To improve cancer patient management, international recommendations underline the importance of integrating palliative care (PC) into oncology, and education of future oncologists is key to achieving this. In France, no study has evaluated PC training for oncology residents. This study aims to identify educational needs in PC among French oncology residents and to assess the acceptability of changing their medical training.

A nationwide, descriptive, mixed-methods study was performed between 2021 and 2023. The first qualitative phase used semi-structured interviews with oncology residents to identify their training needs in PC. The second quantitative phase performed a nationwide online survey among all French oncology residents.

The least trained residents were the least keen to receive training, expressing a reductive definition of PC to the end of life, as well as a non-collaborative and integrated vision between PC and oncology. The questionnaire had a participation rate of 24%; 95% (n = 126) were in favour of modifying their PC training. Of these, 98% (n = 123) were strongly in favour of integrating PC training into the national oncology residency programme, and 91.3% (n = 115) were in favour of practical experience in a PC unit during their residency.

This study highlights a need to improve the delivery of PC training both in theory and practice in France. This study corroborates previous reports of inadequate PC training, its heterogeneity, and the benefits to be yielded from improving it. To enable early integrated PC, improving training of oncology residents in PC is an attractive target.

Nasopharyngeal carcinoma (NPC) is a prevalent malignancy characterized by variable outcomes, even after standardized treatment protocols. The American Joint Committee on Cancer (AJCC)/Union for International Cancer Control (UICC) staging system has proven limited in its ability to predict survival, which highlights the necessity for the discovery of new biomarkers.

This study was a retrospective analysis of 842 NPC patients who received platinum-based concurrent chemoradiotherapy (CCRT). The cholesterol-to-lymphocyte ratio (CLR) was calculated and evaluated as a potential prognostic factor. Both univariate and multivariate analyses were conducted to pinpoint independent prognostic variables. Furthermore, CLR-based nomograms were developed and assessed for its predictive accuracy.

Low CLR (≤ 3.06) was significantly linked to both improved overall survival (OS; HR = 0.640, 95% CI 0.473-0.866, P < 0.001)and progression-free survival (PFS; HR = 0.754, 95% CI 0.586-0.970, P = 0.028). Multivariate analysis confirmed CLR as an independent prognostic factor for OS (but only in univariate analysis for PFS). Additionally, age, tumor stage, nodal stage, and body mass index were independently associated with both OS and PFS in multivariate analysis. The CLR-based nomogram showed superior discriminative performance compared to the traditional staging system, with higher C-indices for both OS(0.668 vs 0.635) and PFS (0.655 vs 0.625).

CLR stands as an independent prognostic factor for NPC patients undergoing CCRT. The CLR-based nomogram (incorporating five independent prognostic factors: age, T stage, N stage, BMI, and CLR) provides a tailored approach to predicting survival, enabling healthcare providers to adjust treatment strategies in accordance with individual risk profiles. Further validation of these findings in external cohorts is necessary, as well as exploration of CLR's clinical utility in directing treatment decisions.

Hematological malignancy (HM) patients are at high risk of bloodstream infections (BSIs) due to chemotherapy-induced mucosal barrier injury (MBI), invasive procedures, and prolonged antimicrobial exposure. While conventional nosocomial infection paradigms emphasize catheter-related biofilms, emerging evidence highlights the role of disrupted oral/gut microbiomes in bacterial translocation. This study aimed to identify risk factors for bacteremia secondary to MBI following chemotherapy in patients with HM.

A single-center, retrospective analysis of 72 HM patients, including 24 with mucosal barrier injury laboratory-confirmed bloodstream infection (MBI-LCBI), 22 with non-MBI-LCBI, and 26 controls without BSIs, was conducted. Microbiology profiles, resistance patterns, and risk factors for BSIs were analyzed.

All MBI-LCBI patients had significantly longer neutropenia duration than non-MBI-LCBI patients did (median 6.5 vs. 3.0 days, p = 0.013). Multivariate analysis identified MBI as an independent risk factor for BSIs (OR = 11.467, 95% CI1.287-102.170). Prolonged hospitalization (> 30 days) was associated with BSI occurrence (OR = 6.758, 95% CI 1.102-41.440) and neutropenia duration (OR = 1.112, 95% CI 1.014-1.220). Significant differences in pathogen distribution were observed between groups: Escherichia coli, Klebsiella pneumoniae, and viridans group streptococci predominated in the MBI-LCBI group, whereas Pseudomonas aeruginosa and Staphylococcus spp. were common in the non-MBI-LCBI group. Carbapenem resistance remained below 20% for key gram-negative pathogens.

