Oncology Reviews最新文献

Background and aims: Liquid biopsy offers a minimally invasive tool to detect actionable mutations, monitor minimal residual disease (MRD), and guide therapy in gastrointestinal (GI) cancers. We critically review the clinical utility of circulating tumor DNA (ctDNA), circulating tumor cells (CTCs), and small extracellular vesicles (sEVs) across GI malignancies and propose a framework for their integration into clinical practice.

Methods: We synthesized evidence from over 200 studies, including prospective trials and translational research, to assess diagnostic accuracy, prognostic value, and clinical actionability of each biomarker type in esophageal, gastric, colorectal, pancreatic, hepatocellular, and biliary cancers.

Results: ctDNA has shown strong potential for MRD detection and treatment monitoring, particularly in colorectal and pancreatic cancer. CTCs offer insights into metastatic risk and therapeutic resistance, while sEVs provide molecular cargo relevant to immunomodulation and disease progression. Emerging microfluidics and AI-driven multi-omics approaches may overcome current limitations.

Conclusion: The integration of liquid biopsy technologies into GI oncology holds promise for early detection and precision therapy. We propose a five-phase clinical roadmap and outine the key research gaps that need to be addressed before widespread implementation in routine care.

Osteosarcoma is the most common primary malignant bone tumor, accounting for approximately 20% of all primary malignant bone tumors, and predominantly affects adolescents. The current standard treatment involves a multimodal approach combining neoadjuvant chemotherapy, surgical resection, and postoperative adjuvant chemotherapy. However, patient responses to chemotherapy vary significantly, with response rates (defined as patients achieving ≥90% tumor necrosis) ranging from 30% to 60%. Chemotherapy sensitivity is one of the most critical prognostic factors, and this heterogeneity underscores the importance of predictive tools for optimizing individualized treatment and improving clinical outcomes. In recent years, radiomics has emerged as a revolutionary paradigm in medical imaging analysis. By extracting high-throughput, deep-layer feature information from medical images, it provides a novel technical pathway for quantitative tumor phenotyping. Advanced computer vision algorithms enable the automated extraction of thousands of quantitative metrics-including morphological (shape features), intensity (first-order statistics), and texture (second- and higher-order features)-from multimodal imaging data such as Computed Tomography (CT), Magnetic Resonance Imaging (MRI) and 18F-Fluorodeoxyglucose Positron Emission Tomography (18F-FDG PET/CT) These features not only precisely characterize tumor heterogeneity and the microenvironment but also overcome the subjectivity and reproducibility limitations of traditional manual image interpretation. Leveraging these advantages, radiomics has demonstrated significant value in predicting neoadjuvant chemotherapy efficacy in osteosarcoma.

Objective: Esophageal cancer (EC) ranks as the sixth leading cause of cancer-related deaths globally, with over 500,000 new cases annually. Understanding trends in individuals over 60 is critical for enhancing treatment and the success of early diagnosis and screening.

Materials and methods: This study analyzed global, regional, and national trends in EC management among individuals aged 60 years and older, spanning from 1990 to 2021, utilizing data from the Global Burden of Disease Study 2021. We employed the integrating differential equations to enhance the accuracy of incidence, prevalence, mortality, and Disability-Adjusted Life Years (DALYs). The Bayesian Age-Period-Cohort (BAPC) model was also used to forecast future trends up to 2050.

Results: Our findings indicate significant shifts in the EC burden among those over 60, with a notable increase in absolute numbers from 1990 to 2021, despite a decline in age-standardized rates. The incidence rose by 185%, while the age-standardized prevalence rate decreased by 17.02%. Socioeconomic factors, indicated by the Social Demographic Index, revealed varying trends across different regions and income levels, highlighting the influence of economic status on EC outcomes.

Conclusion: Analysis indicates varying trends across different regions. Behavioral risk factors, particularly smoking and alcohol use, significantly contribute to the burden of EC, especially among males. Projections suggest that despite declining age-standardized rates, the absolute number of cases, deaths, and DALYs will continue to rise due to population growth and aging, highlighting the ongoing global challenge of EC.

Adriamycin (ADM) resistance remains a major clinical obstacle in breast cancer chemotherapy, driven by complex mechanisms including enhanced drug efflux, apoptosis inhibition, and protective autophagy. This review explores a novel regulatory axis centered on eukaryotic initiation factor 3b (eIF3b) and its interplay with autophagy and the Wnt/β-catenin signaling pathway in ADM resistance. Emerging evidence indicates that eIF3b, a crucial subunit of the translation initiation complex, is significantly overexpressed in ADM-resistant breast cancer tissues and cell lines. Crucially, our preliminary experimental findings demonstrate that downregulation of eIF3b suppresses autophagy and concurrently sensitizes resistant breast cancer cells to ADM. While protective autophagy is a well-established resistance mechanism, and the Wnt/β-catenin pathway significantly contributes to multidrug resistance, the specific role of eIF3b and its potential crosstalk with these pathways in ADM resistance is poorly understood. This review synthesizes current knowledge, highlighting the strong evidence suggesting eIF3b acts as an upstream regulator of autophagy to promote ADM resistance. Furthermore, it discusses the potential involvement of the Wnt/β-catenin pathway in this regulatory network, and proposes several hypothetical models of interaction among eIF3b, autophagy, and Wnt/β-catenin signaling. Elucidating the precise molecular mechanisms by which eIF3b drives autophagy and potentially interacts with Wnt/β-catenin holds significant promise for identifying novel therapeutic targets to overcome ADM resistance and improve breast cancer treatment outcomes. Ultimately, targeting the eIF3b-autophagy-Wnt/β-catenin axis could provide a innovative translational strategy to reverse chemoresistance in breast cancer patients.

