South Asian women, like many other culturally and linguistically diverse populations in Australia, remain under-represented in breast cancer screening, perpetuating inequities in early detection and treatment. To explore perspectives of South Asian women and general practitioners (GPs) to identify barriers, facilitators and strategies to improve breast screening participation.

A qualitative study using semi-structured interviews was conducted with South Asian women (aged 35-65 years) and GPs in Victoria, Australia. Data were analysed using inductive and deductive reflexive thematic analysis, with findings mapped to the individual, interpersonal, organisational, community and policy levels of the Socio-Ecological Model, and interpreted using the Consolidated Framework for Implementation Research. Reporting followed the COREQ checklist.

Thirty-four participants (25 South Asian women and nine GPs) were interviewed. At the individual level, barriers included fear of pain or cancer diagnosis, modesty and competing priorities that reduced breast screening participation; whereas facilitators included preventive attitudes, awareness of the benefits of early detection and autonomy. Interpersonally, limited GP prompting and spousal permission restricted participation, whereas proactive GP communication, shared decision-making and family support encouraged it. Organisational barriers included difficulties navigating screening pathways and long waiting times, whereas cultural sensitivity and availability of female staff facilitated engagement. Community-level barriers included stigma around discussing breast health and language difficulties, whereas trusted translators and leveraging community networks promoted participation. Recommendations from participants for health policy level included proactive GP-patient communication, family-inclusive messaging, promoting awareness of female staff and policy reforms, such as automated, multilingual text reminders.

Breast screening participation is shaped by interacting individual, interpersonal, organisational, community and policy-level factors. Primary care has an important role in improving screening awareness and participation through culturally sensitive communication, proactive screening discussions and community-based outreach strategies.

A growing body of evidence supports prehabilitation in cancer patients, but the findings have been inconsistent. This overview aimed to identify, evaluate and summarise the effect of prehabilitation on the clinical outcomes of cancer patients.

Overview of systematic reviews.

PubMed, Embase, Cumulative Index to Nursing and Allied Health Literature, Cochrane Library and the JBI Evidence Synthesis database (Joanna Briggs Institute, University of Adelaide, Australia; hosted on Ovid) were searched from inception to January 2025. The search was updated in May 2026, and no new articles were included.

We included systematic reviews of randomised controlled trials (RCTs) involving adult cancer patients with a clinically established diagnosis who received prehabilitation interventions prior to surgical treatment. We excluded abstract-only citations, narrative reviews and scoping reviews. Reviews were excluded if ≥50% of the included studies were postoperative interventions, or if preoperative subgroup data could not be extracted.

Two reviewers independently extracted data on participants' characteristics, types of interventions, outcomes, synthesising methods and pooled anticipated absolute/relative effects for outcomes meta-analysed. Two reviewers assessed methodological quality using the A MeaSurement Tool to Assess Systematic Reviews 2 (AMSTAR 2) tool and assessed the certainty of evidence for prehabilitation using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) framework. Overlap among included systematic reviews was quantified using the corrected covered area (CCA).

Twenty systematic reviews (137 RCTs and 18 941 participants) were included. Low- to moderate-certainty evidence indicated that prehabilitation may improve preoperative physical fitness (eg, 6-minute walk test, preoperative cardiopulmonary function, preoperative lung function), reduce surgical complications and shorten the length of hospital stay. None of the included systematic reviews demonstrated a statistically significant effect on preoperative handgrip strength, 30-day readmission, mortality, anxiety or depression. Findings regarding physical activity and quality of life remained inconsistent. Overlap among included reviews was slight (CCA=4.15%).

Low- to moderate-certainty evidence suggests that prehabilitation may improve preoperative physical fitness, reduce surgical complications and shorten the length of hospital stay in adult cancer patients undergoing surgery, whereas current evidence does not support a beneficial effect on 30-day readmission, mortality, quality of life or psychological status. Given the predominantly low-to-moderate certainty of the evidence and the methodological heterogeneity across the included systematic reviews, these findings should be interpreted with caution. Methodologically robust and transparently reported RCTs and systematic reviews are needed to strengthen the certainty of evidence and to inform clinical implementation of prehabilitation.

CRD 42024533214.

