RESUMO
Background: There is growing evidence that brain metastases (BM) have no well-defined boundaries and that conventional microsurgical circumferential dissection of BM is often inadequate to prevent local tumor recurrence. Previous studies have suggested that supramarginal resection can significantly improve local tumor control. We retrospectively analyzed the local tumor control in a series of patients with BM from lung adenocarcinoma. Methods: We retrospectively analyzed 48 patients with BM for lung adenocarcinoma in Shenzhen Second People's Hospital from May 2015 to May 2020. 26 resected lesions were located in eloquent areas and underwent standard gross total resection (GTR group); 22 resected lesions were located in ineloquent areas, after standard gross total resection, the periphery was expanded and resected by 5 mm (MTR group). The postoperative tumor recurrence was compared between the two groups. Results: During the follow-up period, the local recurrence rates in the GTR group and the MTR group were 61.5% and 27.3% (p = 0.022), respectively. Within 6 months after surgery, the local recurrence rates in the GTR group and the MTR group were 42.3% and 13.6% (p = 0.029), respectively. Within 12 months after surgery, the local recurrence rates in the GTR group and the MTR group were 57.7% and 22.7% (p = 0.014), respectively. The median progression-free survival time after surgery was 7.0 months (95% CI 4.0-10.0 months) in the GTR group and 14.0 months (95% CI 11.4-16.6 months) in the MTR group (Log-Rank p = 0.008). Compared with the MTR group, the HR of local recurrence in the GTR group was 3.74 (95% CI 1.38-10.39, p = 0.010). Cox multivariable analysis showed no other factors associated with local recurrence except for the surgical method (p = 0.012). Conclusions: On the basis of conventional surgical total resection, expanded peripheral resection of 5 mm around the brain metastases of lung adenocarcinoma can significantly reduce the local recurrence rate and prolongs the progression-free survival time.
RESUMO
Cranial diploe hematoma is a hematoma that occurs between the inner and outer layer of the skull and is often in infants and young children. Hemophilia A is an inherited X-linked bleeding disorder caused by a deficiency of coagulation factor VIII (FVIII) . Epidemiological survey results show that the prevalence of hemophilia in 24 provinces and cities in China is 2.73/100,000, while only about 5% of patients are registered . Hemophilia is mainly characterized by bleeding, which can occur anywhere in the pa-tient's body and manifest as intracranial, gastrointestinal, or pharyngeal bleeding, which can be life-threatening in severe cases. This article shares a case of a patient with he-mophilia A complicated by a chronic giant diploe hematoma.
RESUMO
The long noncoding RNA WEE2 antisense RNA 1 (WEE2-AS1) plays an oncogenic role in hepatocellular carcinoma and triple negative breast cancer progression. In this study, we investigated the expression and roles of WEE2-AS1 in glioblastoma (GBM). Furthermore, the molecular mechanisms behind the oncogenic actions of WEE2-AS1 in GBM cells were explored in detail. WEE2-AS1 expression was detected using quantitative real-time polymerase chain reaction. The roles of WEE2-AS1 in GBM cells were evaluated by the cell counting kit-8 assay, flow cytometric analysis, Transwell cell migration and invasion assays, and tumor xenograft experiments. WEE2-AS1 expression was evidently enhanced in GBM tissues and cell lines compared with their normal counterparts. An increased level of WEE2-AS1 was correlated with the average tumor diameter, Karnofsky Performance Scale score, and shorter overall survival among GBM patients. Functionally, depleted WEE2-AS1 attenuated GBM cell proliferation, migration, and invasion in vitro, promoted cell apoptosis, and impaired tumor growth in vivo. Mechanistically, WEE2-AS1 functioned as a molecular sponge for microRNA-520f-3p (miR-520f-3p) and consequently increased specificity protein 1 (SP1) expression in GBM cells. A series of recovery experiments revealed that the inhibition of miR-520f-3p and upregulation of SP1 could partially abrogate the influences of WEE2-AS1 downregulation on GBM cells. In conclusion, WEE2-AS1 can adsorb miR-520f-3p to increase endogenous SP1 expression, thereby facilitating the malignancy of GBM. Therefore, targeting the WEE2-AS1miR-520f-3pSP1 pathway might be a promising therapy for the management of GBM in the future.
