Circulating tumor cell (CTC) is an evidenced biomarker for early cancer diagnosis and assessment of treatment response. This necessitates increasing attempt to develop new method for detection of CTCs with highly enriching and anti-interference capacity. Herein, we built a simple platform for CTC detection by combining aptamer-mediated specific recognition with affinity magnetic levitation (Maglev). The method involved modification of DNA tetrahedron (TDN) using SYL3C aptamer as tentacles, assembly of aptamer conjugated-TDN on microsphere by azide-alkyne click chemistry, enrichment of CTCs by the activated microspheres, and detection of CTCs by affinity Maglev. These yielded an aptamer sensor resembling octopus tentacles to enhance the capture selectivity and efficiency of CTCs. Once CTCs were captured, a microsphere@TDN@CTCs complex was formed, resulting in a change in the overall density. The number of CTCs was calculated by measuring the levitation height difference between microspheres pro- and post-binding of CTCs in affinity Maglev. An example study on MCF-7 cells exhibited a detection of 8.81 cells mL^-1 in buffer solution, with repeatability characterized by a relative standard deviation of less than 4.48%, in comparison to 9.08 cell mL^-1 in mimic clinical sample with a relative standard deviation of 6.98%. Analysis of mimic clinical samples demonstrated that the method was effective for the specific detection of CTCs with robust resistance to interference from co-existing substances in plasma. It is possible to serve as an early diagnostic alternative for clinically relevant cancers once large number of clinical trials are performed.

This article summarizes hereditary conditions associated with adrenal tumors, emphasizing the importance of germline genetic testing in patients with adrenocortical carcinoma (ACC) and pheochromocytoma/paraganglioma (PPGL). ACC is strongly linked to syndromes such as Li-Fraumeni, Lynch, and Beckwith-Wiedemann, while PPGL has one of the highest hereditary rates among endocrine tumors, often involving SDHx genes and other susceptibility genes, including VHL, RET, NF1, MAX, and TMEM127. The article outlines clinical features, gene-specific risks, management considerations, and evolving surveillance guidelines. Identifying hereditary predispositions improves patient care, guides targeted surveillance, and allows cascade testing for at-risk family members.

Socioeconomic deprivation is increasingly recognized as a determinant of care, yet its relationship to spine surgery remains poorly characterized. The Area Deprivation Index (ADI) provides a validated, neighborhood-level measure of socioeconomic disadvantage. This study characterizes ADI's associations among patients undergoing posterior spine surgery.

1,038 adult patients who underwent posterior spine surgery at a quaternary academic center between 2022 and 2024 were included in the retrospective cross-sectional study. National- and state-level ADI ranks were linked to addresses using 9-digit ZIP codes. ADI ranks represent either the percent (national) or decile (state) for any given ZIP code with higher ranks representing worse neighborhood conditions. Associations between ADI and diagnostic category (ICD-10), admission source, demographic variables, and preoperative clinical characteristics were evaluated using nonparametric testing with multiple comparisons using false discovery rate adjustment. Ordinal logistic regression modeled variance in neighborhood deprivation.

National-level ADI rank varied significantly between diagnostic categories (p = 0.018, p = 0.374 not significant for State-level ADI rank, Kruskal-Wallis). Patients undergoing surgery for neoplastic pathology demonstrated higher national-level ADI ranks compared with those treated for degenerative disease (q = 0.028). Female sex was also associated with worse state-level ADI rank (p = 0.026, national-rank p = 0.066 ns, Mann-Whitney). In ordinal regression, diagnosis of neoplasm remained independently associated with national ADI rank (OR 1.74, p < 0.001). In the models for both national and state-level ADI rank higher body mass index was also (OR 1.24, p < 0.001 and OR 1.23, p < 0.001 respectively), and female sex (OR 0.77, p = 0.020, OR 0.77, p = 0.018 respectively) were significantly associated with worse ADI ranks.

Among patients undergoing posterior spine surgery, neighborhood socioeconomic deprivation is associated with higher rates of spinal neoplasms, female gender, and larger BMIs. These findings suggest that socioeconomic context influences access to spine surgical care prior to operative intervention and highlight the importance of incorporating neighborhood-level factors into evaluations of spine care delivery. Future studies will examine how these presentation-level disparities relate to postoperative outcomes and resource utilization.

