With advancements in lymphoma treatment leading to improved survival rates, the time burden associated with cancer care has emerged as a significant concern. Time toxicity can disrupt daily life and impact treatment decisions; however, lymphoma-specific evidence regarding patients' subjective experiences remains limited. This study aimed to investigate the experiences of time toxicity and the coping strategies employed by young and middle-aged lymphoma patients in China.

This descriptive qualitative study took place from June to December 2025 in the haematology department of a tertiary hospital in Hangzhou, China. We employed purposive sampling with maximum variation to recruit patients aged 18-50 years who were undergoing lymphoma treatment. The study was informed by Time-Geography Theory. Data collection involved face-to-face semi-structured interviews, and the data were analysed using conventional content analysis.

The study involved fifteen participants, revealing five interconnected themes: (1) the multidimensional time burden driven by treatment; (2) the disruption of social roles and restructuring of daily life rhythms; (3) healthcare mobility constrained by time and space; (4) emotional distress associated with time toxicity; and (5) multilevel coping strategies for managing time toxicity. Time toxicity manifested not only as the cumulative time spent on healthcare activities but also as disruptions to daily routines, role functioning, healthcare mobility, and psychological well-being. Participants reported substantial time burdens due to frequent hospital visits, prolonged waiting times, and complex care pathways, particularly for those requiring cross-city care. Despite these challenges, patients employed various coping strategies, including active time management, Health-oriented self-management, cognitive adjustment, and family support.

Time toxicity in young and middle-aged lymphoma patients is a multidimensional and contextually embedded experience shaped by the interaction between healthcare demands and everyday life. These findings highlight the importance of considering patients' temporal and spatial circumstances when coordinating lymphoma care and developing supportive interventions.

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy. In this paper, we present DZ-ART1, a first-in-class, dual-function therapeutic. This innovative agent is composed of a tumor-targeting heptamethine carbocyanine dye conjugated to artemisinin (ART). Near-infrared imaging demonstrated precise tumor localization of DZ-ART1 in mice. DZ-ART1 accumulated 5- to 10-fold more in cancer cells compared to normal cells. DZ-ART1 significantly decreased the survival of eight PDAC cell lines with little effect on normal cells. It increased the lethal effect of chemotherapies in vitro and in vivo. Functional assays confirmed DZ-ART1's ability to disrupt mitochondrial bioenergetics, deplete ATP, and induce reactive oxygen species production. Mitochondrial depletion of cancer cells decreased DZ-ART1 uptake and cytotoxicity, highlighting its mechanistically unique, mitochondria-dependent action. Transcriptomic profiling revealed DZ-ART1's broad reprogramming of PDAC pathways related to cell survival, cancer stemness, and metastasis. In three rigorously validated preclinical models - Kras^þ/LSLG12D;Trp53^þ/LSLR172H;Pdx-1^-Cre (KPC) transgenic, syngeneic, and patient-derived xenografts (PDX) - DZ-ART1 markedly suppressed tumor growth and metastasis and prolonged survival, all without toxicity to normal tissues. DZ-ART1 represents a new class of anti-cancer therapeutics that uniquely combines diagnostic imaging and cancer cell organelle-specific targeting.

The etiopathogenesis of prostate cancer (PCa) is complex and involves multiple hormonal and environmental factors. Among these, the role of infectious agents remains controversial. Human papillomavirus (HPV) is known to promote carcinogenesis in epithelial tumors and has also been detected, albeit inconsistently, in PCa tissues. This systematic review, meta-analysis, and real-world cohort study aimed to clarify the prevalence and the prognostic role of intratumoral (IT)-HPV detection in locally advanced and metastatic PCa. We performed a systematic literature search including studies reporting IT-HPV detection in locally advanced (LA-PCa) and metastatic PCa (mPCa). Pooled prevalence estimates were calculated using random-effects models. In parallel, HPV DNA was analyzed using archival tissue in a single-center real-world retrospective cohort of 196 metastatic PCa patients. Twenty-three records met the inclusion criteria, comprising 22 full-text publications and one abstract. Nineteen datasets, encompassing 837 patients, contributed to the quantitative synthesis of stage III-IV disease. Pooled IT-HPV prevalence in mPCa was 18.5% (95% CI, 6.4-34%), while including also LA-PCa was 14.6% (95% CI, 5.2-26.8). Eastern countries showed higher IT-HPV prevalence in both mPCa and LA-PCa (40% and 34.3%, respectively) compared with Western regions (0.8% and 0.3%; p < 0.0001). HPV-positive PCa was associated with a higher Gleason score (>7) in advanced stage (pooled OR 6.32, 95% CI, 3.13-12.78) compared with IT-HPV-negative PCa; however, no studies reported data on its association with survival outcomes. Within our retrospective cohort, IT-HPV DNA was detected in 3.1% of cases (6/196) and exhibited typical PCa driver alterations, such as TP53, SPOP, PIK3CA, and AR amplification. IT-HPV seems to be infrequent in metastatic and locally advanced PCa in Western populations and more prevalent in Asian cohorts and might be associated with a higher Gleason score. IT-HPV-positive advanced PCa seems to exhibit typical PCa driver alterations. Data on the association between IT-HPV status and survival outcomes in PCa are lacking. Standardized molecular assays and multicenter prospective studies are needed to delineate its significance in PCa.

