Background Esophageal squamous cell carcinoma (ESCC) is a major cause of cancer mortality in Asia, where histopathological diagnosis of endoscopic biopsy specimens remain challenging. Methods To address this challenge, we developed an AI-based ESCC diagnostic system in biopsies (AI-EDS) using 1 104 H&E-stained whole slide images (WSIs) from one center, which were divided into three datasets at the patient level: 515 WSIs (including 226 malignancies) for training, 50 WSIs (22 malignancies) for validation, and 539 WSIs (149 malignancies) for internal testing. Lesion areas were annotated using an iPad-based system, and the DeepLab-v3 model, supported by a ResNet-50 backbone, was trained for analysis. AI-EDS was subsequently applied to 945 esophageal biopsy WSIs (351 malignancies) from four additional hospitals. Finally, we also assessed the model's performance on surgical resection and endoscopic submucosal dissection (ESD) specimens with a total of 173 WSIs (131 malignancies). Results The AI-EDS demonstrated high accuracy in distinguishing malignant from benign lesions in an internal test dataset, achieving an AUC of 0.986 (95.36% accuracy, 99.49% sensitivity, and 84.56% specificity). In multicenter validation across four external hospitals (945 WSIs), the system maintained strong performance (AUC range: 0.966-0.998). Notably, the AI-EDS matched diagnostic accuracy of junior pathologists (89%) while reducing interpretation time by more than half. Furthermore, the system demonstrated robust generalization capability in surgical resection and endoscopic submucosal dissection specimens (173 WSIs, AUC = 0.827). Conclusions This multicenter validation confirms that the AI-EDS serves as a reliable, interpretable tool for computer-aided ESCC diagnosis, particularly valuable in resource-limited regions.

Hyperglycemia markedly exacerbates cerebral ischemia/reperfusion (I/R) injury, yet the underlying neuroprotective mechanism of selenium remains poorly defined. This study investigates whether sodium selenite (Se) promotes mitochondrial biogenesis via the selenoprotein H (SelH)-mediated AMPK/SIRT1/PGC-1α signaling pathway to alleviate hyperglycemia-aggravated cerebral I/R injury. In a streptozotocin-induced diabetic rat model subjected to middle cerebral artery occlusion/reperfusion (MCAO/R), in vivo administration of Se significantly reduced cerebral infarct volume, decreased neuronal apoptosis, and improved mitochondrial ultrastructure. Meanwhile, Se upregulated the protein levels of p-AMPK, SIRT1, PGC-1α, NRF1, and TFAM. In vitro, HT22 hippocampal neurons were subjected to high glucose combined with oxygen deprivation/reoxygenation (OD/R). Treatment with Se or SelH overexpression significantly enhanced cell viability, reduced lactate dehydrogenase (LDH) release and intracellular calcium ion levels, restored mitochondrial membrane potential (MMP), inhibited the production of reactive oxygen species (ROS) and malondialdehyde (MDA), and enhanced superoxide dismutase (SOD) activity. Mechanistically, the AMPK activator AICAR potentiated these protective effects; conversely, SIRT1 gene silencing or its inhibitor EX-527 significantly attenuated the protective effects of Se and SelH overexpression, confirming the AMPK/SIRT1/PGC-1α axis as a key downstream pathway. This study reveals for the first time that Se promotes mitochondrial biogenesis by activating the AMPK/SIRT1/PGC-1α signaling pathway through SelH, thereby alleviating hyperglycemia-aggravated cerebral I/R injury, providing a new target for clinical intervention.