Melanoma recurrence risk is highest within the first 2 years after diagnosis and progressively declines thereafter. Current surveillance strategies remain largely guided by clinicopathologic risk stratification, with the comprehensive medical history, physical examination, and complete skin assessment forming the cornerstone of follow-up. Although cross-sectional imaging and lymph node ultrasound are used in selected higher-risk patients, routine intensive imaging has not consistently demonstrated survival benefit and may increase costs and false-positive findings. Emerging technologies are reshaping melanoma surveillance and clinical management. Circulating tumor DNA (ctDNA) has shown promise as a minimally invasive biomarker capable of detecting molecular residual disease and anticipating clinical recurrence. Persistent or newly positive ctDNA after surgery is consistently associated with inferior recurrence-free survival. However, ctDNA does not reliably detect all recurrence patterns and its sensitivity varies according to disease burden and metastatic site. Prospective validation and clarification of how ctDNA should guide adjuvant therapy or imaging strategies remain necessary. In parallel, CD8-targeted positron emission tomography (CD8 PET) has emerged as a novel functional imaging modality capable of noninvasively visualizing whole-body T-cell dynamics. By differentiating tumor burden from immune infiltration and capturing early T-cell recruitment, CD8 PET offers predictive insights into immunotherapy response. Nevertheless, limitations of this technique include dependence on optimal imaging timing, limited tracer availability, cost, and an inability to directly assess T-cell functionality. Together, ctDNA and immune-focused imaging approaches represent promising steps toward precision surveillance and management of melanoma. Further robust prospective studies are required to define their integration into clinical decision making and optimize patient outcomes.

Over the past 50 years, advances in systemic therapy, radiotherapy, surgery, and supportive care have dramatically improved cancer outcomes. Yet, growing concern exists that in our race for biomedical innovation, the metrics used to evaluate progress have drifted away from the outcomes that matter most to people living with cancer. In addition, we have not built health care systems that adequately recognize the psychosocial, relational, and existential dimensions of illness. Many medical therapies approved through regulatory pathways in the past decade offer modest clinical benefit while imposing substantial burdens on patients and the sustainability of health systems globally. These patterns reflect the convergence of global structural forces-including clinical trial design, regulatory standards, practice guidelines, and reimbursement systems-that often prioritize innovation and access over greater certainty that therapies meaningfully improve clinically relevant outcomes. In this review, we examine how these interconnected forces influence patients' experiences of cancer care worldwide. We argue that sustaining meaningful progress requires a reanchoring of oncology to outcomes that reflect what patients consistently value: longer survival, preserved function, improved quality of life, and timely access to high-value care.

Most oncology trials define superiority according to dichotomized P value thresholds, which are frequently misinterpreted. Posterior probability, however, directly estimates the probability of the hypothesis at hand. Here, we reanalyze a large collection of modern phase III trials and benchmark posterior probability versus the standard trial interpretation based on statistical significance.

Outcomes from 194,129 patients were manually reconstructed from the primary end points of 230 phase III, superiority-design oncology trials. Posterior probabilities of treatment effect were then calculated across multiple priors and several effect sizes of clinical relevance, including minimum clinically important difference (MCID) defined as hazard ratio (HR) < 0.8 per ASCO criteria or HR < 0.64 per European Society of Medical Oncology (ESMO) criteria.

All trials interpreted as superior using P value thresholds had probabilities >90% for achieving at least marginal benefits (HR < 1). However, only 62% of positive trials (74/120) had >90% probabilities of achieving the ASCO MCID (HR < 0.8), even under an enthusiastic prior, including 70% of trials (57/82) leading to regulatory approval. Only 30% of positive trials (36/120) had >90% probability of achieving the ESMO MCID (HR < 0.64). Conversely, 24% of trials (26/110) interpreted as not superior had >90% probability of achieving marginal benefits (HR < 1), even under a skeptical prior.

Bayesian models, although often in agreement with statistical significance thresholds, add considerable unique interpretative value for a subset of phase III oncology trials. Posterior probability may provide a solution for overcoming the discrepancies between refuting the null hypothesis and detecting clinically relevant effects.

Pancreatic cancers, whose incidence increases with age, are often refractory to treatment. Here, we identified a core mechanism shared by physiological homeostasis, senescent cell accumulation during aging, and pancreatic cancers. Pancreatic acinar cells, when stressed, secrete CXCL13, which protects stressed cells while transiently activating paracrine Hippo/YAP signaling to induce proliferation and PD-L1-mediated immune protection to maintain organ homeostasis. In the aged pancreas, CXCL13/YAP/PD-L1 signaling permits senescent cells to survive, driving feedforward chronic inflammation and steatosis. Because of prolonged CXCL13/YAP/PD-L1 activation in pancreatic cancers, neighboring noncancerous cells, activated for proliferation and immune-protected, eventually transform and accelerate tumor progression. CXCL13 blockade removed senescent cells and ameliorated steatosis in the aged pancreas while suppressing tumor growth in pancreatic cancer models, highlighting the CXCL13/YAP/PD-L1 axis as a potential therapeutic target. Together, our findings demonstrate the stress-induced CXCL13/YAP/PD-L1 axis as a central regulator of cell-state transitions in the pancreas, providing a unifying principle by which organ homeostasis, aging, and tumorigenesis are governed.