Hepatocellular carcinoma (HCC) progression and metastasis are closely associated with the acquisition and maintenance of a mesenchymal phenotype. The transforming growth factor (TGF)-β/SMAD signaling pathway stabilizes the mesenchymal state of HCC, whereas the inflammatory cytokine interleukin-1β (IL-1β) is abundantly expressed in the HCC tumor microenvironment and activates p38 mitogen-activated protein kinase (MAPK), a key mediator of cell migration and invasion. However, the role of inflammatory cytokines in modulating TGF-β-mediated mesenchymal phenotypes remains unclear. Therefore, this study aimed to determine the function of IL-1β in the regulation of mesenchymal phenotypes in SK-Hep1 cells and elucidate the roles of the TGF-β/SMAD and p38 MAPK signaling pathways.

Cells were treated with TGF-β1, IL-1β, or both in combination and mesenchymal marker expression was assessed by western blotting and immunofluorescence. Cell migration and invasion were evaluated by wound healing and Matrigel transwell invasion assays. The selective p38 inhibitor SB202190 was used to determine pathway dependency.

TGF-β1 induced fibronectin and N-cadherin expression and increased their migratory and invasive capacities, whereas IL-1β further enhanced these effects. Mechanistically, IL-1β markedly increased the p38 MAPK phosphorylation and enhanced the TGF-β1-mediated SMAD2/3 phosphorylation and nuclear trans-localization. Furthermore, SB202190 decreased fibronectin and N-cadherin expression and reduced the migratory and invasive capacities of SK-Hep1 cells.

These results indicate that IL-1β enhances TGF-β1-mediated mesenchymal phenotypes in SK-Hep1 cells via the activation of a p38 MAPK pathway that is associated with TGF-β/SMAD signaling. Considering that inflammation accelerates HCC progression and metastasis by enhancing the mesenchymal phenotype, these findings support further investigation of anti-inflammatory strategies for HCC management.

Breast cancer (BC) constitutes the most prevalent malignancy globally, with an incidence of approximately 80%-85% for invasive ductal carcinoma (IDC) and 10%-15% for invasive lobular carcinoma (ILC), and a persistently high mortality and morbidity rate. Although IDC and ILC originate from distinct cellular lineages (ductal and lobular epithelial cells, respectively), they frequently develop in the context of hormonal dysregulation and chronic proliferative stimuli. Recent evidence accumulated over the past decade has demonstrated a role for cytokines belonging to the interleukin-6 (IL-6) family in the pathogenesis and progression of BC. These cytokines exert their effects via the activator of transcription (JAK/STAT) pathways, activating downstream Janus kinase/signal transducer, and gp130 receptor subunit activation. As a member of the IL-6 family, Oncostatin M (OSM.) is critically involved in the processes of autoimmune disorders, inflammation, and oncogenesis, particularly in BC. It has been demonstrated that the overexpression of OSM and OSM receptor (OSMR) plays a pivotal role in cancer cell remodeling and promotes cell proliferation, angiogenesis, survival, invasion, and other hallmark features of BC. However, owing to the involvement of multiple signaling pathways, OSM can exert context-dependent and even contradictory effects in certain cancer types. This review aims to examine the emerging roles of OSM in BC, elucidate its multifunctional role in tumor regulation and progression, and ultimately explore therapeutic strategies developed to modulate this cytokine in the context of BC.

