World journal of clinical oncology最新文献

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.

Pancreatic cancer remains a highly lethal malignancy, primarily due to late-stage diagnosis. Current screening paradigms, which focus exclusively on high-risk individuals, leave the vast "low-risk" population unscreened. This conventional binary risk stratification, based predominantly on family history and known genetic syndromes, fails to incorporate emerging risk dimensions such as polygenic risk scores, lifestyle factors, and novel biomarkers. We propose a paradigm shift from this static model towards a dynamic, multidimensional risk stratification framework. By integrating genetic susceptibility (e.g., newly identified variants in NOC2L, HNF4G), lifestyle metrics (e.g., new-onset diabetes), and liquid biopsy biomarkers (e.g., circulating tumor DNA, carbohydrate antigen 19-9 dynamics), we can reclassify a subset of "low-risk" individuals who may benefit from targeted screening. The integration of artificial intelligence for prospective validation, as seen in ongoing trials, is crucial for implementing this approach.

Background: Patients with esophageal cancer exhibit marked variability in prognosis, highlighting the need for metabolism-related biomarkers. Although metabolic reprogramming is considered to be correlated with the prognosis of patients with esophageal squamous cell carcinoma (ESCC), its specific association mechanisms remain unclear.

Aim: To explore the triglyceride-glucose (TyG) index and its derivatives - indicators for insulin resistance, a core feature of metabolic syndrome. Given their controversial associations with cancer and limited research on their dynamic changes in ESCC patients post-treatment, this study aims to analyze these dynamic changes.

Methods: The present retrospective study analyzed 360 East Asian patients with ESCC who received definitive chemoradiotherapy to explore the associations of TyG, TyG-body weight, and TyG-body mass index (both pre- and post-treatment) with overall survival.

Results: Elevated levels of post-treatment TyG and its derivatives (postTyG, postTyG-body weight, postTyG-body mass index) were significantly associated with a reduced risk of death, showing a superior prognostic value compared to the baseline levels (preTyG). Restricted cubic spline analysis confirmed the presence of non-linear or monotonic associations, with more pronounced correlations observed in male patients.

Conclusion: Post-treatment TyG and its derivatives may serve as independent prognostic indicators for East Asian patients with ESCC, providing a basis for personalized diagnosis and treatment.

Transarterial chemoembolization is a common treatment modality that significantly improves prognosis in patients with intermediate-advanced hepatocellular carcinoma. However, this procedure is associated with a spectrum of potential arterial and biliary complications, ranging from mild self-limiting ones to those severely affecting patient outcomes. This review systematically integrates recent studies to explore the epidemiological characteristics, risk factors, and management strategies of these two groups of complications. Arterial complications, primarily hepatic artery stenosis, pseudoaneurysm, and arterial rupture hemorrhage, exhibit a biphasic distribution pattern with the majority occurring within 72 hours postoperatively, while a notable portion occurs within 1-4 weeks. Biliary complications, including biliary fistulas, biliary strictures, and ischemic cholangitis, exhibit higher incidence rates and more insidious clinical manifestations than arterial complications. Risk factors include the severity of cirrhosis, tumor location, procedural technique, and chemotherapeutic drug toxicity. Management strategies emphasize careful preoperative planning (primarily with computed tomography angiography), standardized intraoperative procedures (like superselective embolization), and multi-pronged postoperative monitoring (imaging combined with laboratory indicators of liver function). Interventional embolization or surgical reconstruction is used for arterial complications, while endoscopic therapy or surgical drainage is selected based on the severity of injury for biliary complications. Future research should further explore individualized treatment regimens and novel embolic materials to reduce complication rates and enhance the safety of transarterial chemoembolization.

Background: The technical complexity and potential for complications associated with endoscopic submucosal dissection (ESD) pose limitations on the widespread use of this procedure for stage 1 rectal neuroendocrine tumors (NETs), despite its high success rate in achieving complete resection (R0).

Aim: To examine the results of ESD and hybrid ESD, a simpler adaptation of the ESD technique, for stage 1 rectal NETs.

Methods: Seventy-nine patients with 84 lesions of clinical stage 1 rectal NETs who received treatment at Sun Yat-sen University Cancer Center from January 2010 to June 2021 were reviewed retrospectively.

Results: Sixty-one lesions in 58 patients were treated with ESD, while 23 in 21 patients were treated with hybrid ESD. The 84 rectal NETs had a median diameter of 8 (5) mm (range, 3-20 mm), with the median lesion size 8 (5) mm for ESD and 8 (4) mm for hybrid ESD (P = 0.359). For ESD, the median duration of procedure was 46.00 (14.00) minutes, while for hybrid ESD, it was 32.00 (15.00) minutes (P < 0.001). Both the ESD and hybrid ESD groups had identical rates of en bloc resection (100.00% vs 100.00%, P = 1.000), R0 resection (86.89% vs 86.96%, P = 1.000), perforation (1.64% vs 0.00%, P = 1.000), and delayed bleeding (1.64% vs 4.35%, P = 0.475). After a median of 27.50 (30.00) months of observation, neither group had recurrence.

Conclusion: For endoscopic excision of stage 1 rectal NETs, both ESD and hybrid ESD were well tolerated and produced positive results, with similar efficacy and safety.

The consumption of ultra-processed foods (UPFs) is continuously increasing, and there is growing evidence that these foods contribute to the development and progression of cancer. For oncology patients alone, maintaining nutritional status is crucial for tolerating treatments and improving survival. The aim of this paper is to review the role of UPFs in the diet of oncology patients, highlighting their potential health-damaging effects (e.g., increased inflammation, microbiome disruption, nutrient deficiencies) and potential benefits (e.g., easy accessibility, high energy content, specially formulated nutritional supplements) particularly in the context of addressing the energy and nutrient needs and nutritional challenges of patients experiencing cancer-related cachexia or anorexia. Using a literature review, we examine how the UPFs can impact oncology patients' health, supporting the quality of life and clinical outcomes of oncology patients.