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Background Scalp metastases from anaplastic oligodendroglioma (AO) are extremely rare and mostly involve intracranial recurrence or widely metastatic disease. Here we describe an exceptional case of histopathologically proven scalp metastasis of AO 6 years after surgical resection and postoperative adjuvant radiation. Case Description A 42-year-old woman presented with several months of progressive headache and dizziness. Preoperative magnetic resonance imaging (MRI) showed an irregular enhancing lesion in the left frontal lobe extending to the ependymal surface. Left frontal craniotomy was performed through a coronal approach, and gross total resection was achieved. Pathologic examination confirmed a World Health Organization grade III AO. The patient subsequently received 60 Gy of external beam radiotherapy in 30 fractions over 6 weeks. During 8 years of follow-up, the patient remained symptom free, and no evidence of intracranial recurrence was found. However, 6 years after intracranial tumor resection, the patient noticed a subcutaneous mass in her right frontal scalp, which was the site contralateral to her craniotomy. MRI revealed a homogeneously marked enhancing nodular lesion in the subcutaneous tissue of the right frontal scalp without intracranial recurrence. Gross total resection was performed, and the pathologic findings, which identified the mass as an AO, were consistent with those of the primary left frontal tumor. Conclusions This study presents a rare case of long-term AO scalp metastasis without intracranial recurrence. Intraoperative seeding and longer survival for oligodendroglial tumors may cause this rare entity. Optimal surgical strategies and standard operative procedures can promote the prevention of iatrogenic seeding.

To investigate clinical characteristics and outcomes of chronic subdural hematomas (CSDHs) in different age ranges.A retrospective collection of data from CSDH patients ≤40 years, 41-79 years, and ≥80 years of age between August 2011 and May 2017 was performed. The differences and similarities of clinical data and outcomes among three groups were analyzed.A total of 1118 CSDH patients were included. We found that 64.5% patients had arachnoid cyst/ventriculoperitoneal shunt in patients ≤40 years, 4.3% in the 41-79 years group, and 3.2% in the ≥80 years group (P 0.001). Headache was the most frequent symptom in the ≤40 years group (88.2%) and the 41-79 years group (60.9%), while the most frequent symptom in the ≥ 80 years group was limb weakness (80.4%). The history of head trauma was not significantly different between the three groups. After burr hole drainage craniostomy, the disappearance or alleviation of symptoms, duration of catheter drainage, and length of hospital stay were not significantly different, while the recurrence rate was also not significantly different between the three groups. Post-operation complications are an independent risk factor contributing to the death of patients of 41-79 years (P0.001, B = 3.140, Exp (B) = 23.103, 95% CI = 5.142-103.809) and of ≥ 80 years (P = 0.001, B=2.831, Exp (B) = 16.970, 95% CI = 3.365-85.567). The history of antithrombotic drug was an independent risk factor of complications in patients of 41-79 years (P = 0.042, B =1.341, Exp (B) =3.823, 95% CI = 1.048-13.942) and patients of ≥ 80 years (P = 0.026, B=1.399, Exp (B) = 4.052, 95% CI = 1.178-13.933), while complications were also an independent risk factor contributing to the outcome in patients of 41-79 years (P 0.001, B =2.254, Exp (B) =0.314, 95% CI = 0.089-1.103) and patients of ≥ 80 years (P = 0.006, B=2.074, Exp (B) = 7.953, 95% CI = 1.791-35.313). In the ≤40 years group, all patients had a good outcome (MRS score 0-3), while 98.2% (851/867) of the cases in the 41-79 years group and 94.3% (149/158) of the cases in the ≥ 80 years group saw a good outcome (P = 0.001).Our results clearly display the common and different clinical data of CSDH in all age ranges, which is crucial to improve the management and treatment of patients with CSDH.

