Search Results (6,838)

Introduction: Breast cancer-related lymphedema (BCRL) affects quality of life (QoL) and increases healthcare costs. Resistance training (RT) is proposed as a preventive strategy, although its safety and effectiveness remain uncertain. Objective: To evaluate the effectiveness and safety of RT in preventing BCRL in women at risk. Methods: MEDLINE, Embase, CENTRAL, PEDro, and LILACS databases were searched from their inception to January 2025, along with the gray literature, trial registries, and preprints. Risk of bias was assessed using RoB 2, and certainty of the evidence (CoE) was assessed using GRADE. Primary outcomes were the occurrence of lymphedema and overall QoL; secondary outcomes included pain, upper limb function, range of motion (ROM), grip strength, and adverse events. Results: Eight RCTs (n = 1131) were included. The effects of RT on lymphedema and arm volume are very uncertain (very low CoE). For QoL, pain, ROM, and grip strength, the findings were inconsistent and uncertain (low to very low CoE). Adverse events were mild and transient, with no serious complications. Conclusion: RT is probably safe in women at risk of developing BCRL. Its preventive effectiveness is highly uncertain. Well-designed RCTs with standardized diagnostic criteria, patient-centered outcomes, and long-term follow-up are needed to establish their role in BCRL prevention with greater certainty. Ethics and dissemination: This study did not require ethical approval. The results will be disseminated through publications in peer-reviewed journals and academic presentations. Registration: PROSPERO (CRD42023455720). Full article

Background: Photodynamic therapy (PDT) has emerged as a powerful minimally invasive modality for cancer treatment. However, its efficacy as a monotherapy is often limited by oxygen dependence and limited light penetration. Combining PDT with systemic anticancer drug therapies offers a promising strategy to achieve synergistic effects and overcome resistance. Objective: This review aims to provide a systematic analysis of the mechanisms and clinical potential of combining PDT with chemotherapy, targeted therapy, and immunotherapy, focusing on recent advancements and nanotechnology-based delivery systems. Methods: A comprehensive literature search was performed using PubMed and Scopus databases. The analysis focused on peer-reviewed studies published over the last 10 years addressing synergistic molecular pathways, co-delivery nanoplatforms, and clinical trial outcomes. Results: The combination of PDT with chemotherapy enhances drug accumulation via vascular photosensitization and can overcome multi-drug resistance. Integration with immunotherapy, particularly immune checkpoint inhibitors and tumor vaccines, triggers immunogenic cell death (ICD), leading to systemic antitumor responses. Nanotechnology provides a versatile platform for the targeted co-delivery of photosensitizers and pharmacological agents, significantly reducing systemic toxicity. Conclusions: Combined PDT–drug regimens demonstrate superior therapeutic efficacy compared to monotherapies. Future clinical translation requires the standardization of dosimetry and the development of multifunctional nanomedicines to enable personalized treatment protocols. Full article

Background/Objectives: Anaplastic thyroid carcinoma (ATC) is one of the most aggressive and lethal forms of malignant neoplasm of the endocrine system, and osteopontin (OPN) has been shown to be aberrantly expressed in this tumor type. Among the five OPN splicing isoforms (OPN-SI), OPN-4 has been recently reported in several tumor types, including ATC, but its functional role(s) have not yet been elucidated. Methods: To characterize OPN-4 roles in ATC cells, OPN-4 was ectopically overexpressed in the c643 ATC cell line, generating the c643/OPN-4 cells. OPN-roles were evaluated by cell functional assays, including cell proliferation and viability, using Carboxyfluorescein Succinimidyl Ester (CFSE), crystal violet, and trypan blue assays. For migration, clonogenicity, cell cycle and apoptosis assays were used. For assessment, c643/OPN-4 cells were cultured in two-dimensional (2D) monolayers or three-dimensional (3D) spheroids with the latter being maintained in a bespoke microfluidic system. Results: OPN-4 overexpression led to a significant reduction in cell proliferation, viability, migration and clonogenicity. c643/OPN-4 cells displayed a significant accumulation in the G0/G1 phase and a decrease in the S phase of the cell cycle; however this did not affect cell death or the expression levels of other OPN-SI. In a spheroid model of c643/OPN-4 cells, no significant differences were found in spheroid size or viability when compared to those formed by control cells. Notably, OPN-4 overexpression enhanced the effects of sorafenib on cell viability under dynamic treatment conditions involving continuous perfusion. Conclusions: These early findings point to the fact that OPN-4 may reduce some aspects of tumor progression features in ATC cells and open new avenues for investigating OPN-4 as a biomarker of therapeutic response in personalized treatment strategies. Full article