Primary liver cancers, including hepatocellular carcinoma and intrahepatic cholangiocarcinoma, are one of the leading causes of cancer-related mortality. Transarterial chemoembolisation (TACE) and radioembolisation (TARE) are established palliative treatments yet they are traditionally performed during inpatient hospitalisation. Recent technical and organisational advances allow for safe same-day ambulatory procedures. In particular, the extent to which ambulatory intra-arterial therapy aligns with patients' expectations, comfort and quality of life remains poorly documented. The Care pathway for Hepatic intra-arterial Oncology in an ambulatory Context study (CHOC) trial aims to evaluate the implementation and effectiveness from both patient-centred and clinical perspectives of an ambulatory care pathway for intra-arterial treatment of primary liver cancer in a multicentre randomised hybrid type 1 trial.

CHOC is a pragmatic, multicentre, randomised controlled hybrid type 1 trial comparing ambulatory versus conventional inpatient care for patients undergoing TACE or TARE for primary liver cancer. A total of 206 patients (103 per arm) will be randomised 1:1 and followed for 7 months. The primary outcome is the patient's global satisfaction score, measured 3 days post-procedure using the EORTC PATSAT-C33 questionnaire. Secondary outcomes include quality of life, safety, clinical outcomes, cost analysis and an embedded qualitative implementation study assessing acceptability, adoption, feasibility and sustainability across centres. Economic analyses will estimate both per-patient costs and the 5-year budget impact for the French national health insurance.

The study has received ethical approval from the Protection of Persons Committee and adheres to the Declaration of Helsinki, good clinical practice and French regulatory requirements. Findings will be disseminated through peer-reviewed publications, conferences and participating centres to guide broader implementation of ambulatory interventional radiology care.

NCT06990659.

Oral carcinoma is the sixth most prevalent cancer type with a poor 5-year survival rate. mRNA-lipid nanoparticle-based immunotherapy can overcome the challenges associated with conventional treatment options. Here, we investigated the immunogenicity and antitumor efficacy of survivin antigen encoded mRNA lipid nanoparticles (LNPs) in combination with anti-CTLA-4 immune checkpoint inhibitor. Survivin mRNA was synthesized by in vitro transcription technique after cloning the antigenic target sequence into an expression vector. The mRNA-LNPs were prepared with lipids, ALC-0315, DOPE, and cholesterol using a droplet-based microfluidic device. The average particle size, polydispersity index and encapsulation efficiency of mRNA-LNPs was found to be 305 ± 68 nm, 0.11, and 65 ± 3.9%, respectively. Survivin mRNA-LNPs incubated with mouse-derived bone marrow dendritic cells showed activation of tumor-associated antigen specific T-cells. The co-culture of splenocytes, and cheek cells derived from C57BL/6 mouse administered with survivin mRNA-LNPs and CTLA-4 inhibitor with MOC-1 oral carcinoma cells showed significant (P < 0.05) reduction in the cancer cell viability compared with control group. The oral cancer cytotoxicity is attributed to the upregulation of MHCI and MHCII, CD8 + and CD4 + T-lymphocytes and reduction in the T-regulatory cells. Taken together, this study provides preliminary evidence for further development of survivin mRNA-LNPs and CTLA-4 inhibitor combination for oral cancer immunotherapy.

The hyaluronic acid receptor is typically overexpressed in cancer cells, and hyaluronic acid targeting has gained attention in cancer treatment. In this work, cytotoxic potential of magnetic iron oxide nanoparticles co-conjugated with hyaluronic acid and limonene in the MDA-MB-231 cell line was characterized. Physicochemical characteristics of the nanoparticles were studied by FT-IR, XRD, TEM, SEM-EDS, DLS, zeta potential and VSM analyses. Cytotoxic effects of Fe₃O₄@Glu-HA-LIM NPs in cancer and normal cells were studied by MTT assay. Flow cytometry and AO/PI staining were employed to study cell cycle phases and cell apoptosis levels in the cancer cells. ROS levels in the treated and control cells were also quantified. According to physicochemical characterization, Fe₃O₄@Glu-HA-LIM NPs were correctly synthesized and exhibited spherical shape, particle diameter of 29 to 69 nm, surface charge of -52.5mV, hydrodynamic size of 245.4 nm and magnetic saturation of 60.607emu/g at 9000Oe. The 24 -hour IC₅₀ of Fe₃O₄@Glu-HA-LIM NPs in the MDA-MB-231 cell line was 227 µg/mL and Fe₃O₄@Glu-HA-LIM NP displayed lower cytotoxicity in the normal cell line (24-hour IC₅₀=483 µg/mL), which is potentially attributed to hyaluronic acid receptor targeting and induction of significant oxidative stress in cancer cells. Treatment of cancer cells with Fe₃O₄@Glu-HA-LIM NPs caused cell cycle arrest mainly at the S and G2/M phases. Moreover, exposure to Fe₃O₄@Glu-HA-LIM NPs elevated ROS levels in the cancer cell line by 9.27 folds. This study demonstrates the promising cytotoxic potential of Fe₃O₄@Glu-HA-LIM NPs in the MDA-MB-231 cell line, which can be considered for chemotherapy of triple-negative breast cancer.

