The trends and contributors of racial and ethnic disparities in causes of death among patients with clear cell renal cell carcinoma remain unclear. We analyse SEER data (2000-2019) and find that Black patients have the highest 5-year cumulative incidence of death (22.4% vs. 21.7% in whites). Despite a decreasing trend in mortality, the disparities persist between Black and white people (HR 1.15, 95% CI 1.09-1.22) and between AIAN and white people (1.25, 1.10-1.43). Disparities in death from cardiovascular disease between Black and white people increase over time. Stage at diagnosis, receipt of surgery, income, and geographic factors partially explain the observed disparities in mortality patterns. This study identifies specific, measurable contributors to mortality disparities, suggesting that interventions targeting earlier detection, equitable treatment, and socioeconomic barriers are needed.

Robotic gastrectomy has been adopted for gastric cancer. However, operative time remains longer than that of laparoscopic surgery. Junk time has been proposed as a major contributor to prolonged operative duration. This study evaluated intraoperative time structure during the initial clinical experience with the minimally invasive laparoscopic and robotic (MILAR) approach using the da Vinci SP system.

This retrospective exploratory workflow analysis included consecutive patients who underwent robot-assisted distal gastrectomy with D1+/D2 lymphadenectomy between May 2024 and June 2025. Patients were divided into the SP (MILAR) group and the conventional multi-port robotic (Xi) group. Operative videos from skin incision to gastric transection were reviewed to quantify effective time and junk time.

A total of 40 patients were analyzed (SP, n = 11; Xi, n = 29). Total operative time was significantly shorter in the SP group than in the Xi group (148.0 vs. 204.0 min, p = 0.001). Junk time was significantly reduced (30.4 vs. 36.6 min, p = 0.034), accompanied by fewer robotic instrument exchanges (4 vs. 46, p < 0.001). Effective time was shorter in the SP group; although this finding may have been influenced by surgeon expertise and case complexity. No increase in procedure-related complications was observed in the SP group.

The present exploratory study describes differences in intraoperative time structure observed during the initial clinical experience with the MILAR approach using SP system. These findings provide insight into workflow characteristics of a hybrid team-based approach and warrant further evaluation in prospective studies.

Glioblastoma (GBM) remains one of the most aggressive primary brain tumors, with poor prognosis, high recurrence, and limited therapeutic options. Although substantial progress has been made in drug development, effective clinical translation is still constrained by inefficient delivery across the blood brain barrier (BBB) and blood brain tumor barrier (BBTB), insufficient tumor accumulation, intratumoral heterogeneity, acquired therapeutic resistance, and dose limiting systemic toxicity. Nanomedicine offers a promising strategy to address these barriers through tunable physicochemical properties, flexible surface functionalization, improved pharmacokinetics, and controllable drug release. In this review, we systematically summarize recent advances in nanomedicine enabled GBM therapy from four interrelated perspectives: the optimization of nanomaterial properties, the development of goal-oriented targeting strategies, the rationalization of delivery routes, and the engineering of smart stimuli-responsive nano-systems. Rather than only cataloguing representative nanoplatforms, we emphasize how material parameters, biological targeting mechanisms, delivery routes, and release behaviors are mechanistically linked to BBB or BBTB penetration, tumor accumulation, therapeutic efficacy, and translational feasibility. Importantly, we also incorporate a key failure case analysis of representative clinical and preclinical studies, highlighting why promising nanotherapeutic concepts may fail because of inadequate intratumoral distribution, insufficient survival benefit, poor patient selection, manufacturing complexity, safety concerns, or impractical trial design. By integrating delivery mechanisms, cross platform comparison, translational barriers, and future optimization principles, this review provides a critical and forward looking framework for the rational design of precise, effective, and clinically translatable nanomedicine strategies for GBM treatment.

Lymphadenectomy around the left recurrent laryngeal nerve is one of the most technically demanding steps in esophagectomy. Even in robot-assisted esophagectomy, the operative field easily becomes wet and achieving on-demand suction remains challenging.

Between July 2024 and November 2025, 11 patients underwent robot-assisted esophagectomy in the prone position. We developed a simple on-demand suction technique by suturing gauze to a commercially available suction tube, allowing both the surgeon and the assistant to perform suction as needed. The modified tube can be manipulated using either robotic instruments or assistant forceps and can also be used for gentle tracheal rolling during lymphadenectomy. Furthermore, to evaluate the feasibility and safety of this technique, we conducted a retrospective comparison with 11 cases performed using the conventional method (tracheal traction with a robotic Cadiere forceps) between March 2023 and May 2024. All procedures were performed by a single surgeon.

This simple and low-cost technique facilitates maintenance of a dry operative field during robot-assisted esophagectomy. Furthermore, in comparison with the conventional method, no significant differences were observed in operative time, blood loss, or the incidence of recurrent laryngeal nerve palsy; however, there was a trend toward reduced intraoperative manipulation time. These findings suggest that this technique offers comparable safety to the conventional approach while potentially contributing to improved operative field management.