Myelofibrosis (MF) is a chronic myeloproliferative neoplasm characterized by progressive bone marrow fibrosis, extramedullary hematopoiesis (particularly symptomatic splenomegaly), constitutional symptoms, progressive cytopenias, and, in a subset of patients, leukemic transformation. The advent of the JAK1/2 inhibitor ruxolitinib has revolutionized the management of MF, substantially improving splenomegaly, symptom burden, and, in some settings, overall survival. However, a substantial percentage of patients fail to achieve sustained benefit, are intolerant, or become refractory; real-world and clinical trial data indicate that approximately half of treated patients discontinue ruxolitinib treatment within 3 years and up to approximately 75% within 5 years, with poor outcomes after discontinuation (median survival in several series is approximately 12–14 months). In recent years, several new small molecules that act beyond the JAK-STAT axis have emerged in clinical development. These include agents targeting telomerase (imetelstat), epigenetic regulation via BET inhibition (pelabresib/CPI-0610), the MDM2-p53 axis (navtemadlin/KRT-232), erythroid maturation and the bone marrow microenvironment (luspatercept), PI3K signaling (parsaclisib), and PIM inhibitors (nuvisertib). Early clinical data show promising results for symptom and splenic control in specific settings and, importantly, suggest potential disease-modifying activity (improvements in marrow fibrosis and molecular responses) for some compounds. This review summarizes the biological rationale, key clinical data (efficacy and safety), ongoing randomized trials, and remaining knowledge gaps for these non-JAK small molecules in MF and offers practical considerations for integrating them into contemporary treatment algorithms. Full article

Background: Somatostatin receptors (SSTRs) are pivotal diagnostic and therapeutic targets in well-differentiated neuroendocrine neoplasms (NENs). SSTR-directed treatment strategies rely on sufficient SSTR2 expression. Thus, receptor loss during dedifferentiation limits therapeutic efficacy. Preclinical data suggest pharmacologic modulation of SSTRs’ expression. However, there are no robust data on the effect of NEN-specific systemic treatments on SSTRs’ expression and function. Methods: We systematically evaluated the effects of six systemic agents commonly used in NEN therapy—isplatin, etoposide, 5-fluorouracil (5-FU), streptozotocin (STZ), temozolomide (TMZ), and everolimus—on SSTR2 and SSTR5 expression, as well as on uptake of ⁶⁸Ga-DOTATOC, in BON-1 and QGP-1 cells, as well as the MS-18 cell line. Analyses included qRT-PCR, Western blotting, immunohistochemistry, and radiopeptide uptake assays. Results: Systemic agents modulated SSTR expression and radioligand uptake in a drug- and cell line-dependent manner. Etoposide consistently upregulated SSTR2 expression and significantly increased radioligand uptake across all three cell lines. TMZ enhanced SSTR2 expression and uptake in BON-1 cells, but reduced uptake in QGP-1 and MS-18 cells. In contrast, 5-FU, STZ, cisplatin, and everolimus showed heterogeneous, compound- and cell line-specific effects on SSTR2 expression and ⁶⁸Ga-DOTATOC uptake, including both up- and downregulation depending on the model. Conclusions: All agents under investigation affect SSTR expression in vitro, while etoposide is identified as the most consistent enhancer of SSTR2’s expression and function across cellular NEN models. Our findings highlight both the potential and the risks of systemic therapy-induced receptor modulation and therefore support further investigation of treatment sequencing strategies to optimize SSTR-targeted approaches. However, further studies are required to translate these observations to a clinical setting. Full article