Adoptive cellular therapies may expand treatment options for pediatric brain tumors by focusing activity on tumor antigens and limiting off-tumor effects. We systematically reviewed preclinical and clinical evidence for CAR T cells, TCR-engineered T cells, and NK or γδ T-cell platforms directed against HER2, B7-H3 (CD276), EGFR806-reactive EGFR, GD2, IL13Rα2, and EphA2 or EphA3, with attention to delivery route, safety, persistence, and combination strategies. Following PRISMA, we searched PubMed, Embase, and Scopus from inception through September 17, 2025, restricted to English. The search yielded 324 records; 103 duplicates were removed; 221 titles and abstracts were screened; 180 full texts were reviewed; and 34 studies were extracted by two independent reviewers. We captured design, tumor and molecular features, product engineering, route and schedule, lymphodepletion, toxicities including cytokine release syndrome, immune effector cell associated neurotoxicity, and tumor inflammation associated neurotoxicity, radiographic or clinical response, survival, and correlatives such as persistence or trafficking in blood, cerebrospinal fluid, or tumor tissue, cytokines, and antigen dynamics. In vivo studies showed reproducible antitumor activity for HER2 in medulloblastoma, GD2 in diffuse midline glioma, and multi-antigen constructs incorporating IL13Rα2 and EphA2 in medulloblastoma and ependymoma, with significant survival advantages compared with controls. γδ T cells targeting the EphA axis selectively killed medulloblastoma with neural sparing; GD2 CAR NK-92 inhibited diffuse intrinsic pontine glioma growth. In early clinical programs, route shaped safety and pharmacodynamics. For GD2, low-dose intravenous induction followed by repeated intraventricular dosing produced objective radiographic regressions and manageable tumor inflammation associated neurotoxicity, while dose-limiting cytokine release syndrome was confined to higher intravenous doses. Intraventricular B7-H3 CAR T cells, given without lymphodepletion, enabled multi-cycle dosing with mainly grade 1 to 2 events and cerebrospinal fluid localized persistence. Weekly intracranial EGFR806 CAR T cells were feasible and well tolerated, with stable disease as the best response in a small cohort. Across trials, persistence and immune activation were most evident in cerebrospinal fluid, supporting cerebrospinal fluid centered pharmacodynamic monitoring. Mechanism-based combinations, including IGF-axis inhibition in diffuse midline glioma and epigenetic priming of GD2 with an integrated safety switch in medulloblastoma, enhanced activity. The evidence supports pediatric-centric antigen selection and a CNS-first, locoregional dosing approach to increase on-tumor exposure and reduce systemic toxicity. Priorities include multi-antigen strategies to prevent escape, incorporation of safety switches, earlier deployment when tumor burden is low, and prospective cerebrospinal fluid pharmacodynamics in multisite phase II studies.

Despite advances in treating acute lymphoblastic leukemia (ALL), resistance to asparaginase (ASNase) remains a major clinical hurdle. Recent evidence suggests that leukemic cells may evade ASNase-induced cytotoxicity by upregulating the glutamate/aspartate transporter EAAT1 (SLC1A3). This study aimed to evaluate whether pharmacological inhibition of EAAT1 using UCPH-101 could enhance the inhibitory effects of ASNase in T-ALL models.

Using patient-derived samples and established T-ALL cell lines (MOLT-4 and Jurkat) we assessed the effects of ASNase and UCPH-101, both alone and in combination. Combinations were designed based on IC₅₀-based fixed-ratio dosing, including sub-IC₅₀ and supra-IC₅₀ concentrations. Effects on cell viability, apoptosis, and apoptosis related gene expression were evaluated using standardized in vitro assays. Synergy was evaluated using the combination index (CI) method on the Chou-Talalay model.