Gastritis cystica profunda (GCP) is a benign lesion characterized by the submucosal proliferation of cystic gastric glands. It most frequently occurs in patients with a history of gastric surgery but is infrequently found in those with an unoperated stomach. While generally benign, GCP has been associated with gastric adenocarcinoma in some cases. We report a case of early gastric cancer (EGC) arising from GCP in a 69-year-old man with no history of gastric surgery. The lesion, which had remained in the stage of high-grade intraepithelial neoplasia for nine years, was successfully treated with endoscopic submucosal dissection (ESD). This case highlights the diagnostic challenges posed by GCP-associated lesions and suggests that such lesions may exhibit an indolent clinical course. In 2016, a gastroscopic examination revealed a 0-IIa + IIc lesion of approximately 40 mm in diameter on the greater curvature of the gastric antrum, close to the posterior wall. A biopsy confirmed high-grade intraepithelial neoplasia. The lesion was deemed indicated for ESD. However, during the procedure, a poor lifting sign following submucosal injection led to the suspicion of submucosal infiltration, and the treatment was subsequently aborted. The patient declined further treatment and opted for clinical follow-up. In 2025, a follow-up gastroscopy showed no significant change in the lesion compared to its 2016 appearance. A second ESD was successfully performed. Histopathological examination of the resected specimen confirmed the diagnosis of GCP with well-differentiated adenocarcinoma (confined to high-grade intraepithelial neoplasia). All lateral and deep margins were free of neoplasia, with no evidence of lymphatic, vascular, or perineural invasion. The surrounding gastric epithelium showed normal mucosa without dysplasia. This case highlights the diagnostic challenges posed by GCP-associated lesions and suggests that, in selected instances, such lesions may follow a relatively indolent clinical course.

Ischemic stroke remains the leading cause of long-term disability globally, underscoring the urgent need for novel therapeutic strategies. Here, we explore a microbiota-gut-brain axis that provides valuable insights for achieving this objective. Utilizing a distal middle cerebral artery occlusion (dMCAO) mouse model, we observed a marked reduction in Duncaniella muris (D. muris) post-stroke, alongside dysregulated tryptophan metabolism, characterized by elevated levels of indole-3-lactic acid (ILA) and decreased indole-3-propionic acid (IPA). D. muris supplementation restored metabolic balance by converting ILA to IPA, leading to significant improvements in neurological recovery. Mechanistically, IPA exerted neuroprotective effects by attenuating neuroinflammation through TREM2-dependent modulation of microglial activation, promoting an anti-inflammatory phenotype and inhibiting NLRP3 inflammasome-mediated pyroptosis. These findings highlight the therapeutic potential of the D. muris-IPA-TREM2-pyroptosis axis as a novel target for ischemic stroke treatment, providing a basis for future microbiome-based interventions aimed at improving stroke outcomes.

IntroductionDiabetes mellitus complicated with depression (T2DD) is different from a single disease. It leads to more severe damage to nerve cells and cognitive dysfunction, and has a poor prognosis. Existing evidence indicates that ferroptosis—a form of programmed cell death driven by iron accumulation and lipid peroxidation—is involved in both diabetes and depression. Glutathione peroxidase 4 (GPX4) and long-chain acyl-CoA synthetase family member 4 (ACSL4) are key regulators of ferroptosis, but their roles in T2DD-associated neural damage remain unclear.MethodsIn this study, we established a T2DD rat model using a high-fat diet combined with streptozotocin injection and chronic unpredictable mild stress and performed behavioral tests to assess depressive-like behaviors. Meanwhile, HT22 hippocampal neuronal cells were exposed to high glucose and corticosterone to simulate an in vitro model of T2DD. We investigated the role of the GPX4/ACSL4 axis in ferroptosis in the primary somatosensory cortex.ResultsIn vivo, T2DD rats exhibited reduced spontaneous activity, aggravated neuronal damage, Fe2+ accumulation in the cortical region, elevated oxidative stress, upregulation of CSL4/NCOA4 expression, and downregulation of GPX4/SLC7A11 expression, indicating that T2DD exacerbates neural damage. In vitro, high glucose (50 mM) and corticosterone (200 μM) synergistically reduced HT22 cell viability, increased reactive oxygen species (ROS) levels, and induced JC-1 and Ca2+ alterations suggesting mitochondrial depolarization and aggravated mitochondrial damage, further complementing the above conclusions. Notably, treatment with the ACSL4 inhibitor AS252424 reversed the abnormalities in reactive oxygen species, Fe2+, and malondialdehyde levels induced by RSL3 (a GPX4 inhibitor), while restoring glutathione (GSH) levels and Adenosine Triphosphate suggesting that dysregulation of the GPX4/ACSL4 axis may be the central mechanism underlying ferroptosis and neuronal damage in T2DD.ConclusionThis study reveals the role of ferroptosis in the T2DD model and provides new insights into therapeutic interventions targeting lipid metabolism pathways.