Background: Pancreatic neuroendocrine neoplasms (PanNENs) represent a heterogeneous tumor entity with a steadily rising incidence, mainly due to advances in imaging and growing diagnostic awareness. In pancreatic ductal adenocarcinoma (PDAC), the mesopancreas (MP) has been identified as a frequent site of microscopic tumor spread and a key determinant of circumferential resection margin (CRM) status, leading to the concept of standardized mesopancreatic excision (MPE). While its oncological relevance in PDAC is increasingly recognized, the role of the mesopancreas in PanNENs remains unclear. This study aimed to systematically evaluate mesopancreatic infiltration in PanNENs and to identify associated clinicopathological predictors. Methods: Consecutive patients undergoing oncological pancreatoduodenectomy, spleen-preserving distal pancreatectomy, or distal splenopancreatectomy for PanNENs and PanNECs were included. The mesopancreas was histopathologically examined for tumor infiltration within CRM assessment. Results: MP infiltration was detected in 60% of patients. It was associated with higher Ki-67 index, larger tumor size, lymph node involvement, venous invasion, and positive CRM status. A Ki-67 index ≥ 5% and tumor size ≥ 21.5 mm were identified as predictors of MP infiltration. Higher T stage predicted reduced overall survival (OS), whereas MP infiltration, lymphatic (L1) and venous (V1) invasion, and Ki-67 ≥ 5% were associated with impaired disease-free survival (DFS). Conclusion: Mesopancreatic infiltration is frequently present in PanNENs and correlates with aggressive tumor characteristics. Given its association with CRM positivity and reduced DFS, consideration of the mesopancreas in staging and surgical strategies appears oncologically justified. Larger studies are required to validate these findings. Full article

Background: Intraductal papillary mucinous neoplasm (IPMN) is a mucin-producing pancreatic tumor with variable malignant potential. While most are asymptomatic and indolent, a subset progress to invasive carcinoma or cause local complications such as pancreatitis. Spontaneous fistulation into adjacent organs is an increasingly recognized phenomenon with impact on prognosis and management. The incidence of fistulation in IPMN in the reported literature is 1.9–6.6%. The most common sites are the stomach, duodenum and bile duct. Reported outcomes are poor, with a median survival of approximately 16 months. Methods: We describe four patients with IPMN complicated by fistula, confirmed by endoscopic or histopathological evaluation with CT and MRI images and discuss the available literature of fistulating IPMN. Results: Fistulation occurred at the common bile duct, stomach, duodenum and duodeno-jejunal junction. Two of four patients passed away at 4.8 and 24.8 months from detection of fistula. Histology revealed high-grade dysplasia or invasive carcinoma in most patients, highlighting the aggressive nature of IPMNs complicated by fistulae. Conclusions: Our findings reinforce the importance of recognizing fistula formation as a marker of aggressive disease in IPMN. Although surgical resection remains the treatment of choice in suitable candidates, the rarity of this entity means that standardized management guidelines are lacking. Full article

Background: Higher-risk myelodysplastic neoplasms ( HR-MDS) are associated with poor survival and a substantial risk of leukemic transformation. Although azacitidine is a standard treatment in this setting, comparative real-world data remain limited. We evaluated the association between azacitidine exposure and clinical outcomes in patients with HR-MDS. Methods: We performed a retrospective single-center cohort study including 72 adults with HR-MDS, defined by the Revised International Prognostic Scoring System(IPSS-R) as High or Very High risk. Patients were categorized as azacitidine-treated (Aza, n = 44) or managed with best supportive care alone (No Aza, n = 28). Overall survival (OS) was defined from diagnosis to death from any cause. Progression-free survival (PFS) was defined as the time to acute myeloid leukemia transformation or death. Leukemic transformation (LT) was analyzed using Kaplan–Meier estimates and competing-risk cumulative incidence, with death without prior LT treated as a competing event. Univariable and multivariable Cox regression models were applied. Results: Azacitidine exposure was associated with longer OS compared with best supportive care, with a median OS of 13 vs.10 months and 24-month OS rates of 27% vs. 14% (p = 0.0239). PFS was also prolonged in the Aza group, with a median of 11 vs. 7 months (p = 0.0406). LT-related outcomes similarly favored azacitidine. In multivariable analyses, azacitidine remained independently associated with improved OS, PFS, and LT-related outcomes. IPSS-R Very High risk remained an adverse prognostic factor across endpoints, while a higher baseline bone marrow blast percentage independently predicted leukemic transformation. Conclusions: In this real-world HR-MDS cohort, azacitidine exposure was associated with improved survival outcomes and delayed leukemic transformation compared with best supportive care alone. Full article

