BMC Cancer最新文献

Background: Prostate cancer is a leading cause of cancer-related morbidity and mortality among men worldwide. Despite its growing burden, screening uptake remains low in many low- and middle-income countries, including Ethiopia. Early detection through screening is essential, yet awareness and access remain limited.

Methods: This systematic review and meta-analysis followed PRISMA guidelines. We searched PubMed, Scopus, Web of Science, AJOL, and Google Scholar for studies published 30 August 2025 using terms related to prostate cancer, screening, and Ethiopia. Observational studies of prostate cancer screening were included. Two reviewers independently screened studies, extracted data, and assessed quality using the Newcastle-Ottawa Scale. Pooled prevalence was estimated with a random-effects meta-analysis; heterogeneity and publication bias were evaluated using I² and funnel plots with Egger's test. Significant factors were summarized narratively.

Results: Twelve studies, including 7,526 participants from Addis Ababa, Southern, Central, and Amhara regions, were analyzed. The pooled prevalence of prostate cancer screening was 30.37% (95% CI: 20.49-40.25% I² = 96.7%, p < 0.001). Subgroup analysis showed the highest prevalence in the Wolaita Sodo (63.08%, 95% CI: 58.73-69.22%), followed by Amhara region (47.97%( 95% CI: 42.02-53.92), and the lowest in central Ethiopia region (7.19%, 95% CI: 4.75-9.67%). Significantly associated factors included awareness of prostate cancer screening (AOR = 3.36, 95% CI: 1.87-6.85), age of the patients > 45 years (AOR = 3.53, 95% CI: 1.69-5.46), regular checkup of cancer (AOR = 3.65, 95% CI: 1.09-6.20), average income ≥ 5000 ETB (AOR = 3.80, 95% CI: 2.28-5.31), family history of prostate cancer (AOR = 3.87,95% CI: 2.30-5.45), and ever heard about prostate cancer (AOR = 3.15,95% CI: 1.43-4.88).

Conclusion: Prostate cancer screening in Ethiopia remains low, with marked regional differences. Uptake is higher among older men, those with higher income, prior awareness, family history, or regular health checkups. Targeted educational programs and improved access to screening are urgently needed. Nationwide, longitudinal, and mixed-method studies are essential to evaluate interventions and understand behavioral, cultural, and systemic factors affecting screening practices.

Conclusion: Prostate cancer screening in Ethiopia remains low, with marked regional differences. Uptake is higher among older men, those with higher income, prior awareness, family history, or regular health checkups. Targeted educational programs and improved access to screening are urgently needed. Nationwide, longitudinal, and mixed-method studies are essential to evaluate interventions and understand behavioral, cultural, and systemic factors affecting screening practices.

Background: Physical activity is critical for older breast cancer survivors. We explored the experiences and recommendations of older breast cancer survivors from the IMPROVE trial, including a sizable number of older African American and socioeconomically disadvantaged survivors, to inform future implementation and dissemination of sustainable programs.

Methods: Participants included women, ≥ 65 years, within five years of treatment completion for stage I-III breast cancer who were enrolled into a randomized controlled trial of supervised group moderate-intensity exercise for 20-weeks followed by 32 weeks of unsupervised exercise versus support group (SG) plus Fitbit intervention. Semi-structured exit interviews were conducted at study completion. Interviews were audio-recorded, transcribed verbatim, and analyzed using thematic analysis with constant comparison. Two researchers independently coded transcripts, discussing discrepancies to enrich interpretation. The Social Cognitive Theory and the Transtheoretical Model guided interpretation of results.

Results: Between 2016 and 2020, 213 older breast cancer survivors were randomized into the exercise arm, (n = 108) or a SG + Fitbit arm, (n = 105). At study completion, 145 (68%) opted to participate in exit interviews. This included 75 Exercise and 70 Support Group participants. Participants described a range of experiences and recommendations that clustered into five broad themes: program experiences, transition challenges, Fitbit experiences, program impact, and recommendations. Survivors consistently highlighted camaraderie, peer bonding, and accountability as central benefits of participation, with enjoyment of activities and staff support further enriching their experience. Many described difficulties sustaining activity after program completion, underscoring the need for ongoing group-based support. Experiences with Fitbit were mixed: some found it motivating, while others reported technical barriers. Survivors also noted increased energy, health awareness, and reduced isolation. Recommendations included extending program duration, adding nutrition content, reducing survey burden, and addressing transportation challenges.

Conclusion: Older breast cancer survivors, including those underrepresented in survivorship research, emphasized the importance of social support, structured exercise, and wearable technology in sustaining physical activity. Their recommendations highlight strategies for tailoring future interventions to enhance accessibility, sustainability, and long-term impact.

Trial registration: ClinicalTrials.gov Identifier: NCT02763228.

Background: SLC38A1 has been identified as a carcinogenic factor in the progression of colorectal, gastric, pancreatic, and other cancers. However, its involvement in lung adenocarcinoma (LUAD) remains unexplored in the literature.

Methods: The expression levels, diagnostic relevance, and clinical significance of SLC38A1 in LUAD were evaluated using data from the TCGA, XENA, and LCE databases, along with validation in samples from 10 LUAD patients at our hospital. Prognostic nomograms and risk models based on SLC38A1 were constructed. The functional roles and mechanisms of SLC38A1 in LUAD were investigated through CCK-8 assays, migration and invasion assays, Western blotting, GO and KEGG pathway analyses, and correlation analysis to explore its relationship with the immune microenvironment.