Hyperglycemia aggravates cerebral ischemia/reperfusion (I/R) injury, a severe ischemic stroke complication with few treatments. Selenium exerts neuroprotective effects, yet its molecular mechanisms in this injury remain unclear. This study explored whether sodium selenite alleviates the injury via regulating the p53/PUMA apoptotic pathway and the role of selenoprotein H (SelH). In vivo, Sprague-Dawley rats (including PUMA-knockdown models) were subjected to middle cerebral artery occlusion/reperfusion; in vitro, HT22 cells (PUMA-knockdown/SelH-overexpressing) were treated with high glucose and oxygen-glucose deprivation/reoxygenation. Results showed hyperglycemia exacerbated neurological deficits, infarct volume, neuronal apoptosis and mitochondrial damage in vivo, and induced ROS overproduction, mitochondrial dysfunction and apoptosis in vitro. Sodium selenite reversed these injuries, downregulated p53/PUMA pathway-related proteins, upregulated the bcl-2/Bax ratio, and elevated SelH expression. PUMA knockdown enhanced its neuroprotection, while SelH overexpression attenuated cell damage by inhibiting the p53/PUMA pathway (not direct oxidative stress reduction). Thus, sodium selenite mitigates hyperglycemia-aggravated cerebral I/R injury through the SelH-p53/PUMA pathway, providing novel therapeutic targets for diabetic stroke.

Hyperglycemia exacerbates cerebral ischemia/reperfusion (I/R) injury, apoptosis pathways playing a key role. Sodium selenite (SE) exhibits neuroprotective effects, however, whether the Fas/FasL/PUMA pathway is involved in this neuroprotective effects remains unclear. For help to make this clear, hyperglycemic-aggravated cerebral I/R models (SD rats) and in vitro high-glucose oxygen deprivation/reoxygenation (OD/R) models (HT22 cells) were applied in this study. This study showed that the cerebral infarct volume and neuronal damages in the hyperglycemic I/R rat indeed were alleviated by the selenite treatment. And the lost neurological functions were improved by selenite treatment also. In the HT22 cells, the SE treatment enhanced viability and reduced reactive oxygen species (ROS) accumulation. Mechanistically, this study showed that the SE treatment downregulated the expressions of Fas, FasL, p-NF-κB, PUMA, Cleaved Caspase-3, and Cytochrome c, while increased the Bcl-2/Bax expression ratio. The SE’s anti-apoptotic effects were potentiated by PUMA knockdown or autophagy inhibitor 3-MA co-treatment. These findings confirm that SE alleviates hyperglycemia-exacerbated cerebral I/R injury by inhibiting the Fas/FasL/PUMA apoptotic pathway, providing a therapeutic strategy for hyperglycemia ischemic stroke. Conclusion Sodium selenite alleviates hyperglycemia-exacerbated cerebral I/R injury by modulating the Fas/FasL/PUMA signaling pathway. Significance statement： The finding that sodium selenite alleviates hyperglycemia - exacerbated cerebral I/R injury by modulating the Fas/FasL/PUMA signaling pathway advances knowledge in neuroscience by revealing a novel mechanism through which a compound can mitigate the harmful effects of hyperglycemia on cerebral I/R injury, and it deepens our understanding of how apoptotic pathways in the nervous system can be regulated to protect against such injuries.

Histiocytic sarcoma (HS), reclassified in the WHO fifth edition as a Histiocytic/dendritic cell neoplasms, represents a rare hematopoietic malignancy with extranodal predominance and aggressive clinical behavior. This study reports the case of a 53-year-old female diagnosed with primary pulmonary HS, who presented with a 60-mm mass in the right middle lobe and later developed fatal brain metastases. Using a combination of pathology, whole-exome sequencing, and fusion gene analysis, we identified key molecular drivers of tumor development and spread. Major findings include the concurrent activation of the RAS/MAPK and PI3K/mTOR pathway activation (118 combined gene variants), TP53 biallelic inactivation, HLA locus alterations, and persistent LOC285045 fusions. Drug sensitivity profiling suggested potential responses to sunitinib and MEK inhibitors. By comparing this case with nine other reported cases of lung HS, we found that lung HS has a significantly worse survival (p=0.03) than HS at other sites. A high cell growth rate (Ki-67 >30%) and large tumor size (>50 mm) were identified as critical indicators of poor prognosis.

