Vaginal cuff recurrence of endometrial cancer is generally managed with radiotherapy, and surgical reports are scarce. We report a laparoscopic resection technique for isolated vaginal cuff recurrence.

A 57-year-old woman underwent laparoscopic hysterectomy with bilateral salpingo-oophorectomy for grade 1 endometrioid carcinoma (FIGO stage IA) without adjuvant therapy. Nine months postoperatively, she was referred to our hospital with suspected vaginal cuff and pelvic lymph node recurrence. Imaging revealed no invasion of adjacent organs, and lymph nodes were deemed resectable.

Laparoscopic resection of the vaginal cuff tumor and pelvic lymphadenectomy were performed. Following the principles of radical hysterectomy, the bilateral cardinal ligaments, uterosacral ligaments, and the anterior and posterior layers of the vesicouterine ligaments were divided. The vaginal canal was circumferentially incised, and the recurrent tumor was excised. As paravaginal tissue invasion was not suspected, the hypogastric nerves were preserved. Specimens were retrieved transvaginally in protective bags. Histopathological examination confirmed recurrent grade 3 endometrioid carcinoma with negative margins and pelvic nodal metastases. Postoperative chemotherapy was administered, and the patient remains disease-free.

This technique represents a valuable therapeutic option, providing safe and definitive resection for patients with vaginal cuff recurrence.

Primary graft failure is a rare but life-threatening complication after umbilical cord blood transplantation (UCBT), especially in pediatric patients with relapsed acute lymphoblastic leukemia (ALL). Optimal salvage strategies, including conditioning regimens and donor selection for second transplantation, have not been established. This report describes the case of a 9-year-old boy with relapsed B-cell precursor ALL who developed primary graft failure following the first UCBT performed during his second complete remission. The initial transplant had used a cord blood unit with a low CD34-positive cell dose and significant human leukocyte antigen (HLA) and ABO mismatch. Despite myeloablative conditioning, neutrophil engraftment failed, and donor chimerism remained minimal. An urgent second UCBT was performed using a different cord blood unit with improved HLA compatibility and markedly higher total nucleated and CD34-positive cell doses, following reduced-intensity conditioning with fludarabine and low-dose total body irradiation. Sustained neutrophil engraftment was achieved on day +34, with stable full donor chimerism thereafter. Post-transplant complications, including hemophagocytic syndrome, sinusoidal obstruction syndrome, acute graft-versus-host disease, and viral reactivation, were successfully managed. This pediatric case demonstrates that, in the absence of a suitable donor and with prompt intervention, a second UCBT is a feasible salvage option after primary graft failure.

Mesenteric lymphangioma is a rare cystic lesion that may present as acute abdomen due to events such as axial torsion. This is a case report of a small bowel mesenteric lymphangioma presented with axial torsion, which required emergency surgery after repeated abdominal symptoms and hospital visits failed to identify the lesion. This report includes a review of the literature.

A 7-year-old boy was presented with abdominal pain and vomiting. Abdominal ultrasound and contrast-enhanced CT revealed the whirlpool sign, leading to a diagnosis of small bowel volvulus. Emergency surgery was performed. A multilocular cyst measuring approximately 8 cm in diameter was identified in the mesentery of the small bowel, approximately 150 cm proximal to the ileocecal junction. The mesentery exhibited volvulus. A partial small bowel resection and cystectomy were performed. Pathological examination revealed irregularly dilated lymphatic lumens with endothelial cells positive for CD31 and D2 - 40, resulting in a diagnosis of mesenteric lymphangioma.

Surgical resection is the standard treatment for mesenteric lymphangioma. Even when symptoms improve with conservative management, this disease carries the potential for serious complications requiring emergency surgery. Therefore, patients presented with abdominal symptoms, this condition should be considered, and early intervention should be contemplated.

The incidence of head and neck cancer (HNC) is rising globally, with patients undergoing extensive surgical resection for advanced disease frequently requiring prophylactic tracheostomy to secure the airway in the early postoperative period. Specialised HNC nurses undertake extended scope tracheostomy procedures, including tube changes and decannulations, yet practice varies widely between institutions and no standardised training framework exists.

To benchmark the roles and responsibilities of specialised HNC nurses in tracheostomy management across Australia, and to explore the facilitators, barriers and enablers of nurse-led extended practice.

National mixed-methods study.

An online REDCap questionnaire was distributed to nurses with inpatient HNC tracheostomy experience within the past 5 years (n = 22). A subset participated in semi-structured interviews (n = 11), analysed using inductive thematic analysis.

