Masculinity has been identified as a potential influence on psychological and physical health outcomes among male cancer survivors. This systematic review synthesized quantitative research examining associations between masculinity-related constructs and survivorship outcomes, including mental health, physical functioning, and health-related quality of life (HRQoL).

A systematic search of PsycINFO, CINAHL, and PubMed was conducted through March 2025, following PRISMA guidelines. Studies were included if they quantitatively assessed masculinity-related variables in male cancer survivors and reported associations with HRQoL, mental health, or physical health outcomes. Study quality was assessed and a narrative synthesis was conducted.

Thirty-one studies met inclusion criteria. Traditional masculine norms (e.g., self-reliance, dominance, stoicism) and cancer-related masculine threat were consistently associated with poorer mental health, lower HRQoL, and greater symptom burden. In contrast, masculine self-esteem, a positive appraisal of one's masculinity post-cancer, was linked to better psychosocial outcomes and HRQoL across samples. Most studies were cross-sectional and focused on prostate cancer survivors, often lacking demographic diversity.

Masculinity-related constructs are meaningfully associated with cancer survivorship outcomes. Future work should prioritize longitudinal designs, cultural diversity, and clinical translation to develop gender-sensitive interventions targeting masculine identity disruption and promoting adaptive self-concepts.

The incidence of prostate cancer continues to increase, making it the second most common malignant tumor among men worldwide. Immunotherapy has emerged as a key therapeutic strategy for treating tumors. Numerous studies have established that the efficacy of tumor immunotherapy is closely associated with the tumor microenvironment and T cell subsets. However, the specific functions of certain T cell subsets in prostate cancer remain incompletely characterized. Therefore, this study aimed to systematically investigate the distribution patterns of T cell subsets within the tumor microenvironment of prostate cancer patients and their correlations with clinicopathological parameters. Therefore, we investigated the impact of T cells on the tumor microenvironment of prostate cancer at the single-cell level. We employed a variety of analytical methods to reveal the functions of T cells, including cell interaction analysis, time-series analysis, enrichment analysis, immune infiltration analysis, and other analytical approaches. By integrating bulk RNA-seq data, we constructed and validated a prognostic risk model based on T cell marker genes. Finally, we utilized the ssGSEA and ESTIMATE algorithms to explore the relationship between the prognostic risk model and immunotherapy. After quality control, 16,999 cells from the single-cell data were retained for downstream analysis. Our study focused on T cells, revealing the communication between various cell types and T cells. Pseudotime analysis showed that different T cell marker genes exhibited differential expression at various time points, corresponding to distinct biological processes. Enrichment analysis indicated that T cell marker genes were enriched in several immune-related pathways. From our analysis, BCAS2, EIF2S2, RIOK3, and ATP6V1E1 were ultimately identified as prognostic markers. Immune infiltration analysis revealed that high-risk patients had lower immune scores, stromal scores, and ESTIMATE scores and greater tumor purity compared to low-risk patients. We analyzed the mechanisms involving T cells in prostate cancer from multiple perspectives, constructed a prognostic model, and conducted immune infiltration analysis. Our findings contribute to the understanding of prostate cancer and its prognosis, providing valuable insights for future research and prognostic assessments in prostate cancer.

People with neurofibromatosis type 1 (NF1) have an 8%-13% lifetime risk of developing malignant peripheral nerve sheath tumors (MPNST). Atypical neurofibromas (AN) and atypical neurofibromatous neoplasms of uncertain biologic potential (ANNUBP) have been described as precursors to MPNST. AN/ANNUBP often appear as distinct nodular lesions (DNL) that are ≥3 cm in longest diameter. To assess the hypothesis that most MPNST originate in preexisting DNL, we performed a retrospective review of MRIs obtained prior to the MPNST diagnosis in people with NF1.

Study subjects were identified at two NF centers, University Hospital Hamburg-Eppendorf in Germany and the National Cancer Institute in Bethesda, Maryland, USA. We confirmed the location of MPNST on the MRI performed at the time of histopathological diagnosis and analyzed distinguishing imaging features at the site of MPNST on prior MRIs.

Thirty subjects with NF1 and 35 histologically confirmed MPNST were included in the analysis. Twenty-six MPNST (74%) were detected incidentally on surveillance MRI. In 32 of 35 MPNST (91%), a pre-existing DNL could be detected at the site of subsequent malignancy on prior MRIs. Thirteen DNL gradually emerged within a plexiform neurofibroma (PN) during observation, and 19 DNL were already established on the first available scan. The median time from DNL detection to MPNST diagnosis was 5.1 years (range 0.5-15.7).