Reactive oxygen species (ROS)-induced DNA oxidative damage is a significant manifestation of oxidative stress in the body and is closely associated with the onset and progression of various diseases. Although Pyripyropene A (PPPA) exhibits anti-tumor and anti-inflammatory activities, its antioxidant and protective effects against DNA oxidative injury remain unclear. In this study, using a hydrogen peroxide-induced oxidative injury model of L02 cells, it was found that PPPA could significantly reduce intracellular ROS and malondialdehyde (MDA) levels, enhance the activities of catalase (CAT) and reduced glutathione (GSH), and increase the 2,2-Diphenyl-1-picrylhydrazyl (DPPH) clearance rate, confirming its antioxidant effect. Comet assay showed a reduction in DNA breakage, and down-regulation of phosphorylated histone (γ-H2AX) and 8-hydroxydeoxyguanosine (8-oxodG), indicating that it effectively alleviates DNA oxidative injury. Meanwhile, the upregulated expression of poly ADP-ribose polymerase (PARP) suggests that PPPA may promote repair by activating the DNA damage response (DDR). This study systematically clarify for the first time that PPPA exerts a protective effect by synergistically antioxidizing, reducing DNA injury, and potentially activating repair pathways, providing a theoretical basis for its application in neoplasm and oxidative stress-related diseases.

Hyperglycemia aggravates cerebral ischemic reperfusion injury (CIRI). Neuroprotective drugs that are effective in reducing CIRI in animals with normoglycemic condition are ineffective in ameliorating CIRI under hyperglycemic condition. This study investigated whether quercetin alleviates hyperglycemic CIRI by inhibiting endoplasmic reticulum stress (ERS) through modulating the SIRT1 signaling pathway. A middle cerebral artery occlusion/reperfusion (MCAO/R) model was induced in STZ-injected hyperglycemic rats. High glucose and oxygen glucose deprivation/reoxygenation (OGD/R) models were established in HT22 cells. The results demonstrated that hyperglycemia exacerbated CIRI, and quercetin pretreatment decreased the neurological deficit score and cerebral infarct volume, and alleviated neuron damage in the cortex of the penumbra in hyperglycemic MCAO/R rats, indicating that quercetin could be a candidate for treating hyperglycemic CIRI. Moreover, quercetin pretreatment reduced apoptosis, inhibited the expression of the ERS marker proteins GRP78 and ATF6, and mitigated the expression of the ERS-mediated proapoptotic protein CHOP in hyperglycemic MCAO/R rats, suggesting that quercetin alleviated hyperglycemic CIRI by inhibiting ERS and ERS-mediated apoptosis. Furthermore, quercetin upregulated Sirt1 expression in HG+OGD/R treated HT22 cells and inhibited PERK, p-eIF2α, ATF4, and CHOP expression. In contrast, the SIRT1 selective inhibitor EX-527 blocked the effect of quercetin on protein expression in the SIRT1/PERK pathway and aggravated HT22 cell injury. These findings indicate that quercetin inhibits ERS-mediated apoptosis through modulating the SIRT1 and PERK pathway. In conclusion, quercetin alleviates hyperglycemic CIRI by inhibiting ERS-mediated apoptosis through activating SIRT1 that consequently suppressed ERS signaling.

Objective To investigate the intervention mechanism of sodium selenite in alleviating hyperglycemia-induced cerebral ischemia/reperfusion (I/R) injury through the Fas/FasL/NF-κB/PUMA pathway. Methods The SD rat model of hyperglycemia-induced cerebral I/R injury and the HT22 cell model of high-glucose oxygen deprivation/reoxygenation (OD/R) were constructed to systematically evaluate the neuroprotective effect of sodium selenite and its regulatory effect on the Fas/FasL/NF-κB/PUMA pathway. Results The infarct volume, neurological dysfunction, metabolic level, and apoptosis level in the HG group were significantly higher than those in the NG group. Sodium selenite improved the infarct volume, neurological dysfunction, metabolic level, and apoptosis level in the HG group, and regulated the Fas/FasL/PUMA apoptotic pathway to alleviate injury. In vitro experiments showed that sodium selenite significantly improved morphological damage caused by high-glucose OD/R, increased cell viability, and reduced the expression of apoptotic factors. The application of Fas and FasL inhibitors and knockdown of PUMA expression indicated that sodium selenite alleviated cell apoptosis by inhibiting the activation of the Fas/FasL/PUMA pathway. Conclusion Sodium selenite alleviates hyperglycemia-exacerbated cerebral I/R injury by regulating the Fas/FasL/NF-κB/PUMA signaling pathway. ### Competing Interest Statement The authors have declared no competing interest.

