World journal of clinical oncology最新文献

Background: Magnetic resonance imaging (MRI) and endoscopic ultrasonography (EUS) are recommended in combination for screening pancreatic cancer in high-risk individuals. However, in clinical practice, MRI and EUS are increasingly utilized for pancreatic surveillance during routine health examinations.

Aim: To investigate the feasibility of these imaging modalities for screening in low-risk individuals.

Methods: This retrospective study included patients at low risk for pancreatic cancer who underwent MRI or EUS at two health evaluation centers between March 2019 and December 2024. Basic characteristics, laboratory data, and imaging results were collected.

Results: A total of 3364 low-risk individuals underwent pancreatic screening: 1553 (46.1%) received MRI, and 1811 underwent EUS. No significant differences were observed in age or sex distribution between the groups. In imaging screening, EUS demonstrated a higher detection rate of abnormal pancreatic lesions (12.8% vs 2.6%; P < 0.001). MRI detected more cystic lesions than did EUS (P < 0.001). EUS identified smaller nodular lesions compared to MRI (9.2 mm vs 18.0 mm; P = 0.044). The MRI group had a higher number of confirmed intraductal papillary mucinous neoplasms (P = 0.031), whereas the EUS group identified more suspected branch-duct intraductal papillary mucinous neoplasms (P < 0.001). Pancreatic adenocarcinoma was found in three patients (0.08%), with no significant difference in detection rates between EUS and MRI (0.11% vs 0.06%; P = 0.656).

Conclusion: In low-risk individuals, MRI and EUS offer comparable effectiveness for pancreatic cancer surveillance. The choice of imaging strategy for health evaluation depends on cost considerations and degree of invasiveness.

Background: Pseudoachalasia mimics primary achalasia in symptoms and diagnostic findings, as observed in gastroscopy and barium swallow studies. However, pseudoachalasia, often associated with malignancies like metastatic breast cancer, requires prompt differentiation to avoid misdiagnosis and inappropriate treatment. This report highlights a rare case of pseudoachalasia secondary to metastatic breast cancer and highlights the diagnostic value of esophageal motility changes.

Case summary: A 52-year-old woman presented with a one-year history of intermittent dysphagia following breast cancer surgery. Initial examinations suggested achalasia, but the patient's high-resolution manometry (HRM) results showed a rapid shift from ineffective esophageal motility to type II achalasia within four months. Further investigations revealed metastatic adenocarcinoma of the cardia, originating from the breast.

Conclusion: In patients with a history of malignancy, rapidly evolving esophageal motility abnormalities should raise suspicion of pseudoachalasia. HRM plays a crucial role in differentiating between primary and secondary achalasia. Early diagnosis through advanced imaging and pathology is essential for proper management.

Background: Dissection of the right paraesophageal lymph node (RPELN) in managing papillary thyroid carcinoma remains a contentious issue. This meta-analysis assesses previously established and novel risk factors associated with RPELN metastasis.

Aim: To evaluate previously established and novel risk factors associated with RPELN metastasis in patients with papillary thyroid carcinoma papillary thyroid carcinoma through a comprehensive meta-analysis.

Methods: We searched MEDLINE (via PubMed), ScienceDirect, Scopus and EMBASE up to December 2024. Studies were assessed using the Newcastle-Ottawa Scale. Statistical analysis was conducted with RevMan version 5.4, using the Q-test and I ²-test for heterogeneity. Sensitivity was evaluated with the leave-one-out method, and publication bias with the Egger regression test and funnel plot.

Results: Of 2444 articles retrieved, 26 were included in our meta-analysis with 16427 patients. The RPELN metastasis rate was 12.98% [95% confidence interval (CI): 12.46%-13.50%]. The pooled results suggested that age < 55 years [odds ratio (OR) = 1.71, 95%CI: 1.35-2.16, P < 0.00001], sex (OR = 0.60, 95%CI: 0.54-0.67, P < 0.00001), tumor size 1 cm (OR = 3.37, 95%CI: 2.69-4.21, P < 0.00001), multifocality (OR = 1.81, 95%CI: 1.49-2.20, P < 0.00001), capsular invasion (OR = 2.94, 95%CI: 2.05-4.20, P < 0.00001), vascular invasion (OR = 2.16, 95%CI: 1.56-2.99, P < 0.00001), extra-thyroid extension (OR = 3.30, 95%CI: 1.82-5.98, P < 0.0001), central lymph node metastasis (OR = 7.77, 95%CI: 4.73-12.76, P < 0.00001), lateral lymph node metastasis (OR = 6.94, 95%CI: 6.11-7.89, P < 0.00001), Hashimoto thyroiditis (OR = 0.79, 95%CI: 0.69-0.92, P = 0.002), micro-calcifications (OR = 2.29, 95%CI: 1.20-4.37, P = 0.01), and echogenicity (OR = 0.62, 95%CI: 0.40-0.98, P = 0.04) should be considered with RPELN metastasis.