[18F]fluoromisonidazole ([18F]FMISO) positron emission tomography (PET) imaging has been explored for its potential use as an added modality for the assessment of gliomas. The aim of this review was to synthesize the existing literature investigating this topic. A comprehensive search of the PubMed/MEDLINE, Scopus, and Embase databases was performed to identify eligible original research investigating the role of [18F]FMISO PET imaging for the evaluation of gliomas. Thirty-tree studies were included in the present review. Overall, the findings reported suggest that [18F]FMISO PET may have relevant clinical implications in glioma assessment and management, including improved tumor characterization, differential diagnosis between different grades and other neoplasms, prognostic stratification, and potential guidance for personalized therapeutic strategies. The available evidence supports the idea that [18F]FMISO PET can act as a robust and biologically meaningful imaging modality in gliomas. Its strengths lie in tumor grading, prognostication, and treatment monitoring, particularly in glioblastoma. Future research should focus on standardized imaging protocols, integration with molecular classification frameworks, and validation of hypoxia-guided therapeutic strategies. Full article

In the hepatobiliary system, the majority of neoplasms grow within the hepatic parenchyma; however, some arise, grow, and/or spread within the lumen of the intrahepatic large bile ducts and the perihilar/distal bile ducts (collectively referred to as large bile ducts), representing specialized ductal organs associated with unique peribiliary glands and being distinct from the intrahepatic small bile ducts and bile ductules embedded within the hepatic parenchyma. Precursors of cholangiocarcinoma (CCA) arising within the lumen of large bile ducts have recently been proposed. Neoplasms growing and spreading within the lumen of large bile ducts have been categorized into four groups and are discussed here in light of updated pathological findings. (i) Precursor(s) of CCA arising in the large bile ducts (large-duct-type intrahepatic CCA and perihilar/distal CCA): These precursors include high-grade biliary intraepithelial neoplasia (BilIN), intraductal papillary neoplasm of the bile duct (IPNB), and intraductal oncocytic papillary neoplasm (IOPN). High-grade BilIN presents as a flat, microscopic lesion with dysplastic cytoarchitectural alterations and grows along the luminal surface of large bile ducts, whereas the latter two present as grossly visible polypoid or tumorous lesions composed of papillary, villous, or tubular proliferation of neoplastic epithelium with delicate fibrovascular cores. These lesions may eventually progress to invasive CCA. Intraductal tubulopapillary neoplasm of the bile duct (ITPN), previously categorized as another precursor of CCA arising in large bile ducts, appears to represent a heterogeneous group of neoplasms with respect to progression and presumed cell of origin. Some ITPNs are frequently associated with nodular invasive carcinoma resembling small-duct-type intrahepatic CCA (SD-iCCA) and share genetic alterations with SD-iCCA; such cases may arise in association with small bile ducts or bile ductules. In contrast, other ITPNs exhibit cystic changes with tubulopapillary features and may arise in association with peribiliary glands or cysts. (ii) Secondary growth and spread of biliary neoplasms: This category comprises several patterns. First, intraepithelial neoplastic spread directly and continuously from the primary neoplastic lesion is observed in almost all cases of high-grade BilIN, IPNB, and IOPN; it spreads laterally along the luminal surface of the proximal and distal bile ducts and extends vertically into the adjacent peribiliary glands. Intraluminal cast-like spread in the bile ducts adjacent to the primary neoplastic lesion also occurs in some precursor lesions, particularly in ITPN. Implantation of a biliary neoplasm from one part of the biliary tract to another results in discontinuous, multifocal biliary neoplasms, particularly in IPNB, and occurs mainly in the distal bile ducts relative to the main tumor. Multicentric tumorigenesis may contribute to the multifocal development of precursors and CCA in the bile ducts. The accumulation of additional genetic alterations, beyond the common mutations detected in primary tumors, may contribute to metachronous recurrence of CCA after curative resection of the primary biliary tumor. Cancerization of the duct (COD) by CCA may also contribute to secondary growth and spread within the bile duct lumen. Specifically, flat-type cancerization of pre-existing non-neoplastic bile ducts, resembling high-grade BilIN, occurs in approximately one-third of hilar CCA cases. Intraductal polypoid, cast-like cancerization within the lumen of adjacent bile ducts, resembling polypoid precursors of CCA, can also occur in approximately one-tenth of SD-iCCA. (iii) Prominent intraductal polypoid growth of invasive CCA: Invasive CCA rarely presents with predominant intraductal polypoid carcinoma that is continuous with periductal infiltrating CCA; this pattern can be referred to as polypoid invasive CCA. (iv) Nonbiliary neoplasms presenting bile duct tumor thrombus (BDTT): BDTT associated with hepatocellular carcinoma and with extrahepatic malignancies extending into the bile duct lumen can mimic the intraluminal growth and spread patterns of the above-mentioned biliary neoplasms. In conclusion, intraluminally growing biliary neoplasms in the large bile ducts comprise a heterogeneous group that can be reasonably classified into four categories. This categorization may facilitate understanding of these intrabiliary growing neoplasms. Full article

