclofenac on PEP incidences. This multicentre, double-blinded, randomised controlled trial was conducted in nine tertiary centres in China. Patients with low and high risk for PEP and native papilla were randomly allocated (1:1) to receive 100 mg diclofenac or 100 mg indomethacin rectally before ERCP. The primary outcome was the occurrence of PEP defined by the Cotton consensus. The intention-to-treat principle was conducted for the analysis. The trial was terminated early for futility after the predetermined first interim analysis. Between June 2023 and May 2024, 1204 patients were randomised into the diclofenac group (n=600) or indomethacin group (n=604). Baseline characteristics were balanced. The primary outcome occurred in 53 patients (8.8%) of 600 patients allocated to the diclofenac group and 37 patients (6.1%) of 604 patients allocated to the indomethacin group (relative risk 1.44; 95% CI 0.96 to 2.16, p=0.074). PEP occurred in 35 (14.2%) of 247 high-risk patients in the diclofenac group and 26 (9.8%) of 266 high-risk patients in the indomethacin group (p=0.124). PEP incidences were also comparable in low-risk patients between the two groups (18/353 (5.1%) vs 11/338 (3.3%), p=0.227). Other ERCP-related complications did not differ between the two groups. Pre-procedure 100 mg rectal diclofenac was not superior to the same dose of rectal indomethacin regarding preventing PEP. These findings supported current clinical practice guidelines of 100 mg indomethacin or diclofenac for PEP prophylaxis in patients without contraindications. ClinicalTrials.gov (NCT05947461).
Stronger evidence for relaxed selection than adaptive evolution in high-elevation animal mtDNA
Authors: Erik N K Iverson, Abby Criswell, Justin C Havird
Journal: Molecular Biology and Evolution (2025)

Mitochondrial (mt) genes are the subject of many adaptive hypotheses due to the key role of mitochondria in energy production and metabolism. One widespread adaptive hypothesis is that selection imposed by life at high elevation leads to the rapid fixation of beneficial alleles in mtDNA, reflected in the increased rates of mtDNA evolution documented in many high-elevation species. However, the assumption that fast mtDNA evolution is caused by positive, rather than relaxed purifying selection has rarely been tested. Here, we calculated the dN/dS ratio, a metric of nonsynonymous substitution bias, and explicitly tested for relaxed selection in the mtDNA of over 700 species of terrestrial vertebrates, freshwater fishes, and arthropods, with information on elevation and latitudinal range limits, range sizes, and body sizes. We confirmed that mitochondrial genomes of high-elevation taxa have slightly higher dN/dS ratios compared to low-elevation relatives. High-elevation species tend to have smaller ranges, which predict higher dN/dS ratios and more relaxed selection across species and clades, while absolute elevation and latitude do not predict higher dN/dS. We also find a positive relationship between body mass and dN/dS, supporting a role for small effective population size leading to relaxed selection. We conclude that higher mt dN/dS among high-elevation species is more likely to reflect relaxed selection due to smaller ranges and reduced effective population size than adaptation to the environment. Our results highlight the importance of rigorously testing adaptive stories against non-adaptive alternative hypotheses, especially in mt genomes.
Biomimetic Co‐delivery of Lenvatinib and FePt Nanoparticles for Enhanced Ferroptosis/Apoptosis Treatment of Hepatocellular Carcinoma
Authors: Feichao Xuan, Xingyang Zhao, Weiran Pang, Zirong Li, Xiangyi Yin, Weizhong Xie, Xiaojun Zeng, Liming Nie, Junying Yang, Shiying Li, Puxiang Lai, Chihua Fang
Journal: Advanced Healthcare Materials (2025)

Lenvatinib, endorse as a first-line targeted therapy, has demonstrated efficacy in extending the survival span of individuals afflicted with advanced Hepatocellular carcinoma (HCC). However, its therapeutic effect wears off with time, which is ascribed to the cancer cell's tendency to evade and tamper with its usual modes of action, severely limiting its clinical use. This study devises an innovative therapeutic modality involving the synergistic co-delivery of FePt nanoparticles (NPs) and Lenvatinib via poly lactic-co-glycolic acid (PLGA) NPs encase in HCC cell membranes (Len/FePt@CMP NPs). The investigation explores the mechanism through which Lenvatinib induces ferroptosis in HCC, notably by dampening the glutathione peroxidase 4 (GPX4) through the inhibition of fibroblast growth factor receptor 4. FePt NPs are engineered to enhance the efficacy of ferroptosis and apoptosis for HCC treatment. Concurrently, the incorporation of the cancer cell membrane facilitates the targeted accumulation of NPs at the tumor site, leveraging mechanisms of immune evasion and homologous targeting. This enhances ferroptosis/apoptosis treatment efficacy, triggeres by Len/FePt@CMP NPs, is convincingly demonstrated both in vitro and in vivo. The proposed approach has the potential to redefine HCC therapeutic paradigms by overcoming mono-therapeutic limitations in current clinical treatments, showcasing the improved efficacy of a comprehensive strategy.
Variable gene copy number in cancer-related pathways is associated with cancer prevalence across mammals
Authors: Sophie Matthews, Vahid Nikoonejad Fard, Marc Tollis, Cathal Seoighe
Journal: Molecular Biology and Evolution (2025)