Adult T-cell leukaemia/lymphoma (ATL) is an aggressive CD4 +T-cell malignancy caused by the human T-cell leukaemia virus type 1 (HTLV-1). Approximately 3%-5% of infected individuals develop ATL after a prolonged latency of 30-50 years, during which a complex interplay between viral oncoproteins and host genomic alterations drives the transition from viral persistence to overt malignancy. This transformation is orchestrated by the viral transactivator Tax, which initiates cellular transformation, and the HTLV-1 basic leucine zipper factor (HBZ), which maintains the malignant phenotype and promotes survival through immune evasion. Genomic profiling has revealed that over 90% of ATL cases harbour activating mutations in the T-cell receptor (TCR)-NF-κB signalling pathway, enabling the malignant clone to bypass viral dependency. Furthermore, ATL cells survive host immunosurveillance through sophisticated escape mechanisms, including the loss of MHC class I presentation and programed death-ligand 1 (PD-L1) overexpression via 3'-untranslated region (UTR) disruption. Despite the use of antiviral therapies and targeted monoclonal antibodies, therapeutic failure is common due to genomic instability-specifically TP53 mutations compromising Zidovudine/Interferon efficacy and CCR4 antigenic variations leading to mogamulizumab resistance. This review delineates the multi-step journey of HTLV-1-driven clonal evolution and evaluates the molecular barriers to effective clinical management.

Esophageal cancer is an uncommon but devastating complication of achalasia. There is very limited information in the literature about the effect of any type of treatment on the risk of cancer development in patients with achalasia. The aim of the study was to compare the effects of surgical and endoscopic myotomy (SEM) versus non-SEM on the esophageal cancer risk of patients with achalasia.

We performed a population-based analysis using the TriNetX Global Collaborative Network, which provides real-time access to deidentified electronic health records (EHRs) from 146 health care organizations across the United States and 16 other countries. Adult patients (≥18 y) diagnosed with achalasia between 2004 and 2024 were included. In addition, patients with achalasia who developed esophageal cancer were identified. Patients were grouped by treatment: surgery or endoscopic myotomy versus medical or no therapy. To ensure a proper timeline, the esophageal cancer had to be documented only after the diagnosis of achalasia was established. Multivariable logistic regression was used to evaluate associations with cancer risk. Kaplan-Meier analysis compared the time from achalasia diagnosis to cancer development.

Among 50,365 patients with achalasia, 8015 (15.9%) underwent surgical or endoscopic myotomy (SEM). Esophageal cancer occurred in 394 patients (0.78%); of those, 46 (0.57%) were in the SEM group, and 348 (0.82%) were in the non-SEM group. SEM was independently associated with a significant reduction in the risk of esophageal cancer (OR=2.49, 95% CI: 1.93-3.26, P<0.0001) and longer time to diagnosis (586 vs. 92 d, log-rank P=0.0014; HR=0.609, 95% CI: 0.447-0.829). Male sex (OR=2.31, 95% CI: 2.00-2.78) and nicotine dependence (OR=8.77, 95% CI: 7.25-10.43) were significant predictors of increased esophageal cancer risk in patients with achalasia.

Surgical or endoscopic myotomy treatment for achalasia is independently associated with reduced risk and delayed onset of esophageal cancer compared with non-SEM treatment, supporting a potential protective effect.

Colorectal cancer is a major global health burden, with most cases arising from adenomatous polyps. Although colonoscopy is the gold standard for detection, its effectiveness is operator-dependent. Artificial intelligence-assisted systems have been developed to improve adenoma detection, but their comparative performance remains unclear.

We performed a systematic review and Bayesian network meta-analysis of randomized controlled trials comparing artificial intelligence-assisted with standard colonoscopy. PubMed, Scopus, and Google Scholar were searched up to 4 November 2025. Eligible studies included adults undergoing colonoscopy and reporting adenoma detection rate (ADR) and adenomas per colonoscopy (APC). Secondary outcomes included withdrawal time and detection of advanced and sessile serrated lesions. Risk of bias was assessed using Cochrane RoB 2.0, and certainty of evidence was evaluated with CINeMA.

A total of 48 randomized controlled trials (34 106 participants) were included. Artificial intelligence-assisted colonoscopy significantly improved ADR compared with standard colonoscopy. EndoAngel showed the greatest effect [odds ratio (OR): 1.84, surface under the cumulative ranking curve (SUCRA): 0.9], followed by EndoAID (OR: 1.64, SUCRA: 0.7), CAD-EYE (OR: 1.46, SUCRA: 0.5), and GI Genius (OR: 1.45, SUCRA: 0.5). For APC, EndoAID demonstrated the largest benefit (mean difference: 0.62). EndoAngel modestly increased withdrawal time (mean difference: 1.14 minutes). No system significantly improved detection of advanced or sessile serrated lesions. Heterogeneity was low, and certainty of evidence was moderate.

Artificial intelligence-assisted colonoscopy improves adenoma detection; however, differences between systems are small, and benefits for high-risk lesions remain uncertain. Further head-to-head trials and cost-effectiveness studies are needed.