A radiomics-based model to differentiate glioblastoma from solitary brain metastases.

AIM: To differentiate glioblastoma (GBM) from solitary brain metastases (MET) using radiomic analysis. MATERIALS AND METHODS: Two hundred and fifty-three patients with solitary brain tumours (157 GBM and 98 solitary brain MET) were split into a training cohort (n=178) and a validation cohort (n=77) by stratified sampling using computer-generated random numbers at a ratio of 7:3. After feature extraction, minimum redundancy maximum relevance (mRMR) and the least absolute shrinkage and selection operator (LASSO) were used to build the radiomics signature on the training cohort and validation cohort. Performance was assessed by radiomics score (Rad-score), receiver operating characteristic (ROC) curve, calibration, and clinical usefulness. RESULTS: Eleven radiomic features were selected as significant features in the training cohort. The Rad-score was significantly associated with the differentiation between GBM and solitary brain MET (p<0.001) both in the training and validation cohorts. The radiomics signature yielded area under the curve (AUC) values of 0.82 and 0.81 in the training and validation cohorts to distinguish between GBM and solitary brain MET. CONCLUSIONS: The radiomics model might be a useful supporting tool for the preoperative differentiation of GBM from solitary brain MET, which could aid pretreatment decision-making.

Tumour exosomes from cells harbouring PTPRZ1-MET fusion contribute to a malignant phenotype and temozolomide chemoresistance in glioblastoma.

Exosomes are carriers of pro-tumorigenic factors that participate in glioblastoma (GBM) progression, and many fusion genes are strong driver mutations in neoplasia and are involved in tumorigenesis. However, the ability of fusion genes to be transduced by exosomes is unknown. We characterized exosomes from GBM cells harbouring and not harbouring PTPRZ1-MET fusion (ZM fusion). We also determined the effect of the exosomes from ZM fusion cells (ZM exosomes) on pro-oncogenic secretions and showed that ZM exosomes are internalized by the recipient cells. In addition, we studied the effect of ZM exosome-mediated intercellular communication in the GBM microenvironment. MET proto-oncogene expression was higher in ZM exosomes. Moreover, phosphorylated MET was detected only in ZM exosomes and not in exosomes released by non-ZM fusion GBM cells. ZM exosomes transferred to non-ZM fusion GBM cells and normal human astrocytes altered gene expression and induced epithelial-mesenchymal transition. The uptake of ZM exosomes also induced an exosome-dependent phenotype defined by GBM cell migration and invasion, neurosphere growth and angiogenesis. In addition, ZM exosomes conferred temozolomide resistance to the GBM cells, and exosome-derived ZM fusion network proteins targeted multiple pro-oncogenic effectors in recipient cells within the GBM microenvironment. Our findings show that exosomes mediate the aggressive character of GBM and demonstrate the role of ZM fusion in the exacerbation of this effect. These findings have possible implications for the foundation of gene fusion-based therapy for managing GBM.

Multicentric biatrial myxoma in a young female patient: case report.

We report a case of multicentric, biatrial cardiac myxoma in a 29-year-old female who complained of exertional dyspnea, abdominal distension and peripheral edema. Any other associated skin lesions, breast mass or endocrine disorder presenting complex form were' not seen on her. Also, there was no contributory medical history, hypertension and diabetes mellitus. By using transthoracic echocardiography, we identified a biatrial myxoma attached to the interatrial septum. During surgical excision, we found a large right atrial myxoma with extension through the fossa ovalis into the left atrium and small myxoma attached to the right atrial free wall. After successful resection of interatrial septum and free wall, atrial septal defect was created during the resection and safely repaired by bovine pericardial patch.