Most participants were senior metropolitan-based nurses with over 12 years of HNC experience. Nine (41%) performed tracheostomy tube changes and 14 (64%) conducted decannulations. Thematic analysis identified six themes: the central role of the multidisciplinary team; education and patient support; training and skill acquisition; extended scope of practice; challenges to nurse-led management; and benefits of nurse-led management. Skill acquisition was facilitated by mentoring and high-volume exposure; barriers included collegial resistance, equipment access and workload pressures.

Specialised HNC nurses report undertaking extended scope tracheostomy procedures across a range of Australian centres, with mentoring, high-volume clinical exposure and multidisciplinary collaboration described as key enablers. Standardised competency frameworks may help to reduce inter-institutional variation; however, the safety, efficiency and patient-level outcomes of these models were not directly evaluated in this study and warrant formal investigation in future research.

This study provides the first national descriptive data on the role of nurses in tracheostomy management for patients with HNC in Australia and offers a foundation for the development of standardised training pathways. The potential impact of such pathways on efficiency, length of stay and nursing workforce capacity warrants formal evaluation in future studies.

The increasing biological complexity and heterogeneity of cancer have driven a shift in oncology drug discovery from single-target approaches toward system-level strategies capable of capturing multilayered disease regulation. Multi-omics technologies, including genomics, transcriptomics, proteomics, metabolomics, epigenomics, and microbiomics, have emerged as powerful tools for elucidating cancer-driving mechanisms, identifying therapeutic targets, and enabling biomarker-guided drug development. This review examines how integrative multi-omics approaches support cancer drug discovery and therapeutic targeting, focusing on target identification, pathway elucidation, target validation, biomarker discovery, and therapeutic development. Genomics and transcriptomics facilitate the identification of driver alterations and dysregulated signaling pathways, whereas proteomics and metabolomics provide functional insights into protein activity, metabolic reprogramming, and treatment response. We further highlight the contributions of epigenomic and microbiomic profiling to biomarker discovery, therapeutic response prediction, and precision oncology. Given the complexity of multi-omics datasets, the review also explores the application of artificial intelligence (AI) and machine-learning methodologies for data integration, network modeling, biomarker discovery, and drug repurposing, including deep learning, Bayesian frameworks, graph-based models, and explainable AI approaches. Emerging computational frameworks and integration strategies that enable interpretation of heterogeneous molecular datasets and support therapeutic discovery are also discussed. Cancer-focused examples demonstrate how integrative multi-omics frameworks have enabled the identification of clinically relevant biomarkers, therapeutic targets, and rational combination therapies. Furthermore, the clinical translation of biomarker-driven precision oncology, exemplified by HER2-, EGFR-, and MSI-directed therapies, highlights the growing impact of omics-informed approaches on personalized cancer treatment. Overall, AI-enabled multi-omics approaches hold substantial promise for accelerating cancer drug discovery and precision oncology.

Chemotherapy-induced thrombocytopenia (CIT) is a dose-limiting toxicity that can necessitate chemotherapy delays or dose reductions. This review examines evidence that CIT involves injury to both megakaryocytes (MKs) and the bone marrow microenvironment (BMME) and considers the implications for thrombopoietin receptor agonist (TPO-RA) therapy.

PubMed was searched for English-language literature without a publication-date restriction and was comprehensively updated through August 10, 2026. Evidence concerning CIT mechanisms and the mechanistic effects of TPO-RAs was integrated through a predefined narrative thematic framework, with explicit consideration of the directness of evidence for human CIT.

Available studies suggest that TPO-RAs may have effects beyond platelet production, although evidence for vascular, metabolic, and immune microenvironmental effects derives largely from non-CIT or preclinical settings. Persistent rather than nadir CIT, lower endogenous thrombopoietin, and the absence of marrow infiltration, prior pelvic irradiation, or temozolomide exposure may enrich for response. A 2026 phase 3 trial directly demonstrated that romiplostim reduced CIT-induced chemotherapy dose modifications in persistent CIT, but biomarker-guided selection remains to be validated.

The "seed and soil" model organizes previously published evidence and should be regarded as hypothesis-generating in human CIT. Prospective studies are needed before microenvironment-directed combinations or CIT-specific biomarker thresholds can be recommended.

Protein O-fucosyltransferase 1 (POFUT1) has been implicated in several malignancies, but its functional and prognostic significance in glioma remains insufficiently defined. This study evaluated whether POFUT1 expression is associated with glioma progression, patient outcome, and PI3K/AKT pathway activity.

Public glioma transcriptome datasets from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) were analyzed and compared with clinical samples collected from 123 glioma patients. POFUT1 protein levels in clinical specimens were determined by immunohistochemical staining, and its association with patient outcome was analyzed using survival curves. In vitro, glioma cell growth, motility, and invasiveness were examined using MTT and Transwell assays. The effect of POFUT1 on tumor formation was further tested in a subcutaneous xenograft model. RNA sequencing, KEGG pathway enrichment, and pharmacological inhibition were then used to explore the mechanism linking POFUT1 to PI3K/AKT signaling.

