World journal of clinical oncology最新文献

Esophageal cancer poses a severe global healthcare burden, with a dismal prognosis primarily due to late-stage diagnosis - only 10%-30% of patients survive 5 years when symptoms trigger medical attention. Endoscopic submucosal dissection (ESD) has emerged as a transformative minimally invasive therapy for early esophageal neoplastic lesions, offering curative potential while preserving organ function. However, the clinical landscape of early esophageal neoplasia is highly heterogeneous, with low-grade intraepithelial neoplasia, high-grade intraepithelial neoplasia, early-stage carcinoma, and superficial carcinoma differing significantly in biological behavior, endoscopic features, and treatment response. This article examines the recent retrospective study published by Zhang et al, which analyzed 245 patients with 264 lesions treated with ESD between 2014 and 2022. The study fills a critical gap in understanding this heterogeneity by systematically linking lesion stage to clinicopathological characteristics, ESD efficacy, and long-term prognosis. It not only validates ESD's role in early disease but also raises urgent questions about refining stratified management and addressing unmet needs in high-risk populations. This article discusses the implications of the study's findings, contextualizes them within current clinical practice, and outlines directions for future research to advance care for patients with early esophageal neoplasia.

Background: Myeloid sarcoma (MS) is a rare hematological malignancy that may be associated with myelodysplastic or myeloproliferative neoplasms. Herein, we report a case of transformation from myelofibrosis to MS.

Case summary: A 56-year-old male patient was found to have multiple bone lesions by the pelvic magnetic resonance imaging. Pathological analysis of the lesions indicated a myeloid tumor, and immunohistochemistry revealed a TP53 mutation. Bone marrow aspiration was consistent with myelofibrosis. Based on the patient's history of polycythemia and the immunohistochemical findings of the surgically resected lesions, a transformation from a myeloproliferative neoplasm to MS was suggested. The patient developed hematological toxicity after receiving chemotherapy with idarubicin plus cytarabine, and treatment was subsequently adjusted to ruxolitinib combined with venetoclax. However the patient exhibited suboptimal treatment response.

Conclusion: Cases of myelofibrosis transforming into MS are extremely rare. The TP53 mutation is a key molecular marker associated with poor tumor prognosis. Because it can be easily mistaken for other tumors, it is crucial to perform relevant examinations and establish a clear diagnosis as early as possible. This facilitates the timely formulation of an appropriate treatment plan and may help prolong the patient's life.

Background: Lymphoproliferative neoplasms (LPNs) such as chronic lymphocytic leukemia and non-Hodgkin lymphomas are clinically heterogeneous and frequently associated with recurrence and poor outcomes. Immune checkpoint markers, including programmed death-ligand 1 (PD-L1) and programmed cell death protein 1 (PD-1), as well as C-X-C motif chemokine receptor 3 (CXCR3) and inflammation-based indices [systemic immune-inflammation index (SII) and systemic inflammation response index (SIRI)], have shown promise in risk stratification but remain underexplored in Egyptian populations.

Aim: To assess the prognostic value of PD-L1/PD-1 co-expression with CXCR3, SII, SIRI, and CXCR3 expression on monocyte subsets and lymphocytes in Egyptian patients with LPNs.

Methods: A case-control study was conducted at Kafr Elsheikh University Hospitals (January 2024 to January 2025), including 90 patients with LPNs (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, mantle cell lymphoma) and 90 matched healthy controls. All participants underwent clinical evaluation, laboratory testing (including complete blood count, C-reactive protein, lactate dehydrogenase, and ferritin), and flow cytometry for PD-L1, PD-1, and CXCR3. Inflammatory indices (SII, SIRI, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and ferritin-to-lymphocyte ratio) were calculated. Clinical outcomes included remission, recurrence, and survival.

Results: Patients with LPNs had marked hematological and biochemical alterations, including anemia, thrombocytopenia, and reduced neutrophils, with significantly elevated lactate dehydrogenase, C-reactive protein, ferritin, and systemic inflammatory indices (SII, SIRI). Inflammatory ratios (neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio) were lower, whereas the ferritin-to-lymphocyte ratio was higher compared with controls. Immune profiling showed significantly increased PD-L1/CXCR3 and PD-1/CXCR3 co-expression and higher CXCR3 expression on T lymphocytes. Post-treatment, PD-L1/CXCR3, CXCR3/T lymphocyte expression, SII, and SIRI decreased. Prognostic evaluation revealed that SIRI, PD-L1/CXCR3, and PD-1/CXCR3 had high accuracy for identifying stage IV disease, with patients showing low baseline levels achieving superior survival (100% follow-up). Clinically, 21.1% achieved complete remission, 26.7% relapsed, and 15.6% died.