Primary myelofibrosis (PMF) is a myeloproliferative neoplasm frequently treated with the Janus kinase (JAK) inhibitor Ruxolitinib. Perioperative management of Ruxolitinib presents a clinical dilemma. Continued therapy may increase the risk of infection, cytopenia, and impaired wound healing during major surgery, whereas abrupt discontinuation can precipitate Ruxolitinib Discontinuation Syndrome (RDS), an inflammatory rebound syndrome that may be life-threatening. Currently, there are no established perioperative guidelines for the management of Ruxolitinib. We report a case of a 65-year-old patient with PMF undergoing elective coronary artery bypass graft (CABG) surgery. Following multidisciplinary discussion with haematology, Ruxolitinib was withheld for 48 hours perioperatively and prophylactic corticosteroids were administered. The patient underwent uncomplicated surgery and recovery without evidence of infection, thrombocytopenia, or RDS. This case highlights the challenges associated with perioperative Ruxolitinib management and emphasises the importance of multidisciplinary decision-making and individualised risk assessment. Reporting such cases contributes to the limited literature guiding perioperative management of JAK inhibitor therapy in patients undergoing major surgery.

To critically evaluate oligoprogression in advanced gastric and gastroesophageal junction (GEJ) cancer and propose a practical multidisciplinary framework integrating local therapy, systemic treatment decisions, and biomarker reassessment.

We reviewed direct gastric/GEJ evidence and clearly distinguished it from evidence extrapolated from oligometastatic disease and other tumor types.

No prospective comparative study has demonstrated that local treatment with continuation of systemic therapy improves survival specifically in gastric/GEJ oligoprogression. In carefully selected patients, local treatment may be considered to delay the next systemic therapy, prevent or relieve symptoms, maintain local control, or preserve quality of life. Tissue rebiopsy or circulating tumor DNA analysis may be useful when technically obtainable and likely to change management. HER2 reassessment has established clinical relevance after HER2-directed treatment, whereas repeat assessment of CLDN18.2, PD-L1, FGFR2b, and other emerging targets remains exploratory. A negative plasma circulating tumor DNA result does not exclude resistant disease, particularly in low-volume, peritoneal, or central nervous system progression.

Management should remain individualized and multidisciplinary, with explicit recognition that the proposed framework is provisional and that a survival benefit from local therapy with systemic treatment continuation remains unproven.

Monensin, a polyether ionophore widely used in veterinary medicine, has recently emerged as a multimodal anticancer candidate. This review provides a comprehensive overview of preclinical studies showing that monensin exerts selective cytotoxic and anti-progression effects across a wide range of malignancies. Its activity spans breast cancer to leukemia, reflecting both versatility and significant therapeutic potential. In breast cancer, monensin reduces proliferation, induces apoptosis, and enhances chemosensitivity, suggesting a role in combination therapies. In prostate cancer, it disrupts androgen receptor signaling, induces oxidative stress, and triggers mitochondria-dependent apoptosis. In pancreatic cancer, it suppresses EGFR signaling and promotes programmed cell death, while in ovarian and cervical cancers, it inhibits proliferation, migration, and invasion by modulating EGFR and MEK/ERK pathways and enhancing SUMOylation. In renal carcinoma, monensin induces cell-cycle arrest, autophagy, and apoptosis, whereas in bladder and squamous cell carcinoma, it interferes with EGFR-related signaling and lectin-mediated interactions. It selectively kills liver cancer cells through intracellular Na⁺ overload and mitochondrial damage, and in thyroid cancer, it disrupts cellular respiration and AMPK/mTOR signaling. In glioblastoma, it exhibits both anti-tumor and anti-angiogenic effects, while in hematologic malignancies such as leukemia and lymphoma, it induces apoptosis, cell-cycle arrest, and glycosylation alterations. Collectively, these findings highlight monensin as a highly promising, broad-spectrum anticancer candidate. Its multifaceted mechanisms of action and consistent efficacy across diverse tumor types provide a compelling rationale for continued preclinical evaluation and potential clinical translation. These insights position monensin as an innovative therapeutic avenue, offering new hope for the development of versatile and effective cancer treatments.

Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, with tumor-associated macrophages (TAMs), predominantly M2-polarized, shaping a tumor-promoting microenvironment. ETS proto-oncogene 2 (ETS2) is aberrantly upregulated in CRC, but its role in exosome-mediated intercellular communication and TAM polarization remains unclear. Here, public datasets and single-cell RNA sequencing were analyzed to characterize ETS2 expression and cellular distribution in CRC. Co-culture of THP-1-derived M0 macrophages with CRC cells (LoVo and HCT-116), combined with isolation of tumor-derived exosomes, was used to assess exosome-mediated ETS2 transfer and macrophage M2 polarization. CRC cell proliferation, migration, apoptosis, CD8⁺ T cell apoptosis, and macrophage M2 polarization were evaluated by CCK-8, EdU incorporation, flow cytometry, RT-qPCR, and Transwell assays. Chromatin immunoprecipitation and dual-luciferase reporter assays confirmed transcriptional activation of pre-mRNA processing factor 4 (PRPF4) by ETS2, and a xenograft mouse model was used to assess in vivo effects. ETS2 expression was elevated in CRC tissues and TAMs and correlated positively with M2 polarization. Silencing ETS2 inhibited CRC cell proliferation and migration, promoted apoptosis, reduced macrophage M2 polarization, and decreased CD8⁺ T cell apoptosis. Mechanistically, ETS2 activated PRPF4 transcription, and PRPF4 overexpression reversed the inhibitory effects of ETS2 knockdown. CRC-derived exosomes mediated ETS2 transfer to macrophages, promoting M2 polarization, and in vivo PRPF4 overexpression significantly rescued tumor growth suppressed by ETS2 knockdown. These findings indicate that exosomal ETS2 promotes CRC progression and M2 macrophage polarization via PRPF4, highlighting the ETS2/PRPF4 axis as a potential therapeutic target.

Fibroadenoma is the most common benign fibroepithelial lesion of the breast; it occurs most frequently in adolescents and women of reproductive age. While fibroadenoma is considered a non-invasive lesion with a good prognosis, some fibroadenomas may show rapid growth, recurrence, stromal hypercellularity, epithelial proliferative changes and even show radiological overlap with phyllodes tumour and breast carcinoma resulting in significant diagnostic dilemmas. In recent years, molecular pathology and biomarker studies have led to better understanding of the biology of fibroadenomas, and their ability to differentiate between fibroadenomas and malignant breast lesions. This review will provide a comprehensive overview of biomarkers involved in the diagnosis, prognosis, prediction, molecular, genetic, epigenetic, functional, circulating and imaging of breast fibroadenoma and breast cancer. The key biomarkers such as MED12 mutation, Ki-67, p53, Bcl-2, ER/PR, HER2, VEGF, MMPs, γ-H2AX, ctDNA, circulating tumour cells and transcriptomic classifiers are discussed in the context of tumour proliferation, apoptosis, angiogenesis, invasion, genomic instability and malignant transformation risk. The retrieved relevant literature was from 2000 to 2025 from the databases of PubMed, Scopus, Web of Science, and Google Scholar. The review further emphasizes the growing significance of liquid biopsy, radiomics, artificial intelligence, digital pathology, and the integration of multi-omics techniques for enhancing lesion classification, diagnostic accuracy, and personalized risk assessment. Many challenges still exist such as a lack of standardised cut off values for biomarkers, overlap between fibroadenoma and phyllodes tumour, a lack of molecular panels specifically designed for fibroadenoma and a lack of long-term validation studies. Further incorporation of molecular profiling, imaging biomarkers, computational pathology, and precision oncology approaches into the future could greatly enhance the risk stratification and handling of benign and malignant fibroepithelial breast lesions.

Spatial patterns of glioblastoma (GBM) progression inform focal salvage eligibility, but interpretation across studies is limited by heterogeneous spatial definitions, high between-study heterogeneity, and incomplete reporting of non-enhancing/FLAIR-dominant progression. We synthesized reported progression-location involvement after upfront radiotherapy/temozolomide (RT/TMZ) and salvage therapy.

We systematically searched PubMed and Scopus from January 1, 2000, to February 1, 2026, and performed arm-level random-effects meta-analysis of logit-transformed proportions. Enhancing progression was harmonized as non-mutually exclusive local/in-field, marginal/field-edge, and distant/out-of-field involvement among evaluable cases, using each study's spatial framework. The supplementary broad escape-pattern construct was defined as reported progression beyond purely local/in-field enhancing failure.

We included 107 studies (122 arms; 10,529 patients). At first progression after upfront RT/TMZ ± TTF, reported local/in-field enhancing involvement among evaluable cases was 79.2% (95% CI 75.7-82.3; k = 94; n = 6,989; I²=84.8%), and distant/out-of-field involvement was 16.9% (95% CI 14.3-19.9; k = 89; n = 6,493; I²=85.2%). After salvage therapy, local/in-field involvement remained the majority pattern reported among evaluable cases (59.8%, 95% CI 52.8-66.4; k = 27; n = 1,572; I²=80.5%), with distant/out-of-field involvement of 17.5% (95% CI 12.9-23.3; k = 21; n = 1,307; I²=75.5%) and a supplementary broad escape-pattern estimate of 38.6% (95% CI 31.9-45.9; k = 27; n = 1,572; I²=80.1%). Non-enhancing/FLAIR-dominant progression was sparsely and likely selectively reported; only six recurrent/salvage arms contributed data, yielding an exploratory pooled estimate of 27.8% (95% CI 12.8-50.3; n = 216; I²=75.7%).

Published GBM cohorts show predominantly local/in-field enhancing progression after upfront therapy (~ 80%) and persistent majority local/in-field involvement after salvage therapy (~ 60%). Standardized reporting of enhancing, non-enhancing/FLAIR-dominant, disseminated, posterior fossa, and brainstem progression is needed.