Hepatocellular carcinoma (HCC) is a common malignancy characterised by molecular heterogeneity and poor prognosis. The purpose of this study was to determine differences in the expression of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR), Fatty Acid Synthase (FASN), FKBP12-rapamycin-associated protein (FRAP; mTOR), and B-cell scaffold protein with ankyrin repeats 1 (BANK1) between HCC patients and controls. A total of 200 blood samples (100 from HCC patients and 100 from controls) were analysed using Reverse Transcription Polymerase Chain Reaction (RT-PCR), with Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as an internal control. The results demonstrated significant upregulation of FASN and FRAP (mTOR) (p < 0.0001) and downregulation of CFTR and BANK1 (p < 0.0001), suggesting potential oncogenic and tumour-suppressive roles, respectively. Gene expression levels also differed significantly across Stages I, II, III, and IV. The Ct values for BANK1 were higher than those for CFTR, FASN, and FRAP (mTOR). Because the expression measurements for the four genes were obtained from blood rather than tumour parenchyma, these findings were not interpreted as direct evidence of gene expression within tumour tissue. Survival analysis using a public dataset revealed that dysregulation of these genes was associated with lower survival rates. In silico pathway analysis demonstrated complex interactions among the four genes, linking them to metabolic regulation, immune signalling, and cellular proliferation pathways. Overall, the integrated network involving CFTR, FASN, FRAP (mTOR), and BANK1 may have potential as a novel prognostic marker by reflecting combined metabolic and immune pathway activity. A combined four-gene logistic regression model demonstrated promising discriminative performance in the present cohort (AUC = 0.89). However, this finding requires validation in independent cohorts before any diagnostic application can be considered.

Epstein-Barr virus (EBV) is an oncogenic DNA virus that is etiologically associated with multiple malignancies, including nasopharyngeal carcinoma, gastric carcinoma, and lymphomas. Although EBV encodes numerous viral microRNAs (miRNAs), the pathogenic functions of individual miRNAs remain incompletely characterized. In this study, we identify EBV-encoded miR-BART17-5p as a tumor-suppressive miRNA that directly targets ceramide kinase (CERK). CERK expression is significantly downregulated in EBV-associated gastric cancer (EBVaGC) tissues and EBV-positive AGS-EBV cells and inversely correlates with miR-BART17-5p levels. Mechanistic analyses further demonstrate that miR-BART17-5p directly targets the 3' untranslated region (3'UTR) of CERK, thereby regulating its expression. Overexpression of miR-BART17-5p mimics or knockdown of CERK in AGS cells significantly suppresses tumor -associated phenotypes, including cell proliferation, migration, and invasion. Conversely, inhibition of miR-BART17-5p in AGS-EBV cells rescues these phenotypes. Similar results were obtained in SNU719 cells. Mechanistically, miR-BART17-5p inhibits the PI3K/AKT signaling by targeting CERK. Restoration of CERK expression reactivates PI3K/AKT signaling and reverses the inhibitory effects on cell proliferation, migration, and invasion in AGS cells. To evaluate the therapeutic potential of miR-BART17-5p, systemic administration of engineered cholesterol-conjugated miR-BART17-5p agomirs significantly suppresses tumor growth in xenograft models. Collectively, our findings reveal a previously unrecognized EBV-host interaction whereby miR-BART17-5p constrains cancer progression through modulation of CERK/PI3K/AKT signaling activation, highlighting its potential as a preclinical therapeutic strategy for cancer.

During the COVID-19 pandemic, over 100 countries successfully deployed smartphone-based exposure notification (EN) apps alongside conventional contact tracing to mitigate the transmission of SARS-CoV-2. These systems enabled millions of COVID-19-positive individuals to anonymously alert community members of a potential exposure. Although evidence on EN program implementation is limited, leveraging expertise from public health professionals, academics, and global implementers from various disciplines can contribute to addressing this research gap.

This study aimed to explore barriers and facilitators to adoption, identify optimal use cases for these tools, and understand how advancements in technology and policy might maximize EN utility for mitigating other infectious outbreaks.