Conclusion: PD-L1/PD-1 co-expression with CXCR3, combined with SII and SIRI, constitutes a practical prognostic panel for staging and outcome prediction in Egyptian patients with LPNs. These biomarkers may guide personalized management and therapeutic monitoring.

The immunosuppressive tumor microenvironment (TME) of oral squamous cell carcinoma (OSCC) is marked by hypoxia, acidity, and abundant stromal cells, such as cancer-associated fibroblasts, tumor-associated macrophages, and myeloid-derived suppressor cells, along with factors such as tobacco and alcohol exposure, human papillomavirus infection, and microbial imbalance that drive immune evasion and poor immunotherapy responses. This review critically evaluated nanotechnology-driven strategies for reprogramming the OSCC TME, focusing on overcoming immunosuppression, hypoxia, stromal barriers, and OSCC-specific challenges to enhance immunotherapy outcomes. Personalized nanotherapies guided by TME profiling, combination with radiotherapy/chemotherapy, and theranostic nanoparticles show promise despite manufacturing/regulatory challenges. Nanotechnology enables transformative TME reprogramming to potentiate OSCC immunotherapy, necessitating interdisciplinary research and clinical validation.

Background: Early-onset colorectal cancer (EOCRC) is an aggressive malignancy with rising incidence and poor prognosis in young adults. Circulating immune cells may hold prognostic value, yet their role in EOCRC outcomes remains unclear.

Aim: To develop machine learning-based prognostic models using peripheral immune markers in a retrospective cohort of EOCRC patients.

Methods: A cohort of 123 EOCRC patients undergoing radical resection, from January 2017 to December 2020 was included. Data were extracted from medical records with a follow-up till July 2025. Blood samples were processed for flow cytometry to assess immune markers.

Results: Univariable screening identified disease stage and CD16+CD56+ natural killer (NK) cell percentage as top predictors. A parsimonious Cox model integrating stage and high NK cells outperformed random survival forests (concordance index 0.693 vs 0.256). High-risk patients (stage III/IV, high NK cells) had inferior 5-year progression-free survival (61.2%; 95% confidence interval: 49.0-76.5) vs low-risk (86.4%; 95% confidence interval: 78.9-94.6; log-rank P = 0.001). Time-dependent areas under the curve ranged from 0.671 to 0.693, with robust calibration.

Conclusion: This two-factor model offers moderate accuracy for personalized EOCRC risk stratification, highlighting systemic NK cell dysfunction as a potential immunotherapy target. External validation is warranted.

Background: Long-term proton pump inhibitor (PPI) therapy is widely prescribed for acid-related disorders. Emerging evidence associates prolonged use with potential adverse outcomes, including gastric cancer. Despite increasing prescriptions, little is known about patients' awareness of these risks or factors influencing discontinuation. We hypothesized that limited risk awareness and family support significantly affect patients' willingness to deprescribe PPIs.

Aim: To evaluate patients' awareness of PPI risks and factors associated with deprescribing.

Methods: A cross-sectional observational study was conducted in community clinics and pharmacies across Israel, including 3000 adult PPI users recruited consecutively. Participants completed a multilingual survey (Hebrew, Arabic, Russian) assessing risk awareness, family support, and quality of life. A composite risk scale (0-12) was used to quantify perceived cancer risk. Descriptive statistics and multivariate logistic regression were performed to identify factors associated with high-risk awareness and willingness to discontinue PPIs.

Results: Among 3000 participants, fatigue occurred in 20%, constipation in 31.3%, infections in 9.3%, renal issues in 4.6%, and no side effects in 12.5%. Pantoprazole cancer-risk perception was 26.5%. Overall, 30% desired to discontinue PPIs and 15% reported symptom recurrence. High composite risk score (≥ 2) was associated with family support [odds ratio (OR) = 1.9, 95% confidence interval (CI): 1.3-2.8; P < 0.01] and longer PPI use (> 1 year; OR = 1.6, 95%CI: 1.1-2.4; P = 0.02). Attempted discontinuation correlated with high-risk score (OR = 2.1, 95%CI: 1.5-3.0; P < 0.001).