MBI is an independent risk factor for BSI in HM patients, highlighting the need for targeted mucosal protection strategies. MBI-LCBI pathogens primarily originate from the gut/oral flora, and are distinct from catheter-related infections. Carbapenems are recommended for empirical therapy, yet resistance surveillance remains essential.

Specialised outpatient palliative care (SOPC) is an important element of the palliative care concept in Germany. The aim of this study is to compare patient characteristics, care processes and outcomes of patients with heart failure (HF) and oncological diseases, using the latter as a reference group to identify disease-specific needs and support the adaptation of SOPC to non-oncological conditions such as HF.

In this cross-sectional study (22 SOPC providers), clinical data of all palliative care patients who were treated between 2017 and 2021 were retrospectively analysed.

Survival was estimated by Kaplan-Meier analysis. To further examine the relationship between patient survival time and various variables, a Cox proportional hazards model was used. Differences in symptom burden were tested for statistical significance using the McNemar test.

Data from 48 882 patients were analysed, with 5387 (11.0%) identified as having a primary HF diagnosis. This cohort was compared against a large oncological group consisting of 34 287 (70.1%) patients.

For HF patients, the mean number of days spent in SOPC was 30.5±67.7 days and for oncological patients 44.1±72.0 days. A significantly higher proportion of oncological patients died in hospices (14.0%) and hospitals (6.9%) compared with HF (2.9% and 2.2%). Age-adjusted Charlson Comorbidity Index at admission into SOPC was 9.4±3.1 in oncological patients compared with 6.7±1.7 in HF (p<0.001). The median survival time (ie, time spent in last treatment episode) for patients with HF was only 10 days, whereas patients with oncological diagnoses had a median survival of 24 days.

HF patients in SOPC exhibit a different clinical profile compared with oncological patients, characterised by significant symptom burden and shorter survival times. These results emphasise the necessity for tailored palliative interventions to address the specific needs of HF patients.

Prostate cancer (PCa) is the second most common cancer in men worldwide and genetic factors and family history significantly increase the risk of PCa. Men at increased risk for PCa often experience higher PCa-specific anxiety and distress. Comprehensive prevention strategies for men with familial or genetic PCa predisposition are lacking. Consequently, the psychological impact, facilitators and barriers for risk-adapted PCa prevention lack comprehensive study. The novel prospective registry and prevention clinic 'ProFam-Risk' (prevention clinic for familial PCa risk) at the University Hospital Düsseldorf offers personalised risk assessment and risk-adapted prevention recommendations for men with familial or genetic PCa predisposition. As part of this research project, this study ('ProFam-Psych' - risk-adapted prevention clinic for familial and genetic prostate cancer: psychosocial effects; funded by German Cancer Aid) aims to evaluate the longitudinal psychosocial trajectories associated with this novel prevention clinic.

In a longitudinal observational mixed-methods design, psychosocial outcomes will be assessed in participants of the prevention clinic (case group, CAG) and compared with urology patients without increased risk for PCa (control group, COG). Psychosocial outcomes will be collected at four time points in the CAG (T0: baseline; T1: after first visit; T2: after risk stratification consultation; T3: follow-up 6 months after T2) and at two time points in the COG (T0: baseline during inpatient stay; T1: post-inpatient stay). Recruitment started in 2023, and the recruitment target is n=225 participants (CAG) and n=118 participants (COG). Primary endpoint is the longitudinal course of PCa-specific anxiety (Memorial Anxiety Questionnaire for Prostate Cancer) in the CAG. Secondary endpoints include the comparison of T0 and T1 outcomes between the CAG and COG and the assessment of changes in perceived PCa risk and perceived personal control in the CAG. To assess facilitators and barriers to participation in the risk-adapted PCa prevention clinic, a minimum of n=12 semi-structured qualitative interviews will be conducted, with recruitment continuing until data saturation is reached. Qualitative data will be analysed using qualitative content analysis.

Ethics approval from the Medical Faculty of the Heinrich Heine University Düsseldorf was obtained (2023-2551). Results of the main objective and each of the secondary endpoints will be submitted for publication in a peer-reviewed journal.

DRKS.de, DRKS00032350. Prospectively registered with the German Clinical Trials Register (DRKS) on 14 September 2023.

