Cancer Control最新文献

Despite significant advances in oncology, cancer care globally continues to face critical challenges, including stark disparities in access, insufficient preventive focus, fragmented primary health care (PHC) integration, unsustainable financing models, workforce shortages, and inadequate community involvement. This paper revisits the Alma Ata Declaration's principles-health equity, universal access, preventive care, and community participation-as a conceptual framework to address these persistent issues in cancer care. We highlight opportunities to strategically integrate oncology services within strengthened PHC systems, balancing centralized specialist resources with decentralized community-based care. Evidence from diverse settings illustrates how reinforcing PHC infrastructures enhances preventive measures, early detection, and survivorship care, thus mitigating geographic and socioeconomic disparities. Sustainable financing mechanisms and targeted workforce strategies, including task-shifting and multidisciplinary training, are proposed as essential components. Effective community engagement models demonstrate improved care relevance, acceptance, and outcomes. Additionally, we emphasize the critical role of health policy alignment with universal health coverage objectives, robust pharmacoeconomic evaluations, and evidence-based national cancer control plans. Integrating Alma Ata's principles into contemporary oncology provides a viable, scalable model to advance equitable, accessible, and sustainable cancer care globally, laying the theoretical groundwork for future research initiatives and informed policy development.

Background: Oral cancer remains 1 of the biggest health care challenges; it has a poor response to treatment, and treatment often results in severe side effects. Nano-targeted drug carrier-assisted drug delivery systems can improve the benefits of targeted drug delivery and treatment efficacy. A systematic review and meta-analysis was conducted to investigate the effect of targeted nano carrier drug delivery systems on the management of oral cancer.

Methods: A comprehensive literature search was performed using PubMed, ScienceDirect, the Cochrane Library, Google Scholar, and Scopus using PRISMA guidelines, to identify relevant in vitro and in vivo (human) studies. Studies evaluating the impact of nanocarrier-based delivery systems on oral cancer cells or human models were selected. Pooled effect sizes were calculated using random-effects models via RevMan 5.4, and heterogeneity among studies was assessed.

Results: After full-text assessment, 15 research articles were included [14 in vitro studies and 1 randomized controlled trial (RCT)]. In the meta-analysis, the pooled data (IC₅₀) for the impact of the nanocarrier delivery system vs control on oral cancer was -7.67 (95% CI: -41.77, 26.43), with a high heterogeneity (I² = 92%, P < 0.00001). Moreover, in vitro studies had a medium risk of bias, while the RCT had some concerns in the randomization domain.

Conclusion: Nanocarrier-based drug delivery has been found to be a superior approach compared to drug delivery in free form, increasing the efficacy and safety of oral cancer treatment.

IntroductionThis cross-sectional study examined the relationship between paid sick leave and colorectal cancer (CRC) endoscopy screening among employed adults, including the examination of potential pathways.MethodsWe analyzed data from 15,352 employed adults aged 45-75 from the 2021 and 2023 National Health Interview Survey. A generalized structural equation model (GSEM) assessed the direct and indirect pathways between employment status (full-time vs part-time), paid sick leave, health insurance, usual source of care, and CRC endoscopy screening. Survey weights were applied to ensure nationally representative estimates.ResultsFull-time employment was positively associated with paid sick leave (OR = 6.57, 95% CI: 5.85, 7.38) and health insurance (OR = 1.30, 95% CI: 1.07, 1.59). Paid sick leave increased the likelihood of having a usual source of care (OR = 1.57, 95% CI: 1.31, 1.87) and was directly associated with CRC screening (OR = 1.15, 95% CI: 1.03, 1.28). Health insurance increased the likelihood of having a usual source of care (OR = 5.32, 95% CI: 4.30, 6.58) and CRC screening (OR = 3.22, 95% CI: 2.58, 4.02). Usual source of care was also associated with CRC screening (OR = 3.53, 95% CI: 2.89, 4.32).ConclusionsPaid sick leave was associated with CRC endoscopy utilization both directly and indirectly through improved healthcare access. Workplace policies that expand paid sick leave, alongside efforts to strengthen insurance coverage and primary care access, may reduce barriers to CRC endoscopy screening and improve population health.

Adaptive combination therapy is deemed the most intuitive strategy to thwart therapeutic resistance through dynamic treatment tuning that accounts for cancer evolutionary dynamics. However, higher accuracy and reliability of treatment response predictions would be needed, in addition to the need for clinically feasible models of adaptive combination therapy that consider newly approved therapeutics and the growing multimodal data being available about cancer. Grounded in nonlinear system control theory, this review offers a perspective on exploiting GenAI learning and inferencing capabilities to predict treatment response and recommend treatments in the context of adaptive cancer therapy. Results from nonlinear system identification, control theory and deep learning are integrated within an adaptive cancer control framework to leverage the continuously expanding data about cancer and its treatment towards GenAI-enhanced adaptive therapy. The resulting models and their analysis contribute to a much-needed conceptual clarity about the research and translational pathways that would be needed to realize GenAI-assisted cancer treatments. In particular, they underscore that access to clinical data, deep learning opacity, and clinical validation present critical challenges that require adequate attention to pave the way towards acceptance and integration of GenAI in real-world oncology workflows.

