RESULTS: A total of 103 cases with intracranial haemorrhage i.e. intracerebral haemorrhage, extradural haemorrhage, subdural haemorrhage, intraventricular haemorrhage, haemorrhagic contusion and subarachnoid haemorrhage, following motor vehicle accidents was undertaken to study factors contributing to either good or poor outcome according to the Glasgow Outcome Scale. Patients below 12 years of age were excluded. The end point of the study was taken at 24 months post injury. The selected variables were incorporated into models generated by logistic regression techniques of multivariate analysis to see the significant predictors of outcome as well as the correlation between the CT findings with GCS.
CONCLUSION: Significant predictors of outcome were GCS on arrival in the accident emergency department, pupillary reflex and the CT scan findings. The CT predictors of outcome include ICH, EDH, IVH, present of SAH, site of ICH, volumes of EDH and SDH as well as midline shift.
AIM: We here aimed to find out the frequency of BRAFV600E mutation in a series of Malaysian patients with brain tumors and if any association exists between BRAFV600E mutation and clinicopathological features of patients.
MATERIAL AND METHODS: Fresh frozen tumor tissue samples from 50 Malaysian brain tumor patients were analyzed for BRAFV600E mutational status, and its correlation with clinicopathological features (including age, gender, and tumor localization such as intra-axial: within the brain substance or extra-axial: outside the brain substance) was examined.
RESULTS: The overall BRAFV600E mutation frequency was determined to be 22% (in 11 of 50 patients). BRAFV600E was significantly correlated with the tumor location group, which shows BRAFV600E was more frequent in the intra-axial tumor than the extra-axial tumor group. In this study, we also observed that male patients were slightly more susceptible to BRAFV600E mutation, and this mutation was predominant in patients of the age group
RESULT: A total of 24 and 32 somatic variants were identified in presentation and relapse samples respectively with an average of 4.0 variants per patient at presentation and 5.3 variants per patient at relapse, with SNVs being more frequent than indels at both disease stages. All patients have somatic variants in at least one gene that is frequently mutated in AML at both disease presentation and relapse, with most of these variants are classic AML and recurrent hotspot mutations including NPM1 p.W288fs, FLT3-ITD, NRAS p.G12D and IDH2 p.R140Q. In addition, we found two distinct clonal evolution patterns of relapse: (1) a leukemic clone at disease presentation acquires additional mutations and evolves into the relapse clone after the chemotherapy; (2) a leukemic clone at disease presentation persists at relapse without the addition of novel somatic mutations.
CONCLUSIONS: The findings of this study suggest that the relapse-initiating clones may pre-exist prior to therapy, which harbor or acquire mutations that confer selective advantage during chemotherapy, resulting in clonal expansion and eventually leading to relapse.