Glioma is the most common type of primary brain tumors in the central nervous system (CNS). Migfilin occurs in human glioma and enhances cellular motility via the epidermal growth factor receptor (EGFR) pathway. However, the underlying molecular mechanism is not fully understood. In this study, we found that Migfilin promoted matrix metalloproteinase-2 (MMP-2) activity, and restrained the expression of tissue inhibitor of metalloproteinase 2 (TIMP2), which is an MMP-2 inhibitor. Functional and structural studies showed that the LIM1 domain of Migfilin was required for Migfilin-mediated TIMP2 expression inhibition and MMP-2 activity, and was also necessary in promoting cell motility. Furthermore, Migfilin-induced EGFR phosphorylation was greatly reduced by MMP-2 inhibitor (GM6001) or siRNA, while Migfilin-induced MMP-2 activation was also blocked by the EGFR inhibitor (AG1478) or siRNA. MMP-2 and EGFR inhibitors and their siRNAs can block Migfilin-induced migration and invasion, respectively. These results demonstrated that EGFR and MMP-2 signalings may form a positive feedback loop to enhance Migfilin-induced migration and invasion. Finally, we detected that the expression of Migfilin, EGFR phosphorylation (Tyr1173) and MMP-2 activity had a positive correlation in the clinical glioma sample. Taken together, these results suggest that Migfilin is a critical regulator in cellular motility by driving the EGFR-MMP-2 feedback loop, and may be considered as a potential therapeutic target in glioma.

Tumor necrosis factor receptor-associated protein 1 (TRAP1), an important member of mitochondrial heat shock protein 90 family, is involved in multiple biological processes in several types of tumors. However, its pathological role in esophageal squamous cell cancer (ESCC) remains unknown. Herein, we demonstrated the clinical value of TRAP1, and its role in apoptosis and motility in ESCC. The clinical potential of TRAP1 was investigated through immunohistochemical analysis in 328 ESCC samples, which revealed that strong TRAP1 expression was associated with increased risk of lymph node metastasis, while high TRAP1 expression correlated with poor prognosis. Expression of TRAP1 was found to be an independent prognostic factor for patients with ESCC. Additionally, the upregulation of TRAP1 antagonized cisplatin-induced apoptosis while its downregulation sensitized cells to cisplatin-induced apoptosis. As revealed by the transwell assay, TRAP1 overexpression promoted cellular migration and invasion as compared to the control groups. In contrast, silencing of endogenous TRAP1 expression attenuated the ability of migration and invasion. Finally, the molecular mechanism investigated in the present study demonstrated that TRAP1-mediated migration and invasion occurred through STAT3/MMP2 signaling pathway. In conclusion, TRAP1 may be considered as a molecular predictive marker for prognosis and a novel molecular candidate for therapeutic target in ESCC.

Background: The oncogenesis and developmental mechanisms of glioma must be clarified to control the disease. Results: Migfilin relates to pathological grades, prognosis of glioma, and regulates motility of glioma cells. Conclusion: Migfilin mediates migration and invasion through EGFR-induced PLC-γ and STAT3 pathways. Significance: Migfilin helps us better understand the pathogenesis of glioma, and Migfilin may be a molecular marker in diagnosis and an indicator in prognosis., Migfilin is critical for cell shape and motile regulation. However, its pathological role in glioma is unknown. Using an immunohistochemical staining assay, we demonstrate that there is a significant correlation between expression of Migfilin and pathological tumor grade in 217 clinical glioma samples. High Migfilin expression is associated with poor prognosis for patients with glioma. Investigation of the molecular mechanism shows that Migfilin promotes migration and invasion in glioma cells. Moreover, Migfilin positively modulates the expression and activity of epidermal growth factor receptor, and Migfilin-mediated migration and invasion depend on epidermal growth factor receptor-induced PLC-γ and STAT3-signaling pathways. Our results may provide significant clinical application, including use of Migfilin as a molecular marker in glioma for early diagnosis and as an indicator of prognosis.