The leucine-rich pentatricopeptide repeat-containing (LRPPRC) protein, a member of the pentatricopeptide repeat (PPR) family, is a mitochondria-associated protein that regulates various biological processes, including cell cycle progression and mitochondrial gene translation. LRPPRC has also been identified as an important causative gene in several mitochondrial diseases. N6-methyladenosine (m6A) is the most prevalent and extensive modification of mRNA in eukaryotes, playing a significant role in cellular proliferation, differentiation, and oncogenesis. As an m6A regulator, LRPPRC has been shown to play an important role in the development of various human metabolic diseases and malignant tumors. This review mainly focuses on summarizing the biological roles of LRPPRC in a variety of human malignant tumors, emphasizing the molecular mechanisms LRPPRC is involved in and its potential impact on tumor prognosis.

IntroductionNucleophosmin 1 (NPM1), FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD), and de novo methyl transferase 3 A (DNMT3A) triple-mutated acute myeloid leukemia (AML) represents a distinct entity with poor outcomes.MethodsWe explored the gene mutation spectrum and clinical characteristics of 165 AML patients retrospectively, particularly comparing patients with NPM1/FLT3-ITD/DNMT3A triple-mutations and those without.ResultsOur results demonstrated significantly elevated white blood cell counts (P < 0.001), bone marrow blast percentages (P = 0.037), and platelet counts (P = 0.007) in the triple-mutated cohort (6.7%) compared to the non-triple-mutated patients. Furthermore, all triple-mutated cases were classified as the M4/M5 subtype of the French-American-British classification (P = 0.017). Although no significant difference in complete remission rates was observed between the groups after initial treatment, the median overall survival for triple-mutated AML patients was only 4 months. Using the Gene Expression Omnibus (GEO) database and bioinformatics, we compared AML^{NPM1mutFLT3-ITDmutDNMT3Amut} and AML^{NPM1mutFLT3-ITDmutDNMT3Awt}. A total of 246 AML patients from the GEO dataset were included to evaluate the expression profiles of differentially expressed genes. The guanine nucleotide-binding protein subunit γ 4 (GNG4) was differentially expressed between AML^{NPM1mutFLT3-ITDmutDNMT3Amut} and AML^{NPM1mutFLT3-ITDmutDNMT3Awt}, which had the most adjacent nodes among hub genes. The prognostic value of GNG4 was further validated in AML patient samples through qRT-PCR.ConclusionClinical validation indicated a substantial downregulation of GNG4 in AML^{NPM1mutFLT3-ITDmutDNMT3Amut} compared to AML^{NPM1mutFLT3-ITDmutDNMT3Awt} patients. Thus, GNG4 may play a role in the low survival rate of AML^{NPM1mutFLT3-ITDmutDNMT3Amut} patients, offering novel insights into the prognosis, therapeutic targets, and prognostic evaluation of AML.

Breast cancer remains a critical public health challenge in low- and middle-income countries (LMICs), where late-stage diagnoses, limited access to care, and fragmented survivorship support exacerbate disparities in outcomes. This manuscript examines the systemic barriers to delivering women-centric breast cancer care in LMICs, including geographic and socioeconomic inequities, underfunded prevention efforts, and gaps in policy implementation. Building on a proposed roadmap for reform, we advocate for culturally adaptive strategies, community co-creation, and investment in scalable care models. By prioritizing women's unique needs and fostering multisectoral collaboration, LMICs can transform breast cancer care from survival-focused to empowerment-driven, even amid resource constraints.

This editorial introduces the "Cancer Control" Special Collection featuring 14 peer-reviewed diverse studies from diverse geographical regions and thematic areas, including screening, HPV vaccination, cancer literacy, genetic and molecular innovations, and culturally tailored interventions. This collection highlights disparities in access, uptake, and awareness across populations emphasizing the urgent need for evidence-based strategies. It calls for integrated approaches in prevention, health education, policy reform, and technological advancements to reduce the global cancer burden, which continues to rise, especially in low- and middle-income countries.

IntroductionColorectal cancer (CRC) is the third most common cancer worldwide and a significant public health threat with far-reaching societal implications. The currently available CRC therapeutic strategies have limitations, thus requiring the development of new strategies. Coxsackievirus B3 (CVB3) exhibits strong oncolytic activity in CRC, although its mechanism of action remains unclear. This study aimed to investigate whether the induction of ferroptosis is a promising treatment strategy for CRC and whether CVB3 could activate ferroptosis during infection.MethodsIn vitro and in vivo experiments were conducted to evaluate whether CVB3 infection activates the ferroptosis pathway by upregulating miR-214-3p to suppress glutathione peroxidase 4 (GPX4) expression. Dual-luciferase assays and rescue experiments were performed to confirm this regulatory mechanism. Clinical CRC tissues and colon cancer xenograft models were used to demonstrate the mediating role of the miR-214-3p/GPX4 axis in the interaction between viral replication and ferroptosis.ResultsCVB3 demonstrated oncolytic virus properties by selectively lysing tumor cells. The in vitro and in vivo experiments confirmed that CVB3 activates the ferroptosis pathway by upregulating miR-214-3p to suppress GPX4 expression, thereby promoting viral replication and tumor regression. Antagonizing miR-214-3p reversed this process.ConclusionmiR-214-3p expression was upregulated during CVB3 infection of CRC tissues and cells, activating the ferroptosis pathway and promoting tumor cell death.