Patients following brain tumour resection experience significant disability, yet rehabilitation is not typically delivered prior to adjuvant treatment such as radiation or chemotherapy. This study aims to characterize the medical and functional profiles, and function outcomes of patients with brain tumour admitted over the past four years to a pilot inpatient prehabilitation programme following brain tumour resection but prior to adjuvant therapy, and to compare these findings with those of patients in a standard acquired brain injury rehabilitation programme. We retrospectively reviewed the charts from a randomly selected sample of 58 prehabilitation inpatients and 112 patients with acquired brain injuries at Toronto Rehabilitation Institute between March 2020 and December 2024. Data abstracted included demographics, medical and functional profiles, Functional Independence Measure (FIM) scores, and discharge parameters. Compared with acquired brain injury subjects, prehabilitation subjects had significantly less physical (47% vs. 86%, p < 0.0001) but more communication (46% vs. 20%, p = 0.0005) impairments, though with similar mean FIM change (22.5 vs. 26.0, p = 0.082) and FIM efficiency (1.1 vs. 1.0, p = 0.78). While not reaching significance, they also experienced more mood issues during rehabilitation (30% vs. 18%, p = 0.075). These findings support that prehabilitation after brain tumour surgery but before adjuvant therapy is clinically effective within existing ABI rehabilitation programmes. However, prehabilitation programmes may benefit from staffing models that emphasize communication supports and mental health expertise. Full article

Benign parotid tumors are increasingly treated with parenchyma-sparing extracapsular enucleation, yet postoperative salivary collections and Frey syndrome can still generate clinically relevant morbidity; we evaluated whether a standardized intraoperative bundle combining intraparotid botulinum toxin A (BTX-A) and bovine collagen membrane interposition is associated with fewer complications than standard enucleation alone. In this retrospective comparative cohort at a tertiary Head and Neck Surgery Unit, consecutive adults undergoing extracapsular enucleation for pleomorphic adenoma or Warthin tumor (2010–2025) were allocated by institutional era-based protocol to Group A (2010–2017, standard enucleation) or Group B (2018–2025, enucleation plus intraoperative intraparotid BTX-A 50 IU and bovine collagen membrane placement over the repaired parotid fascia). Prespecified endpoints were sialocele/salivary fistula, surgical-site infection (SSI) within 30 days, and clinically recorded Frey syndrome within 6 months; effect sizes with 95% confidence intervals were reported. A total of 188 patients were analyzed (94 per group). Sialocele occurred in 20/94 (21.3%) in Group A versus 2/94 (2.1%) in Group B [Relative Risk (RR) 0.10]. SSI occurred in 14/94 (14.9%) versus 2/94 (2.1%) (RR 0.143), and clinically recorded Frey syndrome in 18/94 (19.1%) versus 4/94 (4.3%) (RR 0.222). This combined protocol was associated with lower complication rates through 6 months; prospective controlled studies with standardized Frey assessment and longer follow-up are warranted. Full article

Background: Penile squamous cell carcinoma is an uncommon neoplasm that arises via two carcinogenic pathways, one linked to HPV infection and the other to chronic inflammation and p53 alterations. Objective/Methods: We assessed the distribution of HPV genotypes in penile tumors and subsequent inguinal metastases in a cohort of 343 patients, analyzing their concordance with p16 stain and histological subtype, as well as the predictive significance of HPV tumor status and the immunohistochemical expression of p16 and p53 in inguinal lymph node metastasis (ILNM). Results: The overall prevalence of HPV in primary penile tumors was 42.9%, with high-risk HPV genotypes detected in 95.2% of HPV-positive cases. HPV16 was the most prevalent genotype identified in both primary tumors and metastases. However, other genotypes, including the low-risk HPV82, were also found in metastatic disease. We observed good concordance between HPV tumor status and histological subtype and very good concordance between HPV tumor status and p16 staining, with Cohen’s kappa (κ) values of 0.80 (p-value < 0.001) and 0.83 (p < 0.001), respectively. Conclusions: In most HPV-positive metastatic cases, the same HPV genotypes were detected in both the metastasis and the penile tumor. Both p16 staining and histological subtype can serve as surrogates for molecular HPV testing in lower resourced settings. In this dataset, no significant association was found between HPV status, p16 expression, or p53 expression and the presence of ILNM, suggesting their limited utility as predictive markers for ILNM in penile cancer. Full article