Previous studies on the correlation between serum selenium and hypertension have yielded inconsistent results. Our previous analysis of participants from the National Health and Nutrition Examination Survey (NHANES) 2011–2018 indicated that elevated serum selenium concentrations were associated with an increased risk of metabolic abnormalities in obese individuals, with the primary effect being on blood pressure in males. The aim of this study was to further elucidate the relationship between serum selenium and the risk of hypertension in obese males. In this study, we examined the correlation between serum selenium concentrations and hypertension in 2,585 male participants with a body mass index (BMI) ≥ 30 kg/m2 aged between 20 and 80 years from the 2011–2018 NHANES database. The associations between serum selenium levels and hypertension were evaluated through weighted generalized linear regression analyses. To examine the saturation threshold effect between serum selenium and hypertension, a generalized additive model (GAM) and a two-piecewise linear regression model were employed. Furthermore, the saturation threshold effect was evaluated separately in subgroups stratified by BMI and age. The weighted prevalence of hypertension (51.84%) was slightly higher than that of nonhypertension (48.16%) in the participants included in this study. After rigorous adjustment for sociodemographic, physical, and laboratory test covariates, the weighted odds ratio (OR) of hypertension increased by 103% for every 1 standard deviation (SD) increase (approximately 24.41 µg) in the serum selenium concentration in participants assigned to the highest serum selenium group (weighted OR = 2.03; 95% CI = 1.24–3.32; P = 0.013). A calculation was subsequently performed to determine the saturation threshold effect of selenium on hypertension among participants in the medium and highest selenium concentration subgroups. The findings indicated that participants with serum selenium concentrations exceeding the saturation threshold (2.56 µM) demonstrated an elevated risk of developing hypertension (weighted OR = 9.58; 95% CI = 2.74–33.46; P = 0.000) in comparison to those with serum selenium concentrations below the threshold. Subgroup analyses demonstrated that serum selenium concentrations exceeding the saturation threshold were associated with an increased risk of hypertension in participants with a BMI ≤ 35 kg/m2 (weighted OR = 9.11; 95% CI = 1.43–58.24; P = 0.030) or those aged less than 55 years or younger (weighted OR = 8.37; 95% CI = 1.71–40.94; P = 0.014). For obese adult males who require additional selenium supplementation to enhancing their overall health and well-being, it is strongly recommended that the serum selenium concentrations be monitored throughout the course of supplementation to ensure that they remain within the relatively safe range (approximately less than 215.75 µg/L).

Here we present FDG PET/CT findings of a 59-year-old woman who developed multiple bone lesions 16 years after enucleation surgery due to left choroidal melanoma. 18 F-FDG PET/CT showed multiple FDG-avid bone metastases with no evidence of local recurrence or other metastatic disease elsewhere. The pathology and immunohistochemistry confirmed the diagnosis of multiple bone metastases from choroidal melanoma.

The role of reactive oxygen species (ROS) in cellular senescence and inflammation has been extensively studied; however, the specific molecular mechanisms underlying these effects have yet to be fully elucidated. By applying a nucleotide pool detection system, oxidative microRNA sequencing, and cytokine chip detection techniques, we found that the levels of 8-oxo-guanosine triphosphate (8-oxo-GTP) increased with age and were positively correlated with elevated levels of oxidized microRNA and increased levels of inflammatory factors. During aging, guanine residues in the seed regions of miR-98-5p that regulates ICAM1, and miR-8085 that regulates CXCL16, were oxidized to 8-oxoguanine. This oxidation weakened the binding affinity of microRNAs to their target genes, thereby promoting the expression of ICAM1 and CXCL16. Oxidized microRNAs can regulate new target genes via o8G:A base mismatches. Our findings reveal that ROS-induced oxidative modifications of microRNAs reshape gene regulatory networks, activate inflammatory pathways, providing new insights into the mechanisms of age-related inflammation.