Most NF1-related MPNST develop from preexisting DNL. However, we cannot estimate what percentage of DNL will transform to MPNST. Assessing the risk of malignant transformation of DNL in NF1 requires prospective studies.

Metal nanoparticles possess unique properties and usage patterns compared to traditional materials owing to their distinctive structures. In recent years, their application scenarios and dosages have considerably expanded. Biosynthetic nanoparticles, particularly those derived from endophytic fungi that help host organisms in adapting to heavy metal environments, hold substantial value and potential for application. This is largely attributed to their simplicity, cost-effectiveness, and energy efficiency. The present review provides an overview of the entire process of metal nanoparticle biosynthesis by plant endophytic fungi and illustrates various scenarios of their applications in oncology treatment. In addition to focusing on the preparation of metal nanoparticles using plant endophytic fungi, this review also explores the characterization of these nanoparticles and clarifies the synthesis mechanisms, including the synthetic pathways and the roles of fungal enzymes. It also comprehensively summarizes the application of biosynthetic metal nanoparticles in cancer, covering their role in diagnosis, enhancement of drug biocompatibility, and improvement of therapeutic efficacy. These nanoparticles exhibit toxicity toward cancer cells by generating reactive oxygen species and inducing oxidative stress, ultimately leading to the death of malignant cells. The biosynthesis of metal nanoparticles by plant endophytic fungi represents a promising, green, and environmentally friendly approach with potential applications in various fields, including cancer treatment, in the future.

X-linked hypophosphatemia (XLH) and tumor-induced osteomalacia (TIO) are characterized by alterations in phosphate metabolism due to elevated levels of fibroblast growth factor 23 (FGF23). These conditions cause significant morbidity due to chronic hypophosphatemia and resulting musculoskeletal disorders.

This study aims to provide clinical strategies for supporting the diagnosis and management of the biochemical profile of patients with XLH and TIO, addressing key considerations beyond the hypophosphatemia and hyperphosphaturia commonly observed in these conditions and addressing the variability and limitations of current biochemical marker detection methods.

A literature search focused on studies published in the last ten years. A multidisciplinary team analyzed the data to integrate the findings into clinical best practices.

The proposed approach emphasizes correctly performing and interpreting tests for serum phosphate, phosphaturia, FGF23, alkaline phosphatase (ALP), parathyroid hormone (PTH), vitamin D, serum calcium, and the calcium-corrected excretion rate. More standardization in screening methods is needed, which affects diagnostic accuracy and management. The recommendations include detailed protocols for patient preparation, sample collection, and interpretation of results.

The recommendations for performing biochemical screening for XLH and TIO promote better clinical practices in patient diagnosis and management. Future research should focus on validating diagnostic methods in diverse populations and standardizing biochemical tests. Multidisciplinary approach to the diagnosis of these patients through the close collaboration of professionals of laboratory medicine and clinical specialties would be pivotal.

Myelofibrosis (MF) is classified among the chronic myeloproliferative neoplasms and presents unique nutritional challenges. Inflammation can trigger metabolic changes that lead to malnutrition and, ultimately, cachexia. Splenomegaly, which may occupy much of the abdomen and compress the stomach, can cause early satiety and further contribute to malnutrition. We investigated associations between nutritional parameters, clinical features, and survival in individuals with MF.

Forty-five individuals with MF (21 males, 24 females) were included and compared with a healthy control group of 351 individuals (157 males, 194 females). Body composition (bioelectrical impedance analysis), resting metabolic rate (RMR), and substrate oxidation (indirect calorimetry) were assessed.

The mean follow-up was 31 ± 8 months, during which seven deaths occurred. MF was associated with malnutrition; patients exhibited lower bioelectrical phase angle values and higher RMR (32.4 ± 4.2 vs. 28.5 ± 3.6 kcal/kg-fat-free mass/24 h; p < 0.001) compared with controls. Kaplan-Meier survival curves showed that a phase angle (PA) below the median was associated with a lower survival rate (p < 0.005). Similarly, spleen length above the median was linked to poorer survival (p < 0.05).

Nutritional factors may serve as important predictors of survival in individuals with MF and should be considered in future supportive interventions aimed at improving both survival and quality of life.