According to the current World Health Organization classification of central nervous system tumors, the angiocentric glioma (AG) assigned a grade 1, characterized by recurrent MYB fusions. However, it also mentions that increased proliferative activity and other anaplastic features have been reported, but the clinical significance of such findings is unclear as an increased proliferative activity alone does not necessarily alter the benign behavior of AGs. Most cases with "anaplasia" were mainly described before the molecular era. Herein, we report the case of a 3-year-old female with epilepsy symptomatic of a left temporo-parietal tumor. Histopathologically, the initial tumor displayed atypical AG morphology and a proliferation index of 1%, without mitoses, or necrosis. RNA sequencing identified a MYB::QKI fusion. After several tumor recurrences, the last tumor sample showed strong evidence of a histopathological transformation into a high-grade tumor with proliferation and mitotic indexes, necrosis and microvascular proliferation. The recurrent tumor still harbored the same MYB::QKI fusion but acquired an hTERT mutation. DNA-methylation analysis classified the initial tumor as an LGG, MYB/MYBL1-altered (AG, MYB/MYBL1-altered with a calibrated score of 0.58) while the progression clustered with glioblastoma, IDH-wildtype, RTK1 (with a calibrated score of 0.33). The copy number variation both at presentation and at last recurrence (CNV) exhibited a chromosome 6 chromothripsis. The patient died from tumor progression after an overall survival of 89 months. This novel observation raises the question of whether this case represents an aggressive form of MYB/MYBL1-altered LGGs driven by an oncogenic MYB fusion, or if they are actually high-grade gliomas that coincidentally exhibit alterations near the MYB locus. Further reports are needed to confirm the existence of malignant forms of LGG, MYB/MYBL1-altered, potentially correlated with a higher grade.

The hypoxic tumor microenvironment, particularly hypoxia-conditioned cancer-associated fibroblasts (CAFs), drives breast cancer (BC) progression and therapy resistance. However, the molecular mechanisms linking hypoxic CAFs to BC plasticity and chemoresistance remain elusive.

Primary CAFs were isolated from high-grade BC tissues (Grade III) and characterized (α-SMA⁺/CD34⁻/pan-CK⁻), with normal fibroblasts (NFs) from reduction mammoplasty as controls. Hypoxic CAF-derived exosomal circSTAT3 stability was validated using RNase R resistance and actinomycin D assays. Exosomes were characterized via transmission electron microscopy (TEM), dynamic light scattering (DLS), and marker profiling (CD63⁺/TSG101⁺/Alix⁺, calnexin⁻). Functional effects of hypoxic CAF exosomes on TNBC cells (MDA-MB-231, SUM159) were assessed through proliferation/migration assays, stemness/epithelial-mesenchymal transition (EMT) marker analysis, and siRNA-mediated circSTAT3 knockdown. Mechanistic studies employed luciferase assays and RNA immunoprecipitation (RIP). Chemoresistance was evaluated by cisplatin half-maximal inhibitory concentration (IC₅₀). In vivo tumor growth and stemness enrichment were analyzed in xenografts. Clinical validation used BC tissues (n = 60) and plasma exosomes from BC patients (n = 40) versus healthy controls (n = 25).

Hypoxic CAF-derived exosomes efficiently transferred circSTAT3 to TNBC cells, promoting proliferation, migration, EMT, and stemness marker expression. SiRNA-mediated circSTAT3 knockdown reversed these effects. Mechanistically, circSTAT3 acted as a competitive endogenous RNA (ceRNA), sponging miR-671-5p to derepress NOTCH1. Hypoxic CAF exosomes increased cisplatin IC₅₀ in TNBC cells, while circSTAT3 depletion restored chemosensitivity. In vivo, hypoxic CAF exosomes accelerated tumor growth, enriched CD44⁺/NOTCH1⁺ populations, and elevated circulating exosomal circSTAT3. Clinically, circSTAT3 was significantly upregulated in advanced BC tissues (p < 0.01) and patient plasma exosomes (p < 0.01), correlating with lymph node metastasis.

This study identifies a hypoxia-driven feedforward loop wherein CAF-derived exosomal circSTAT3 promotes TNBC stemness and chemoresistance via miR-671-5p/NOTCH1 signaling. CircSTAT3 redefines stromal-tumor crosstalk as a circRNA-driven process and serves as both a circulating non-invasive biomarker and a promising therapeutic target to disrupt stromal-mediated resistance in aggressive TNBC.