Conclusion: The male < 55, tumor size > 1 cm, multifocality, capsular and vascular invasion, extrathyroidal extension, lymph node metastasis, and Hashimoto thyroiditis were significantly associated with RPELN metastasis and should be carefully assessed during dissection.

Chimeric antigen receptor T (CAR-T) cell therapy represents a major advance in cancer immunotherapy, offering targeted treatment options, particularly for hematologic malignancies. This review comprehensively explores the structural evolution, production processes, and cytotoxic mechanisms underlying CAR-T function. Therapy involves engineering autologous T cells with synthetic receptors that allow major histocompatibility complex-independent recognition of tumor-associated antigens. Key structural components such as antigen recognition domains, spacers, transmembrane, and intracellular domains are optimized to enhance specificity, persistence, and cytotoxicity. CAR-T therapy exerts antitumor effects via granzyme-perforin degranulation, Fas/Fas ligand signaling, and cytokine secretion. Over time, the development of second- to fifth-generation CARs has incorporated costimulatory molecules, transcriptional regulation, and logic-gated control to improve efficacy and safety. Additionally, novel engineering strategies such as dual CARs, tandem CARs, SynNotch systems, and universal or inhibitory CARs have expanded antigen targeting and reduced off-tumor toxicity. Emerging gene delivery technologies, including viral vectors, transposons, CRISPR/Cas9, and RNA-based electroporation, are improving CAR-T production. Despite notable clinical success, particularly in CD19- and B-cell maturation antigen-targeted therapies, CAR-T applications face challenges, including cell exhaustion, antigen escape, and therapy-induced toxicities, such as cytokine release syndrome and neurotoxicity. Ongoing efforts in engineering innovation, clinical trials, and regulatory support continue to shape CAR-T therapy into a safer, more precise tool for cancer treatment. This review highlights current advances while outlining the barriers and future prospects of CAR-T immunotherapy.

Background: Ectonucleoside triphosphate diphosphohydrolase 6 (ENTPD6), a member of the ENTPD family, has been implicated in certain cancers, yet a comprehensive analysis across multiple cancer types remains lacking.

Aim: To systematically evaluate ENTPD6's expression, prognostic significance, and functions across multiple cancer types.

Methods: In this study, we performed a pan-cancer analysis to investigate the correlation between ENTPD6 expression and various factors, including prognosis, genetic alterations, epigenetic modification, immune infiltration, immunotherapy responses, functional enrichment, and drug sensitivity. A tissue microarray of gastrointestinal tumors was used to validate differential ENTPD6 protein expression.

Results: Pan-cancer analysis revealed that ENTPD6 expression was significantly elevated in many cancers. Immunohistochemistry staining analysis revealed that ENTPD6 expression was significantly higher in esophageal carcinoma, stomach adenocarcinoma, colon adenocarcinoma, rectal adenocarcinoma, and pancreatic adenocarcinoma compared to normal tissues. Furthermore, ENTPD6 expression was strongly associated with immune-infiltrating cells, particularly clusters of differentiation 8+ T cells and natural killer cells, and correlated with immune-related genomic features including tumor mutational burden and microsatellite instability. Pathway analysis indicated that ENTPD6 expression was primarily linked to purine and pyrimidine metabolism pathways. Drug sensitivity analysis revealed that high ENTPD6 expression was sensitive to RDEA119, selumetinib, and PD-0325901.

Conclusion: This pan-cancer study elucidates the pivotal role of ENTPD6 in tumor progression and establishes its potential as a therapeutic target for immunotherapeutic approaches in specific malignancies.

Background: Outcomes of early breast cancer in African women are currently not well defined.

Aim: To analyze survival outcomes and prognostic factors in Moroccan women with operable breast cancer treated with multimodal therapies.

Methods: We retrospectively analyzed the data of a large cohort of 400 patients diagnosed with nonmetastatic breast cancer who completed surgery, chemotherapy, and radiotherapy at the National Institute of Oncology in Rabat, from January 2001 to December 2003.

Results: The mean age at diagnosis was 45 years (range: 22-91 years). Surgery was performed in all cases: Mastectomy in 86% and breast-conserving surgery in 14%. Most tumors (> 87%) were classified as pathologic T2 stage or higher, and axillary lymph nodes were involved in 75.5% of cases. Ninety-five percent of patients completed six cycles of adjuvant chemotherapy, and all received radiotherapy. At a median follow-up of 74.5 months, the 5-year overall survival (OS) was 82.1% [95% confidence interval (CI): 78.1-86.3], and the 5-year disease-free survival was 78.1% (95%CI: 73.8-82.6). In univariate analysis, negative nodal status [pN- vs pN+, hazard ratio (HR) = 0.34, 95%CI: 0.16-0.75; P = 0.007] and lower American Joint Committee on Cancer (AJCC) stage (I-II vs III, HR = 0.29, 95%CI: 0.16-0.52; P < 0.001) were significantly associated with better OS. In multivariate analysis, AJCC stage I-II vs stage III remained the strongest predictor of improved OS (HR = 0.32, 95%CI: 0.15-0.67; P = 0.002), followed by treatment with anthracyclines vs cyclophosphamide, methotrexate, fluorouracil (CMF; HR = 0.58, 95%CI: 0.35-0.94; P = 0.027).