Cancer is a disease of multicellularity, observed across the tree of life. In principle, animals with larger body sizes and longer lifespans should be at increased risk of developing cancer. However, there is no strong relationship between these traits and cancer across mammals. Previous studies have proposed that increased copy number of cancer-related genes may enhance the robustness of cancer suppression pathways in long-lived mammals, but these studies have not extended beyond known cancer-related genes. In this study, we conducted a phylogenetic generalised least squares (PGLS) analysis to test for associations between copy number of all protein-coding genes and longevity, body size, and cancer prevalence across 94 species of mammals. In addition to investigating the copy number of individual genes, we tested sets of related genes for a relationship between the aggregated gene copy number of the set and these traits. We did not find strong evidence to support the hypothesis that adaptive changes in gene copy number contribute to the lack of correlation between cancer prevalence and body size or lifespan. However, we found several biological processes where aggregate copy number was associated with malignancy rate. The strongest association was for the gene set relating to transforming growth factor-beta (TGF-β), a cytokine that plays a role in cancer progression. Overall, this study provides a comprehensive evaluation of the role of gene copy number in adaptation to body size and lifespan and sheds light on the contribution of gene copy number to variation in cancer prevalence across mammals.
Associations of self-identified race and ethnicity and genetic ancestry with mortality among cancer survivors
Authors: Jacqueline B Vo, Derek W Brown, Ian D Buller, Jaimie Z Shing, Naoise Synnott, Rena R Jones, Maria Teresa Landi, Wen-Yi Huang, Mitchell J Machiela, Amy Berrington De Gonzalez, Timiya S Nolan, Peter Kraft, Faustine Williams, Neal D Freedman
Journal: JNCI Journal of the National Cancer Institute (2025)

Self-identified race and ethnicity (SIRE) and genetic ancestry (GA) are potentially associated with disparities in health outcomes; however, independent effects of SIRE and GA on mortality in cancer survivors including when adjusting for multiple risk factors are understudied. Among 23,445 cancer survivors in the Prostate, Lung, Colorectal, and Ovarian Screening Trial, SIRE was associated with mortality among prostate, colorectal, lung, ovarian, and breast cancer survivors; GA was associated with mortality among prostate, colorectal, and breast cancer survivors. Associations were strong when adjusting for age at cancer diagnosis, sex, and tumor characteristics, but attenuated when adjusting for individual-level factors and population-level socioeconomic status. For example, mortality risk was higher among Black vs White prostate cancer survivors and African GA vs European GA, but associations were attenuated after multilevel adjustment. Results suggest SIRE and GA do not solely reflect biologic variation; rather, social factors may drive mortality differences by SIRE and GA.
Effects of exercise on inflammation in female survivors of nonmetastatic breast cancer: a systematic review and meta-analysis
Authors: Francesco Bettariga, Dennis R Taaffe, Anita Borsati, Alice Avancini, Sara Pilotto, Stefano G Lazzarini, Pedro Lopez, Luca Maestroni, Umberto Crainich, John P Campbell, Timothy D Clay, Daniel A Galvão, Robert U Newton
Journal: JNCI Journal of the National Cancer Institute (2025)