Results: SLC38A1 was overexpressed in both unpaired and paired LUAD samples, with a marked increase in early-stage LUAD. Overexpression of SLC38A1 correlated with diagnostic accuracy and poor overall survival (HR = 1.53; 95% CI = 1.15-2.04), disease-free survival (HR = 1.59; 95% CI = 1.1-2.3), and progression-free interval (HR = 1.51; 95% CI = 1.16-1.97). COX regression analysis identified SLC38A1 overexpression as an independent risk factor for poor prognosis in LUAD patients. High-risk scores and nomograms associated with SLC38A1 were significantly linked to adverse clinical outcomes. Genes co-expressed with SLC38A1 were involved in nuclear division, DNA replication, and the cell cycle. Silencing of SLC38A1 expression inhibited LUAD cell growth and migration. Furthermore, SLC38A1 overexpression was associated with immune cell infiltration in LUAD, including Th2 cells, Tcm, T helper cells, and immune markers such as CD8A, CD8B, and CTLA4.

Conclusion: SLC38A1 is upregulated in LUAD, and its overexpression is associated with poor prognosis, diagnostic accuracy, and immune cell infiltration. SLC38A1-based risk models and nomograms offer potential predictive tools for assessing prognosis in LUAD patients.

Background: Tumor-associated macrophages (TAMs) comprise heterogeneous subtypes with context-dependent functions in tumor immunity. Although macrophage senescence influences diverse diseases, its role in neuroblastoma (NB) progression remains undefined.

Methods: Single-cell RNA sequencing (scRNA-seq) data from NB samples (GEO: GSE147766) were analyzed to identify TAM subtypes. Senescence-associated signatures were characterized via pseudotime trajectory, cell-cell communication, and functional assays. A prognostic model was developed using Cox/LASSO regression and validated in independent cohorts (TARGET-NBL, E-MTAB-8248). Drug sensitivity and immune microenvironment differences were compared between risk groups. In vitro validation assessed EIF5's role in TAM senescence and NB progression.

Results: We identified a senescent TAM subset (C0) exhibits a hybrid M1/M2 state with a dominance of M2-like features. Pseudotime analysis revealed differentiation from non-senescent TAMs (C1), accompanied by upregulated LILRB1, LILRB2, IL10, and CXCL8. A 7-gene prognostic signature (AMD1, ARL4A, BRD2, DDX3X, EIF5, SLC43A2, ZEB2) stratified patients into risk groups with distinct survival (P < 0.001). High-risk patients displayed impaired anti-tumor immunity (reduced CD8⁺ T cells, elevated TIDE scores) and differential drug sensitivity. EIF5 knockdown suppressed senescence markers (p21/p16) in macrophages and inhibited NB cell proliferation/migration.

Conclusions: Senescent TAMs influence NB immunosuppression and progression. EIF5 is a key regulator of TAM senescence and a potential therapeutic target. Our risk model may guide clinical stratification and targeted interventions.

Background: Liver hepatocellular carcinoma (LIHC) is one of the most common and aggressive malignancies worldwide, with high mortality rates. PLOD family genes (PLOD1, PLOD2, and PLOD3) play a pivotal role in extracellular matrix (ECM) remodeling, which contributes to cancer progression and metastasis. This study explores the diagnostic, prognostic, and therapeutic potential of PLOD1, PLOD2, and PLOD3 in LIHC.

Materials and methods: Seven LIHC cell lines and five normal liver tissue cell lines were cultured. RT-qPCR was used to assess the expression of PLOD genes. The GSCA and TCGA databases were used for gene expression, pathway analysis, survival, and enrichment analysis. Promoter methylation was analyzed via GSCA and OncoDB, and mutational and CNV analyses were conducted using the cBioPortal database. The KM plotter tool assessed the prognostic significance of PLOD genes, while miRNA-mRNA network analysis was performed using the mirNET and UALCAN databases. Functional assays, including siRNA-mediated knockdown, Western blotting, cell proliferation, colony formation, and wound healing assays, were used to assess the biological roles of PLOD2 and PLOD3 in LIHC.

Results: The expression of PLOD1, PLOD2, and PLOD3 was significantly (p-value < 0.05) higher in LIHC cell lines compared to normal controls. Validation in the TCGA cohort confirmed upregulation of PLOD genes in LIHC tumors, with PLOD2 and PLOD3 showing progressively higher expression across pathological stages. PLOD genes were associated with the activation of oncogenic pathways such as epithelial-to-mesenchymal transition (EMT) and poor survival outcomes. Promoter methylation analysis revealed lower methylation in tumor samples. Kaplan-Meier survival analysis indicated that higher PLOD expression correlated with poorer overall survival (OS) and relapse-free survival (RFS) in LIHC patients. The miRNA-mRNA network identified three miRNAs (hsa-miR-503-5p, hsa-miR-195-5p, and hsa-miR-193a-3p) regulating PLOD genes, with aberrant miRNA expression linked to poor prognosis. PLOD2/3 knockdown in HepG2 and Hep3B cells significantly reduced cell proliferation, colony formation, and migration, highlighting their critical roles in tumor progression.

Conclusion: Our study demonstrates that PLOD1, PLOD2, and PLOD3 are significantly upregulated in LIHC and correlate with poor prognosis. The PLOD genes may serve as valuable biomarkers for diagnosis and prognosis in LIHC. Moreover, targeting PLOD genes could provide new therapeutic strategies to hinder tumor progression and metastasis in liver cancer.