Esophageal squamous cell carcinoma (ESCC) has a significantly low survival rate, primarily due to the lack of diagnostic markers for early diagnosis and effective therapies. Recently, CD98 has been proposed as a specific marker of mature esophageal basal cells, which may be associated with esophageal carcinogenesis. Therefore, we aimed to investigate the clinical significance and biological function of CD98 in ESCC progression, as well as the value of CD98 as a potential new marker for the early diagnosis of ESCC. Through MassARRAY system spectroscopy, DIA proteomics analysis, immunohistochemical and functional experiments, we found hypomethylation-linked upregulation of CD98 expression, which was associated with poor prognosis, promoted cell proliferation by regulating the cell cycle in ESCC. Furthermore, we not only demonstrated that the range of CD98 expression was consistent with that of dysplastic cells in 73.81% of low-grade intraepithelial neoplasia (LGIN) and 83.08% of high-grade intraepithelial neoplasia (HGIN) cases, but also confirmed the expression level of CD98 was positively correlated with the classical diagnosis marker P53. Compared to using P53 alone, the combination of the immunohistochemical markers CD98 and P53 (either one was positive) provided more accurate diagnostic data for LGIN (92.86% vs. 88.10%, p < 0.01) and HGIN (93.85% vs. 73.85%, p < 0.01). In summary, we propose that CD98 is involved in a crucial step in ESCC carcinogenesis, and when combined with P53, may serve as a diagnostic marker for ESCC precancerous lesions.

Abstract Phospholipase C epsilon 1 (PLCE1) is a well-established susceptibility gene for esophageal squamous cell carcinoma (ESCC). Identification of the underlying mechanism(s) regulated by PLCE1 could lead to a better understanding of ESCC tumorigenesis. In this study, we found that PLCE1 enhances tumor progression by regulating the replicative helicase MCM7 via two pathways. PLCE1 activated PKCα-mediated phosphorylation of E2F1, which led to the transcriptional activation of MCM7 and miR-106b-5p. The increased expression of miR-106b-5p, located in intron 13 of MCM7, suppressed autophagy and apoptosis by targeting Beclin-1 and RBL2, respectively. Moreover, MCM7 cooperated with the miR-106b-25 cluster to promote PLCE1-dependent cell-cycle progression both in vivo and in vitro. In addition, PLCE1 potentiated the phosphorylation of MCM7 at six threonine residues by the atypical kinase RIOK2, which promoted MCM complex assembly, chromatin loading, and cell-cycle progression. Inhibition of PLCE1 or RIOK2 hampered MCM7-mediated DNA replication, resulting in G1–S arrest. Furthermore, MCM7 overexpression in ESCC correlated with poor patient survival. Overall, these findings provide insights into the role of PLCE1 as an oncogenic regulator, a promising prognostic biomarker, and a potential therapeutic target in ESCC. Significance: PLCE1 promotes tumor progression in ESCC by activating PKCα-mediated phosphorylation of E2F1 to upregulate MCM7 and miR-106b-5p expression and by potentiating MCM7 phosphorylation by RIOK2.

Anthrax is an acute infectious disease caused by Bacillus anthracis, which can infect various animals and humans. Cutaneous anthrax primarily presents as infiltrative, edematous erythema, surface vesicles, hemorrhagic vesicles, and necrotic eschar; some patients may also experience systemic symptoms such as fever and leukocytosis. With economic development and improvements in public health conditions, naturally occurring cases of cutaneous anthrax have significantly decreased, leading to limited reports on the pathological manifestations of this disease. This article reports a case of a patient with cutaneous anthrax diagnosed and treated in our hospital, aiming to explore the laboratory examinations, imaging, pathological features, and clinical treatment methods of the disease. The goal is to enhance understanding of anthrax and increase vigilance in clinical practice to avoid misdiagnosis and missed diagnosis. The described diagnostic and therapeutic processes are accurate and reliable, with no modifications or exaggerations. It is important to note that the patient’s treatment may have been influenced by local social, economic, health, and epidemiological conditions, which introduces certain limitations. We hope that our colleagues will approach this study with an objective mindset for learning and reference.

Abstract Neuroblastoma presenting as obstructive jaundice due to compression of the extrahepatic bile duct is very rare. An 11-month-old girl had sudden onset of jaundice. Initial imaging suggested a dilated biliary system caused by hepatic hilum mass. 18F-FDG PET/CT showed a lesion with increased 18F-FDG accumulation associated with surrounding enlarged lymph nodes. Surgical pathology confirmed the diagnosis of a poorly differentiated neuroblastoma associated with multiple lymph node metastases.

Supplementary Methods and Materials, supplementary tables, supplementary figure legends