Despite advances in breast cancer treatment, recurrence remains common and contributes to higher mortality risk. Among the potential mechanisms, inflammation plays a key role in recurrence by promoting tumor progression. Exercise provides a wide array of health benefits and may reduce inflammation, potentially reducing mortality risk. However, the effects of exercise, including mode (ie, resistance training [RT], aerobic training [AT], and combined RT and AT) and program duration, on inflammatory biomarkers in breast cancer survivors remain to be elucidated. A systematic search was undertaken in PubMed, CINAHL, Embase, SPORTDiscus and CENTRAL in August 2024. Randomized controlled trials examining the effects of exercise on IL-1β, IL-6, IL-8, IL-10, TNF-α, and CRP were included. A random-effects meta-analysis was undertaken to quantify the magnitude of change. Twenty-two studies were included (n = 968). Exercise induced small to large significant reductions in IL-6 (SMD = -0.85; 95% CI = -1.68 to -0.02; p = .05) and TNF-α (SMD = -0.40; 95% CI = -0.81 to 0.01; p = .05) and a trend for a decrease in CRP. When stratifying by exercise mode, trends toward reduction in IL-6 and TNF-α were observed for combined exercise, whilst changes were not generally affected by exercise program duration. Exercise, especially combined RT and AT, can reduce pro-inflammatory biomarkers, and may be a suitable strategy to reduce inflammation in breast cancer survivors. However, further research is needed to investigate the effects of exercise mode and program duration on markers of inflammation in this survivor group.
Sex-specific radiation-associated lung cancer mortality risks as impacted by smoking among US radiologic technologists
Authors: Cato M Milder, Elizabeth K Cahoon, Sara J Schonfeld, Dale L Preston, Bruce H Alexander, Martha S Linet, Cari M Kitahara
Journal: JNCI Journal of the National Cancer Institute (2025)

The Life Span Study of Japanese atomic bomb survivors estimated greater risks of radiation-associated lung cancer among females than males, with direct implications for occupational radiation safety policy. To evaluate replicability of these findings in radiation workers, we assessed sex-specific radiation-associated risks of lung cancer mortality in a large cohort of U.S. radiologic technologists. Using data from four questionnaires (1983-2013), we reconstructed lifetime smoking history for 83,715 female and 26,650 male technologists. We estimated individual lung occupational radiation doses using badge dose and questionnaire data. We used Poisson regression to investigate joint radiation-smoking effects on sex-averaged and sex-specific lung cancer mortality risk. For 1243 female and 607 male technologists who died from lung cancer, median cumulative lung dose was 16.2mGy (non-cases: 7.7mGy) and 24.5mGy (non-cases: 10.1mGy), respectively. Excess risk of lung cancer increased with increasing radiation dose. However, smoking modified this effect: the radiation effect at 100mGy increased until 16 cigarettes/day, after which it declined. Excess relative risk (ERR) per 100mGy was greater among males (never smoking additive ERR = 1.98; 95%CI = 0.34, 6.25) than females (never smoking additive ERR = 0.40; 95%CI=-0.02, 1.21); sex-differences persisted up to ∼40 cigarettes/day. Our results indicated radiation-associated risks of lung cancer mortality were stronger in males than females, in contrast to the Life Span Study. However, both studies found radiation-associated risks were highest in workers with light-to-moderate smoking intensity. Altogether, these findings reinforce the importance of rigorous radiation protection measures for all radiation workers, regardless of sex, alongside interventions to support smoking cessation.
Long-term (68 weeks) administration of nemolizumab and topical corticosteroids for prurigo nodularis in patients aged ≥13 years: efficacy and safety data from a phase II/III study
Authors: Hiroo Yokozeki, Hiroyuki Murota, Takayo Matsumura
Journal: British Journal of Dermatology (2025)

The biological therapy nemolizumab has been shown to improve the signs and symptoms of prurigo nodularis (PN) to a significantly greater extent than placebo over 16 weeks of treatment. We now report efficacy and safety data over 68 weeks. To evaluate the long-term impact of nemolizumab on pruritus, disease severity, quality of life, and topical corticosteroid usage in patients with PN in Japan, and to confirm the safety profile. Asian patients aged ≥13 years were randomly assigned (1:1:1) to receive nemolizumab 30 mg, 60 mg, or placebo, with concomitant medium-potency topical corticosteroids, every 4 weeks for 16 weeks. For the subsequent 52 weeks, nemolizumab treatment was continued, while placebo-treated patients were reallocated to either the 30-mg or 60-mg nemolizumab groups. Efficacy outcome measures included the Peak Pruritus Numerical Rating Scale (PP-NRS), 5-level itch scale, Investigator's Global Assessment (IGA), the number of PN nodules, Insomnia Severity Index, Dermatology Life Quality Index, and use of topical corticosteroids. Safety measures included the frequency of treatment-emergent adverse events (TEAEs). In the modified intention-to-treat population (n=226), nemolizumab provided sustained and continuing improvements in efficacy between weeks 16 and 68. In patients who received nemolizumab 30 mg, the PP-NRS had decreased by 60.5% at week 16 and 78.6% at week 68; respective decreases in the 60-mg group were 55.1% and 76.5%. Across all treatment groups, a large proportion of patients had improvements indicating a reduction from moderate-to-severe to mild pruritus, IGA improvements indicating a reduction in PN severity, a decrease in the number of nodules, and rapid and durable improvements in sleep and daily life activities. Nemolizumab-treated patients were also able to reduce the daily quantity of medium-potency and higher topical corticosteroids used by at least half. There was no indication of relapse in pruritus, PN severity, or quality of life scores following treatment cessation. Most TEAEs were mild and were similar to those reported in prior studies. Nemolizumab elicited continuous and durable improvements across multiple measures of pruritus, PN severity, and quality of life over 68 weeks of treatment, with no new safety concerns. (Funded by Maruho; jRCT number, 2011200017).
The NuRD-SWI/SNF antagonism regulates the coordinated activation of EMT and inflammation in oral cancer
Authors: Roberto Stabile, Francesco A Tucci, Mathijs P Verhagen, Carmen Embregts, Thierry P P van den Bosch, Rosalie Joosten, Maria J De Herdt, Berdine van der Steen, Alex L Nigg, Senada Koljenović, Jose A Hardillo, C Peter Verrijzer, Adrian Biddle, Robert J Baatenburg de Jong, Pieter J M Leenen, Riccardo Fodde
Journal: JNCI Journal of the National Cancer Institute (2025)