Lung cancer associated with cystic airspaces (LCCAs) is a distinct subtype of lung cancer defined by its unique radiological characteristics. It is increasing in prevalence but is often misdiagnosed. The constantly emerging radiological classification systems help characterize LCCAs and guide certain treatment methods. Compared to non-LCCAs, LCCAs are more likely to be associated with an invasive nature. The natural progression of LCCAs involves the thickening of cyst walls and the emergence of solid nodules, which are indicative of tumor progression. Despite their aggressive features, the overall prognosis of LCCAs was similar to non-LCCAs this review, we aim to systematically address the current understanding of LCCAs, including the epidemiology, radiologic classification, pathology, molecular characteristics, disease progression, and survival prognosis, highlighting the need for further research to standardize the diagnosis and treatment of LCCAs and to better understand their mechanisms of development.

Introduction: In the last two decades, tyrosine-kinase inhibitors (TKIs) have dramatically changed the prognosis of lung and breast cancers, with significant benefits in the metastatic setting and, more recently, in the adjuvant setting for selected groups of patients. Despite their favorable oncological effects, TKIs carry a high risk for drug-drug interactions (DDIs) due to their pharmacokinetics (PK), which depend on both pH-dependent absorption and liver metabolism. However, DDIs are frequently related to "potential DDIs" (pDDIs), and their clinical relevance is often underestimated; there is also a lack of practical guidance for clinicians.

Methods and materials: We conducted a narrative review restricted to the last 20 years, involving adult individuals (aged 18 years or older) with lung or breast cancers treated with TKIs and clinical data on potential DDIs, along with reported toxicities or outcomes.

Results: We summarized the pharmacokinetic profiles and the clinical evidence of 11 TKIs used for lung or breast cancers. Moreover, we provided an easy-to-use guide to help physicians in clinical practice with recommended dose adjustments or cautions necessary to prevent severe adverse events or possible changes in TKI availability in the presence of other interfering drugs.

Conclusion: The level of evidence for DDIs during TKI treatment is low because most available data are from phase I studies in healthy volunteers and few phase II studies in cancer patients. However, since the occurrence of DDIs can be clinically significant and a prompt drug reconciliation process can be useful to prevent them, further prospective, large-sample-size clinical trials should be carried out.

Background: The landscape of oncology varies across countries and regions, and in consanguineous populations such as Saudi Arabia, the clinical management of hereditary cancers poses a distinct challenge. Hereditary breast cancer (HBC), which is a significant public health concern, accounts for approximately 5%-10% of all breast cancer cases. High-risk genes, including BRCA1, BRCA2, PALB2, TP53 and PTEN, with germline pathogenic or likely pathogenic variants (PVs/LPVs), substantially increase the risk of breast cancer and other malignancies.

Method: In this review, we explore the guidelines and the literature to present a comprehensive investigation of the genetic landscape of hereditary cancer syndromes, provide pivotal insights into disease mechanisms and inform precise clinical intervention. Given their marked therapeutic heterogeneity, a tailored precision medicine approach, rather than a uniform strategy of a one-size-fits-all model, is necessary. For high-risk breast cancer patients in Saudi Arabia, the detection rates of PVs/LPVs have reached 24%, underscoring the relevance of targeted interventions.

Results: A comprehensive framework for the management of HBCs is outlined, which focuses on consanguineous populations and adapts global guidelines. We highlight the critical roles of genetic testing in guiding personalised surveillance strategies, especially for regions where data remain limited.

Conclusion: Revealing the genetic variation associated with HBCs mitigates the burden on healthcare providers and the long-term effects of HBCs on affected individuals and their families. Moreover, it is a step ahead towards personalised prevention, treatment and intervention. This knowledge will empower research and innovation in biotechnology.

Exercise is increasingly recognized as a safe and effective adjunct therapy across the cancer care continuum, offering improvements in physiological function, psychological wellbeing, and treatment outcomes. However, conventional one-size-fits-all exercise prescriptions often fall short of addressing the diverse needs of cancer patients, who differ significantly in tumor type, treatment modality, baseline fitness, and comorbidities. Personalized exercise programs offer a tailored, evidence-informed approach that enhances safety, adherence, and clinical benefits. This narrative review synthesizes the current literature on the physiological, psychological, and oncological impacts of exercise in cancer care, emphasizing the rationale, methodologies, and emerging tools for individualized exercise prescriptions. Integration of such programs into oncology practice requires standardized assessments, interdisciplinary collaboration, and digital infrastructure, with a focus on addressing barriers to implementation and ensuring equitable access. Personalized exercise programs have the potential to improve patient outcomes and survivorship experiences across diverse cancer populations.

Cervical cancer (CeCa) remains a significant global health burden, with complex interactions between oxidative stress and immune response playing critical roles in its pathogenesis and progression. This review synthesizes current knowledge on the molecular mechanisms linking oxidative stress pathways and immune evasion, particularly focusing on human papillomavirus oncogenes E6 and E7. We highlight the dual roles of immune components such as Type 17 T helper (Th17) cells and the antioxidant enzyme superoxide dismutase 2 (SOD2), which exhibit context-dependent tumor-promoting and suppressive functions. While extensive mechanistic insights have been gained, translation to clinical practice remains limited, partly due to inconsistent biomarkers and incomplete understanding of therapeutic resistance. Recent advances in targeted therapies, including mitochondrial inhibitors, Immune checkpoint inhibitors (ICIs) (e.g., pembrolizumab, nivolumab), and PARP inhibitors, demonstrate promise but face translational hurdles such as assay variability and immune-related adverse events. Future research must address gaps including predictive biomarker development, noninvasive monitoring via liquid biopsy, and rational combination therapies integrating redox modulation and immunotherapy. Enhanced multi-omics integration and refined preclinical models are essential to advance personalized treatment strategies for CeCa.