Health-related quality of life (HRQoL) of patients with myeloproliferative neoplasms (MPNs) may be impaired across several domains. In this multicenter observational study, we evaluated HRQoL and symptoms in a cohort of MPN patients with validated measures, including the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-Core 30 (EORTC QLQ-C30), the Myeloproliferative Neoplasm Symptom Assessment Form Total Symptom Score (MPN-SAF TSS), and the Functional Assessment of Chronic Illness Therapy-Fatigue Scale (FACIT-Fatigue) questionnaire. The primary objective was to compare the HRQoL profile of patients, by disease subtype, with that of the general population according to the EORTC QLQ-C30. A total of 572 patients with essential thrombocythemia (ET, n = 228), polycythemia vera (PV, n = 207), and myelofibrosis (MF, n = 137) were assessed. Worse statistically and clinically significant differences were observed for role functioning (ET: ∆ = 8.9, P < 0.001; PV: ∆ = 11, P < 0.001; MF: ∆ = 16.7, P < 0.001) and fatigue (ET: ∆ = 5, P < 0.001; PV: ∆ = 8.3, P < 0.001; MF: ∆ = 11.5, P < 0.001) in all three diagnostic groups. However, patients with MF also reported impairments in other important health domains. Fatigue was the most frequently reported and burdensome symptom, with greater severity correlating with a broader and more complex array of associated symptoms. Our analysis also revealed a substantial underestimation of symptoms by treating hematologists in paired physician-patient reports. Current findings may help to disentangle specific HRQoL limitations and symptomatology experienced by patients with MPNs, and underscore the importance of incorporating patient-reported outcomes into routine practice to better reflect the patient's perspective of the disease and treatment-related burden.

Positron emission tomography (PET) scans are widely used for detecting biochemical recurrence (BCR) in prostate cancer, yet evidence for salvage treatments of PET-positive lymph nodes remains limited. This study aimed to analyze the oncologic outcomes of salvage treatments, specifically lymph node dissection (LND) and radiotherapy (RT), in patients with BCR and PET-positive lymph node recurrence.

Systematic reviews and meta-analyses were performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. A comprehensive search of PubMed, Cochrane, and Web of Science databases up to June 2023 was conducted. Inclusion criteria encompassed patients with BCR and PET-positive lymph node recurrence following definitive prostate cancer treatment, who underwent salvage LND or RT.

A total of 38 publications involving 3,559 patients (1391 LND, 2168 RT) were included. Pooled incidence rates after LND and RT were as follows: prostate-specific antigen (PSA) response (56.4% vs. 78.9%), PSA progression (61.3% vs. 36.0%), image progression (44.9% vs. 34.9%), systemic progression (41.3% vs. 35.0%), overall mortality (3.0% vs. 4.8%), and cancer-specific mortality (8.4% vs. 4.1%). Subgroup analyses by prostate-specific membrane antigen (PSMA) PET scan, PSA level ≤2 ng/ml at PET scan, and androgen deprivation therapy usage with salvage therapy revealed varied outcomes.

Despite salvage LND or RT, about half of BCR patients with PET-positive nodal recurrence showed disease progression, suggesting limited effectiveness of focal therapies alone. RT appeared to provide better short-term disease control than LND, highlighting the importance of treatment selection. The study underscores the necessity for further investigation into optimal salvage management strategies for BCR using PET in prospective clinical studies.

LINC01410 is a recently identified long non-coding RNA located on chromosome 9 that plays a multifaceted role in human diseases. Its dysregulation is closely associated with tumor initiation, progression, and therapeutic response. LINC01410 promotes oncogenesis by modulating key signaling pathways, such as PTEN/AKT, Notch, ErbB, and NF-κB, interacting with non-coding RNA networks, and influencing the expression of proteins involved in tumor biology. Beyond these roles, it contributes to cancer metabolism by regulating glycolysis, lipid droplet accumulation, and exosome-mediated intercellular communication, thereby shaping the tumor microenvironment and enhancing malignancy. Intriguingly, LINC01410 exhibits opposite expression patterns in non-malignant conditions such as preeclampsia and diabetic nephropathy, highlighting its context-dependent biological function. Collectively, these findings position LINC01410 as a pivotal regulator linking protein expression, metabolism, and intercellular signaling, underscoring its potential as a biomarker and therapeutic target in oncology.