Poly(lactic-co-glycolic acid) (PLGA) is a widely utilized biodegradable and biocompatible polymer in drug delivery systems, particularly for encapsulating drug molecules with poor solubility and permeability. PLGA nanoparticles, composed of polylactic acid (PLA) and polyglycolic acid (PGA), offer tunable properties such as controlled degradation rates and drug release kinetics. The PEGylation of PLGA nanoparticles results in the formation of a polyethylene glycol (PEG) corona on their surface, which enhances systemic circulation by reducing opsonization and immune system recognition. This extended circulation time increases the likelihood of nanoparticles reaching the target site, a crucial advantage in cancer therapy, as it allows for reduced dosage frequency while improving therapeutic efficacy. Furthermore, surface functionalization with targeting ligands enables selective delivery to specific cells or organs via ligand-receptor interactions, facilitating enhanced cellular uptake and intracellular drug release. This review provides a comprehensive analysis of PEGylated PLGA nanoparticles in cancer diagnosis and therapy, highlighting recent advancements, current challenges, and future perspectives in their clinical translation.

Cancer stem cells are associated with tumorigenesis, aggression, and drug resistance. We aimed to identify stem cell-related subtypes and a prognostic tool, and to investigate potential stem cell-related genes contributing to high-grade serous ovarian cancer (HGSOC).

Stem cell pathways were used to determine tumor subtypes and the least absolute shrinkage and selection operator regression was conducted to construct a prognostic risk model, with robustness validation in external datasets. We assessed immune characteristics and therapeutic responses of risk score. Macrophage subpopulations were identified using single cell data, and pseudo-time analysis revealed the changes of macrophages during cell state transition.

HGSOC patients were stratified into stem cell pathway-related clusters (C1, C2) and stem cell-related clusters (GC1, GC2). Patients in C1 and GC1 exhibited better prognosis, increased ImmuneScore, decreased TumorPurity and low immune escape. Patients in C1 were sensitive to gemcitabine while patients in GC1 were sensitive to cisplatin, cyclophosphamide, gemcitabine and niraparib. Risk score was constructed based on 15 genes (IL2RG, STAB1, C2, CD163, FBXO17, VSIG4, CXCL11, CXCL13, GJB1, GPC3, NPY, KRT16, GRIK5, PI3, and RARRES1) with robustness in prediction. Low-risk patients showed favorable outcomes, high immune infiltration and high immunotherapy response. Novel ligand-receptor pairs LGALS9-HAVCR2 and CD86-CTLA4 were specifically interacted between Macro_1 and T/NK cells. VSIG4 and STAB1 were highly expressed in macrophages and were associated with poor prognosis, high tumor purity and high immune checkpoints.

The results provide novel insights into prognosis prediction and therapeutic responses, and identify VSIG4 and STAB1 as potential biomarkers affecting macrophages in HGSOC.

Papillary thyroid carcinoma (PTC) is a globally widespread inflammation-related cancer, where lymph node metastasis (LNM) poses significant challenges to the prognosis of PTC. The role of the monocyte-to-high-density lipoprotein cholesterol ratio (MHR), a novel inflammation marker attracting increasing attention, in PTC remains unclear.

Clinical data analysis was adopted to preliminarily explore the relationship between clinical features and LNM of PTC. Single-cell RNA sequencing (scRNA-seq) data from the GSE191288 and GSE193581 datasets were integrated to analyze various single-cell infiltration in PTC. A comprehensive suite of in vitro experiments, encompassing immunohistochemistry, co-culture, and Transwell assays were conducted to elucidate the regulatory role of macrophages and PTC.

Clinical data analysis confirmed MHR could be an independent risk factor for LNM (OR = 1.76, 95%CI: 1.20-2.88, P = 0.011). The single-cell analysis identified cell clusters associated with dysregulated cholesterol homeostasis Q1 and CD68 + C3 macrophage subpopulations, as well as their markers GDF15. Further analysis confirmed that they are closely related to PTC metastasis and malignancy, which also implied a significant correlation between MHR and LNM. The in vitro experiments demonstrated PTC may promote metastasis by mediating inducing macrophage differentiation to the M2 phenotype.

This study revealed the potential role of MHR in PTC from the single-cell perspective for the first time. Combined with the results of clinical studies and basic experiments, it was confirmed that mononuclear/macrophage and cholesterol homeostasis significantly promoted the lymph node metastasis of PTC. Overall, these findings informed robust support for MHR as an emerging marker for preoperative LNM prediction of PTC.