Conclusion: Moroccan women with early breast cancer exhibited more aggressive disease compared to women in high-income countries. AJCC stage III was the strongest predictor of poorer OS, followed by chemotherapy regimen (CMF vs anthracycline). A multimodal treatment approach, including surgery, systemic therapy, and radiotherapy, is essential to improve breast cancer outcomes.

Imaging evaluation of lymph node metastasis and infiltration faces problems such as low artificial outline efficiency and insufficient consistency. Deep learning technology based on convolutional neural networks has greatly improved the technical effect of radiomics in lymph node pathological characteristics analysis and efficacy monitoring through automatic lymph node detection, precise segmentation and three-dimensional reconstruction algorithms. This review focuses on the automatic lymph node segmentation model, treatment response prediction algorithm and benign and malignant differential diagnosis system for multimodal imaging, in order to provide a basis for further research on artificial intelligence to assist lymph node disease management and clinical decision-making, and provide a reference for promoting the construction of a system for accurate diagnosis, personalized treatment and prognostic evaluation of lymph node-related diseases.

Proteases are essential for homeostasis, and their primary function is proteolytic in extracellular and intracellular compartments. The deregulation of expression, abundance, and activity of proteases has been related to several pathologies, including cancer. This deregulation contributes to their pro-tumorigenic activity since they participate in the degradation of extracellular matrix components and adhesion molecules, and the activation of growth factors. However, some proteases, such as ADAM metallopeptidase with thrombospondin type 1 motif 8 and kallikrein-related peptidases 5 and 10, have emerged as tumor suppressors due to their antitumoral actions in specific cancer contexts. In this article, we discuss the antitumoral effects of ADAM metallopeptidase with thrombospondin type 1 motif 8, kallikrein-related peptidases 5 and 10 that have been described to date, suggesting their potential use as novel biomarkers and therapeutic targets in cancer.

Background: MicroRNAs play a key role in regulating gene expression in human cells. Single-nucleotide variants in these molecules have been linked to cancer development, particularly breast cancer (BrC).

Aim: To analyze the association of three microRNA polymorphisms with the risk of BrC in women from western Mexico.

Methods: This case-control study included 71 women diagnosed with BrC and 215 women without BrC. Genotypes were determined using a real-time polymerase chain reaction allelic discrimination assay. Multiple genetic models - dominant, recessive, over-dominant, additive, and multiple comparison - were applied to assess the risk.

Results: The over-dominant model showed that the C/T genotype of MIR196A2 (rs11614913) is a protective factor against the ductal histological subtype of BrC in women from western Mexico [odds ratio (OR) = 0.4687, 95% confidence interval (CI): 0.2205-0.9963, P = 0.0489]. A protective effect was also observed for the C/A genotype (OR = 0.2612, 95%CI: 0.0900-0.7582, P = 0.0135) and A allele (OR = 0.2826, 95%CI: 0.0993-0.8044, P = 0.0179) of MIR618 (rs2682818). No significant association was found between MIR200C (rs73262897) and BrC risk.

Conclusion: The C/T genotype of rs11614913 in MIR196A2, and C/A genotype and A allele of rs2682818 in MIR618, are associated with a protective effect against BrC in women from western Mexico.

Cardamonin is a natural chalcone that has been extensively investigated for its anticancer activity. However, its clinical relevance is still not explicit, limiting its progression into clinical trials and highlighting a persistent gap between preclinical evidence and practical application. This review aims to assess the readiness of cardamonin to progress from laboratory research to clinical application as an anticancer agent by examining both scientific evidence and translational challenges. Preclinical pharmacokinetic and pharmacodynamic data suggest that cardamonin's therapeutic potential as an anticancer agent is hindered by its poor oral bioavailability. Although its molecular targets remain undefined, evidence indicates that cardamonin can inhibit various signaling pathways, including nuclear factor kappa-light-chain-enhancer of activated B cells, mammalian target of rapamycin, signal transducer and activator of transcription 3, and Wnt/β-catenin. The lack of in vivo toxicity studies creates uncertainty regarding the balance between its therapeutic benefits and potential adverse effects when moving from laboratory research to human trials. Despite these limitations, cardamonin has, however, demonstrated antiproliferative, anti-metastatic, and chemosensitizing effects, mainly against breast, colorectal, and ovarian cancers. Nevertheless, exploring its combination with standard chemotherapeutic agents may offer a promising foundation for advancing cardamonin into clinical trials.