Prediction of outcomes for symptomatic spinal cavernous malformation surgery: a multicenter prospective clinical study.

PURPOSE: Clinical outcome of spinal cavernous malformation (SCM) varies because of its unclear natural history, and reliable prognostic prediction model for SCM patients is limited. The aim of the present study was to investigate potential factors that predict one-year neurological status in postoperative patients with SCM. METHODS: This was a multicenter prospective observational study in consecutive patients with SCMs. SCMs treated microsurgically between January 2015 and January 2021 were included. Outcome was defined as the American Spinal Injury Association Impairment Scale (AIS) grade at one year after operation. Multivariable analyses were used to construct the best predictive model for patient outcomes. RESULTS: We identified 268 eligible SCM patients. Neurological outcome had worsened from preoperative baseline in 51 patients (19.0%) at one year. In the multivariable logistic regression, the best predictive model for unfavorable outcome included symptom duration ≥ 26 months (95% CI 2.80-16.96, P < 0.001), size ≤ 5 mm (95% CI 1.43-13.50, P = 0.010), complete intramedullary (95% CI 1.69-8.14, P = 0.001), subarachnoid hemorrhage (95% CI 2.92-12.57, P < 0.001), AIS B (95% CI 1.91-40.93, P = 0.005) and AIS C (95% CI 1.12-14.54, P = 0.033). CONCLUSIONS: Admission size of the lesion, morphology, symptom duration, AIS grade and the presence of subarachnoid hemorrhage were strong outcome predictors regarding prognostication of neurological outcome in postoperative patients with SCMs. A decision to surgically remove a symptomatic SCM should be justified by systematic analysis of all factors potentially affecting outcome.

Systematic pan­cancer analysis identifies CDC45 as having an oncogenic role in human cancers.

Cell division cycle 45 (CDC45) is an essential protein required for the initiation of DNA replication. In the present study, the role of CDC45 across 33 cancers was systematically investigated. It was observed that the expression of CDC45 was significantly upregulated in most cancers, exhibiting a marked negative correlation with the overall survival. Next, there was no significant difference in prognosis between the genomically altered and unaltered groups with respect to clinical outcomes. A decreased level of CDC45 at the DNA promoter region was also identified in several cancers. Furthermore, CDC45 expression was associated with the levels of tumor­infiltrating immune cells in some specific cancer types. In addition, CDC45 was associated with m6A methylation, and CDC45 expression was primarily positively correlated with 'writers' and 'readers' in various cancers, particularly HNRNPC, RBM15 and YTHDC1. Gene enrichment analysis was also performed. In addition, the AUC of each cancer with respect to its 1­, 3­, and 5­year survival rates were explored. Finally, CCK­8 assays, EdU assays and cell cycle analysis were conducted. In conclusion, the present study demonstrated that CDC45 may be a potential biomarker and target for cancer treatment.

Pan-cancer analysis indicates that MYBL2 is associated with the prognosis and immunotherapy of multiple cancers as an oncogene.

MYBL2 has been demonstrated to be an oncogene in some cancers, but there is no pan-cancer analysis at the macro level. We used multiple online or offline bioinformatic tools to examine the effects of MYBL2 in human cancers. We first identified that MYBL2 was highly expressed and related to the stage and grade of most cancers. The results of survival analysis from two databases showed that high MYBL2 expression was positively correlated with a poor prognosis for most cancer patients. We observed a significant difference in the promoter methylation level of MYBL2 in cancers such as colon adenocarcinoma and liver hepatocellular carcinoma versus normal controls. We found that MYBL2 can affect the tumor immune microenvironment by influencing the immune infiltration level and expression level of CD4+ T cells, CD8+ T cells, cancer-associated fibroblasts (CAFs) and immune checkpoint-associated cells. Functional enrichment analysis of MYBL2 identified that MYBL2 can play a crucial role in cancers by regulating spliceosomes, DNA replication and the cell cycle. Moreover, we verified the function of MYBL2 in three cancer cells of glioma, breast cancers and liver cancers, and the results showed that MYBL2 can regulate the cell cycle and proliferation ability of cancers.