POFUT1 expression was higher in glioma than in normal brain tissue and increased with tumor grade. Patients with high POFUT1 levels had shorter overall survival, and multivariate Cox analyses supported POFUT1 as an independent prognostic indicator. Incorporating POFUT1 into a nomogram improved prediction of 1-, 3-, and 5-year survival. Functionally, POFUT1 knockdown reduced glioma cell growth, motility, invasion, and xenograft expansion, whereas POFUT1 overexpression produced the opposite phenotype. Transcriptomic and protein analyses indicated that POFUT1 enhanced PI3K/AKT signaling. The PI3K inhibitor LY294002 weakened the tumor-promoting effects caused by POFUT1 overexpression.

POFUT1 as a key driver of glioma malignancy, predominantly through activating the PI3K-AKT signaling pathway. These findings highlight POFUT1 as a promising novel therapeutic target for aggressive glioma.

Neutrophil extracellular traps (NETs), web-like DNA structures released by neutrophils, were initially recognized as key components of the anti-infective immune response but are now implicated in tumor progression. Tumor cells orchestrate the reprogramming of tumor-associated neutrophils (TANs) and trigger NET formation through paracrine signaling, thereby establishing a "tumor cell-TAN-NETs" positive feedback loop. This axis serves not only as a key hub for awakening dormant tumor foci and mediating immune evasion, but also as a core mechanism driving distant metastasis and dictating poor clinical prognosis. Notably, targeted disruption of this axis effectively reverses tumor therapy resistance and significantly sensitizes tumors to radiotherapy, chemotherapy, and immune checkpoint blockade, establishing NETs as novel therapeutic targets poised to overcome the current bottlenecks in cancer treatment. Nevertheless, limitations in detection technologies, prognostic modeling challenges, tumor heterogeneity, and inconsistent research findings constrain clinical translation. Future studies should prioritize optimizing detection methods, conducting rigorous clinical validation, and identifying specific therapeutic targets to accelerate the translational progress of NETs from basic research to clinical practice. This review synthesizes current knowledge on the biological mechanisms, regulatory pathways, and detection approaches of NETs, providing a theoretical basis for their clinical application in precision oncology.

Myeloproliferative Neoplasms (MPNs) are rare hematologic neoplasms. The epidemiology and outcomes of these rare neoplasms warrant an update considering new diagnostic tools and advances in treatment options. NCI's Surveillance, Epidemiology and End Results (SEER)-17 registries were interrogated to analyze adult patients diagnosed with MPN [ICD-O-3 codes: polycythemia vera (PV) 9950/3, essential thrombocythemia (ET) 9962/3, primary myelofibrosis (PMF) 9961/3 and chronic myeloid leukemia (CML) 9875/3] during the years 2000 to 2021. Data of 63,242 (ET, n = 24,172; PV, n = 23,456; PMF, n = 6131; CML, n = 9483) patients were analyzed. The overall incidence rate (IR) for ET, PV, PMF and CML was 1.8, 1.7, 0.5 and 0.7 per 100,000 person-years, respectively. The incidence of ET, PV, and MF increased with age, and the majority of cases were seen after the age of 50. 5-year Relative Survival (RS) for PMF was 50.9% in 2009, to 57.4% in 2013 and 60.6% in 2016. The median overall survival (OS) was 152 months for ET, 150 months for PV, 48 months for PMF, and 202 months for CML. Advancing age was associated with adverse survival across MPN subtypes. Survival of patients with PMF continues to improve over recent years. Important racial and gender variations exist, which were noted in our study.

Metastasis remains the leading cause of cancer-related mortality, yet predicting future metastasis is a major clinical challenge due to the lack of validated biomarkers and effective assessment methods. Here, we present EmitGCL, a deep-learning framework that accurately predicts future metastasis and its corresponding biomarkers. Based on a comprehensive benchmarking comparison, EmitGCL outperforms other computational tools across six cancer types from seven cohorts of patients with superior sensitivity and specificity. It captures occult metastatic cells in a patient with a lymph node-negative breast cancer, who was declared to have no evidence of disease by conventional imaging methods but was later confirmed to have metastatic disease. Notably, EmitGCL identifies HSP90AA1 and HSP90AB1 as predictable biomarkers for future breast cancer metastasis, which we validate by in-vitro pharmacological inhibition of HSP90 that reduced breast cancer cell migration and further support across five independent cohorts of patients (n = 420). Furthermore, we demonstrate YY1 transcription factor as a key driver of breast cancer metastasis, which we corroborate with in-silico, CRISPR-based migration assays, and in vivo mouse lung colonization experiments, suggesting that YY1 is a potential therapeutic target for further investigation.