Phenotypic plasticity and inflammation, two well-established hallmarks of cancer, play key roles in local invasion and distant metastasis by enabling the rapid adaptation of tumor cells to dynamic micro-environmental changes. Here, we show that in oral squamous carcinoma cell carcinoma (OSCC), the competition between the NuRD and SWI/SNF chromatin remodeling complexes plays a pivotal role in regulating both epithelial-mesenchymal plasticity (EMP) and inflammation. By perturbing these complexes, we demonstrated their opposing downstream effects on the inflammatory pathways and EMP regulation. In particular, downregulation of the BRG1-specific SWI/SNF complex deregulates key inflammatory genes, such as TNF-α and IL6, in opposite ways when compared with the loss of CDK2AP1, a key member of the NuRD complex. We showed that CDK2AP1 genetic ablation triggers a pro-inflammatory secretome encompassing several chemokines and cytokines, thus promoting the recruitment of monocytes into the tumor microenvironment (TME). Furthermore, CDK2AP1 deletion stimulates their differentiation into M2-like macrophages, as validated on tumor microarrays from OSCC patient-derived tumor samples. Further analysis of the inverse correlation between CDK2AP1 expression and TME immune infiltration revealed specific downstream effects on the abundance and localization of CD68+ macrophages. Our study sheds light on the role of chromatin remodeling complexes in OSCC locoregional invasion and highlights the potential of CDK2AP1 and other members of NuRD and SWI/SNF chromatin remodeling complexes as prognostic markers and therapeutic targets.
Diagnostic efficacy of an extracellular vesicle-derived lncRNA-based liquid biopsy signature for the early detection of early-onset gastric cancer
Authors: Xin Guo, Weidong Wang, Xin Cheng, Qiying Song, Xinxin Wang, Jiangpeng Wei, Shenhui Xu, Xiaohui Lv, Gang Ji
Journal: Gut (2025)

Early-onset gastric cancer (EOGC) is a lethal malignancy. It differs from late-onset gastric cancer (LOGC) in clinical and molecular characteristics. The current strategies for EOGC detection have certain limitations in diagnostic performance due to the rising trend in EOGC. We developed a liquid biopsy signature for EOGC detection. We use a systematic discovery approach by analysing genome-wide transcriptomic profiling data from EOGC (n=43), LOGC (n=31) and age-matched non-disease controls (n=37) tissue samples. An extracellular vesicle-derived long non-coding RNA (EV-lncRNA) signature was identified in blood samples from a training cohort (n=299), and subsequently confirmed by qPCR in two external validation cohorts (n=462 and n=438), a preoperative/postoperative cohort (n=66) and a gastrointestinal tumour cohort (n=225). A three EV-lncRNA (NALT1, PTENP1 and HOTTIP) liquid biopsy signature was developed for EOGC detection with an area under the receiver operating characteristic curve (AUROC) of 0.924 (95% CI 0.889 to 0.953). This EV-lncRNA signature provided robust diagnostic performance in two external validation cohorts (Xi'an cohort: AUROC, 0.911; Beijing cohort: AUROC, 0.9323). Furthermore, the EV-lncRNA signature reliably identified resectable stage EOGC patients (stage I/II) and demonstrated better diagnostic performance than traditional GC-related biomarkers in distinguishing early-stage EOGC (stage I) from precancerous lesions. The low levels of this biomarker in postsurgery and other gastrointestinal tumour plasma samples indicated its GC specificity. The newly developed EV-lncRNA signature effectively identified EOGC patients at a resectable stage with enhanced precision, thereby improving the prognosis of patients who would have otherwise missed the curative treatment window.