Synergy analysis based on CI values revealed synergistic interactions (CI < 1) at sub and supra IC₅₀ concentrations of both agents in MOLT-4 and Jurkat cells. Dual targeting of amino acid metabolism through ASNase and EAAT1 inhibition resulted in significantly reduced cell viability and increased apoptotic cell death compared to controls. Combinatorial treatment led to significant alterations in the expression of key apoptotic regulators, suggesting a disruption of metabolic adaptation mechanisms in both leukemic cell lines.

These findings demonstrate that EAAT1 inhibition augments ASNase anti-leukemic activity in preclinical ALL models, revealing a metabolic vulnerability that can be exploited therapeutically. The mechanistic insights reported herein support further exploration of EAAT1-targeted strategies to improve outcomes in T-ALL.

Hepatocellular carcinoma (HCC) has an extremely poor prognosis. The emergence of immune checkpoint inhibitors (ICIs) has fundamentally transformed the therapeutic landscape for HCC. However, due to the limited response rate and complex resistance mechanisms of monotherapy, the core of clinical practice has shifted towards ICI-based combination strategies. This article systematically reviews the biological basis-primarily the immune microenvironment-and clinical evidence, including the limitations of monotherapy and the optimization of combination regimens, underlying this paradigm shift, as well as the challenges in achieving precision medicine (such as efficacy prediction and resistance). Finally, it points out that future breakthroughs rely on the integrated application of multi-omics-guided personalized regimens, engineered immune cell technologies, and AI-based predictive models. In summary, advancing HCC immunotherapy from broad combination strategies toward individualized precision combinations represents a promising direction for addressing current limitations and improving therapeutic benefit.

High-level MET gene amplification is a rare but potentially actionable alteration in gastric cancer. Previous phase III trials of MET-targeted therapies enrolled broadly MET-positive populations without prospective selection for high-level MET amplification, and no MET-directed therapy is currently established for this disease. Here, we report a 74-year-old woman with heavily pretreated metastatic gastric adenocarcinoma harboring high-level MET amplification (copy number 21) identified by comprehensive genomic profiling. Following expert panel review, the patient received capmatinib through the BELIEVE trial (NCCH1901; jRCTs031190104) and achieved a confirmed partial response at 8 weeks, with a 43.7% reduction in the sum of target lesion diameters. The response was maintained at 16 weeks; disease progression was observed at 24 weeks, with a progression-free survival of approximately 5.5 months. In the context of a literature review of MET-targeted therapies in gastric cancer, this case supports further investigation of selective MET inhibition in gastric cancer with high-level MET amplification, a rare molecular subset not prospectively enriched in previous clinical trials.

Targeted immunotherapies have transformed the treatment of relapsed and refractory B-cell acute lymphoblastic leukemia (B-ALL), yet their efficacy depends on sustained expression of lineage-associated surface antigens. This review examines how antigen-directed pressure reshapes the biology of resistance, distinguishes canonical antigen escape from lineage plasticity, and clarifies the genomic contexts, diagnostic challenges, and therapeutic implications of these distinct escape routes.

Under antigen-directed pressure, leukemia may escape through antigen downregulation, alternative splicing, acquired genetic alteration, or epitope disruption - mechanisms that generally preserve B-lineage identity and often remain addressable with alternative lineage-directed therapy. A biologically distinct route is lineage plasticity, in which cells destabilize lineage commitment or undergo overt lineage switch; clinical outcomes are poor, with a median overall survival of approximately 4.8 months in the largest reported series. Lineage switch is enriched within permissive genomic contexts, most notably KMT2A-rearranged leukemia, which accounted for the majority of B-ALL-to-acute myeloid leukemia or mixed-phenotype switches in a large international cohort. By contrast, CD19-negative antigen escape is more strongly associated with TP53 mutations and preserves B-lineage identity. Whether switching reflects selection of pre-existing subclones, active epigenetic reprogramming, or both remains unresolved. As antigen-directed therapies move into frontline use, distinguishing antigen escape from true lineage transformation is becoming essential for relapse surveillance, disease classification, therapeutic sequencing, and the design of strategies to prevent resistance.