Conclusion: Patients show limited awareness of long-term PPI risks. Family support and longer treatment duration are strongly associated with higher risk awareness and willingness to discontinue PPIs.

Background: Breast cancer survivors (BCS) demonstrate attenuated immune cell mobilization following acute exercise, with partial restoration following exercise training. Epinephrine (EPI) and norepinephrine (NE) are responsive to exercise-stress and directly regulate immune cell function, indicating a potential role in this restorative process. Similar attenuations in catecholaminergic signaling have been reported in BCS post-exercise; however, it is unknown whether this is maintained within a trained state. We hypothesized that compared to non-cancer controls (CON), acute exercise would induce an attenuated catecholaminergic response in untrained BCS, which would be recovered to levels similar to CON after training.

Aim: To compare acute exercise-induced catecholaminergic responses between BCS and CON before (PRE) and after (POST) completing a community-based exercise intervention.

Methods: Thirteen BCS (age: 56 ± 2 years, body fat: 39.7% ± 1.3%) and 13 CON (age: 56 ± 2 years, body fat: 41.2% ± 1.7%) performed 45 minutes of intermittent cycling at 60% peak power output PRE and POST 16 weeks of community-based exercise training. Blood samples were collected at baseline (BASE), immediately (0 hour), and 1-hour (1 hour) post-exercise for assessment of the acute EPI and NE response. Separate linear mixed models were used for PRE and POST EPI and NE assessment.

Results: At PRE, both BCS and CON demonstrated increases in EPI (+87.4 pg∙mL^-1, P < 0.001) and NE (+1295 pg∙mL^-1, P < 0.001) at 0 hour, with no group differences. At POST, group differences in NE initiation (0 hour-BASE) were not statistically significant (-544.9 pg∙mL^-1, P = 0.115, g = 0.92), despite divergent responses between BCS (+28%, P = 0.175, g = 0.36) and CON (-13%, P = 0.377, g = 0.23). No group differences were observed for NE recovery (1 hour-0 hour) nor for EPI initiation or recovery.

Conclusion: BCS and CON present with similar exercise-induced catecholaminergic responses regardless of training, suggesting an alternative mechanism may have made a greater contribution to the training-induced immune cell revival previously observed.

Melanoma, a highly immunogenic malignancy, has become a paradigm for immune-based therapies. Despite remarkable responses to immune checkpoint inhibitors, many patients exhibit primary or acquired resistance. These outcomes are largely driven by the composition and dynamics of the tumor microenvironment, which shape immune activation, suppression, and therapeutic responsiveness, contributing to immune escape. Moreover, checkpoint molecule expression, altered antigen presentation, and immunosuppressive cytokine profiles further hinder effective immune surveillance. Advances in biomarker discovery have provided valuable insights into predicting therapy response and guiding individualized treatment. This review discusses the interplay between melanoma and its immune microenvironment, explores mechanisms of immune resistance, and highlights emerging predictive biomarkers with potential to refine clinical decision-making and improve outcomes.

Mitochondrial translation relies on the coordinated activity of mitoribosomes, mitochondrial ribosome proteins, mitochondria-specific transfer RNAs, and dedicated translation factors, including mitochondrial initiation factor 2/3, mitochondrial elongation factor Tu, mitochondrial elongation factor Ts, mitochondrial elongation factor G1/G2, mitochondrial elongation factor 4, mitochondrial ribosome recycling factor, and mitochondrial release factor 1A. These components collectively drive the synthesis of 13 essential polypeptides encoded by mitochondrial DNA, all constituting subunits of the oxidative phosphorylation complexes. Although mitochondrial metabolism is increasingly recognized as a key player in cancer, the specific contribution of mitochondrial translation to cancer progression remains poorly explored. This gap in knowledge limits our understanding of how mitochondrial dysfunction contributes to tumor initiation, progression, and therapy resistance. Herein, in this review, we highlight how dysregulation of mitochondrial translation factors can influence major cancer hallmarks such as sustained proliferative signaling, resistance to apoptosis, and increased invasion and metastasis. In addition, we discuss the known molecular mechanisms that link defects in mitochondrial translation to oncogenic features. We also consolidate current insights into the mitochondrial translation machinery and discuss recent evidence of its role in cancer, aiming to emphasize mitochondrial translation as a contributor to malignancy and a potential therapeutic target.