We used the Delphi method to develop a comprehensive online survey comprising closed-ended and open-ended questions. We considered consensus was reached when at least 75% of respondents selected "agree" or "strongly agree" for an item or statement. More than 30 global EN experts known to the investigators were invited to participate in the survey, and those who participated were asked to nominate or recruit others deemed eligible via a peer-to-peer method. We used descriptive and content analyses to summarize key findings from the survey. We invited the same experts to attend virtual focus groups to further probe their insights into the survey findings.

Twenty-two experts from 6 countries, including 10 experts from the United States, representing 3 continents, participated. Respondents were involved in the implementation of various EN technologies that encompassed varying levels of integration with existing public health agencies' infrastructure. Consensus was reached concerning the development of additional functionalities of the system, such as the ability for users to self-report a positive result from a SARS-CoV-2 at-home test, receive additional public health information from the app (ie, information on testing and social services), and receive general venue-based notifications concerning superspreader events. Other items that reached consensus included how the tool could be used for additional epidemiological purposes, such as expanding the technology to other airborne diseases, and the need for integration with surveillance data streams to augment analytics and forecasting.

Global EN systems have the potential to be optimized for public health emergencies beyond COVID-19 and can be used as epidemiological surveillance tools in future disease outbreaks. Decision-makers and experts should revise existing protocols and seek to incorporate new functionality to alleviate the disease burden on both users and public health agencies.

Continuous monitoring of influenza antigenic drift is vital for vaccine strain selection. This study utilized global Department of War (DOW) surveillance data to evaluate circulating influenza strains and inform the 2026-2027 Northern Hemisphere influenza vaccine recommendations by the World Health Organization. From September 2025 through February 2026, the Department of Defense Global Respiratory Pathogen Surveillance Program collected and analyzed respiratory specimens from over 100 sentinel sites globally. Influenza-positive samples underwent next-generation sequencing, phylogenetic analysis, and antigenic characterization. Analysis of 1,300 sequences revealed A(H3N2) as the predominant (80.1%) subtype, followed by A(H1N1)pdm09 (10.6%) and B/Victoria (9.3%), with variations between combatant commands. Significant antigenic drift led to the dominance of subclades K, D.3.1/D.3.1.1, and C.3.1, respectively. Testing indicated that the 2025-2026 vaccine components offered reduced protection against these emerging strains. Antigenic cartography confirms that the 2026-2027 vaccine strains provide significantly improved protection against circulating viruses. Antiviral resistance markers for neuraminidase inhibitors such as oseltamivir remain rare, with only 2 identified in A(H1N1)pdm09. These data are critical for maintaining force health protection and assessing vaccine performance within highly mobile DOW populations. Analysis of 2025-2026 influenza season data revealed the predominance of subclades A(H1N1)pdm09 D.3.1/D.3.1.1, A(H3N2) K, and B/Victoria C.3.1. Antigenic cartography employing recent candidate vaccine viruses from the U.S. Centers for Disease Control and Prevention confirmed that the World Health Organization's strain recommendations for the 2026-2027 Northern Hemisphere influenza vaccine provide the best protection against these circulating strains.

Aim: To investigate the influence of risk factors on the development of recurrent respiratory diseases, to analyze clinical and epidemiological components for the possibility of their prevention.

Materials and Methods: The research was conducted on the basis of the Uzhhorod Children Primary School. Children studied groups (n=118) aged 6-9 years with a diagnosis of "acute recurrent respiratory diseases" were formed.

Results: Childrens inflammatory episodes were most often observed, in particular: bacterial tonsillitis - 86 (72,89%), otitis - 56 (47,46%), pneumonia and sinusitis - 37 (31,36%) (identical indicators). In our study, respiratory infection caused by at least one pathogen was observed in 63,4±4,1% of patients. The proportion of viral infections was 48,34±3,6%, in particular, coinfections were identified in 36,4±2,9% of cases. The distribution of confirmed viruses is as follows: AdV (26,34±1,7%), SARS-CoV-2 (19,5±1,6%), RV (18,2%), RSV (17,8%), influenza A/B (11,4%) and others in minimal structural components (6.8%).

Conclusions: Recurrent respiratory tract infection is a multifactorial disease caused by a complex interaction of environmental and host factors. We suggest that an "additive effect," depending on the number of factors involved, most of which may be underestimated, may be a plausible explanation for the recurrence of respiratory tract infection in a significant proportion of healthy children with unexplained frequent respiratory symptoms.