Background: Rare appendicular pathologies (RAP) are uncommon clinical entities with important diagnostic and therapeutic implications. These conditions frequently mimic acute appendicitis, yet they may require different operative strategies and, in selected cases, oncological management. Methods: We performed a retrospective cohort study including all patients who underwent surgery with the intention of performing an appendectomy at the First Surgical Clinic, Emergency County University Hospital of Cluj-Napoca, between 2018 and 2021. During this interval, 330 appendectomies were performed. Patients with a histopathological diagnosis of RAP were included. Clinical, imaging, surgical, histopathological, postoperative, and follow-up data were analyzed, with particular attention to the preoperative diagnostic work-up and imaging-based suspicion of rare appendicular pathology. Results: Ten patients (3.03%) were diagnosed with RAP, including low-grade appendiceal mucinous neoplasm (LAMN; n = 5), mucinous cystadenoma (n = 2), appendiceal adenocarcinoma (n = 1), appendicular diverticulum (n = 1), and stump appendicitis (n = 1). Computed tomography was the main diagnostic modality, particularly in patients with atypical presentation or suspicion of complicated or neoplastic appendiceal disease, while magnetic resonance imaging and colonoscopy provided additional information in selected cases. Preoperative suspicion of a rare or neoplastic appendiceal pathology was achieved in 70% of patients. Laparoscopic appendectomy was performed in 6 patients, open appendectomy in 1 patient, open ileocecal resection in 1 patient, open right hemicolectomy in 1 patient, and laparoscopic right hemicolectomy in 1 patient. Histopathological examination confirmed the diagnosis in all cases. Immediate postoperative outcomes were favorable, without perioperative mortality or major complications; during follow-up, the patient with adenocarcinoma required oncological treatment and resection of a local recurrence 1 year after surgery. Conclusions: RAP represent a small but clinically significant subset of appendiceal disease. Structured preoperative imaging, intraoperative recognition of atypical findings, and an individualized surgical strategy are essential for optimal outcomes and appropriate oncological management. Full article

Background: Pancreatic tumors in pediatric and adolescent patients are rare, and guidance on prognostication and management is limited. Methods: Using the Surveillance, Epidemiology, and End Results (SEER) database (2004–2021), we analyzed clinicopathological characteristics, treatment patterns, and survival outcomes in patients younger than 20 years with pancreatic tumors. Analyses integrated conventional survival models with machine learning approaches to identify key predictors. Results: The cohort included 203 patients, of whom 108 (53.2%) had solid pseudopapillary neoplasms (SPNs), 59 (29.1%) neuroendocrine neoplasms, 16 (7.9%) pancreatoblastomas, 5 (2.5%) adenocarcinoma variants, 4 (2.0%) acinar cell carcinomas, and 11 (5.4%) other rare histologies. Most patients had localized disease (61.1%) and underwent surgical resection (85.2%). Estimated 5-year and 10-year overall survival rates were 87.8% and 84.0%, respectively. Survival differed significantly by histology, stage, and surgery status (all log-rank p < 0.001). In multivariable analysis, SPN histology was associated with lower mortality (hazard ratio (HR) 0.03, 95% confidence interval (CI) 0.01–0.13; p < 0.001), whereas distant disease was associated with markedly higher mortality (HR 21.49, 95% CI 7.52–133.41; p < 0.001). Surgical resection was independently associated with lower mortality (HR 0.13, 95% CI 0.02–0.29; p = 0.003). Among patients with known 5-year status, the Random Forest and Gradient Boosting models achieved cross-validated area under the curve values of 0.935 ± 0.060 and 0.886 ± 0.093, respectively; stage and surgery were the dominant predictors in both models. Conclusions: Surgery remains the cornerstone of management for pediatric pancreatic tumors, and advanced analytic approaches may enhance risk stratification in this rare population. Full article