BI-05 * MOLECULAR PROFILING OF LOW GRADE GLIOMAS (LGG) IN COLOMBIA (ONCOLGROUP)

Abstract

BACKGROUND: LGG are classified as being astrocytoma (DA), oligodendroglioma (OD) or mixed glioma (OA). TP53-m and 1p19q codeletion have been the main molecular abnormalities recorded to date. IDH1/2 mutations have been described in up to 85% of LGG. It has recently been found that ATRX plays a significant role in glioma oncogenesis. METHODS: We searched for P53 and Olig2 protein expression, MGMT methylation status (pMGMT), 1p19q codeletion and IDH/ATRX status in 63 Colombian LGG patients (pts). Overall survival (OS) rate was estimated and compared between groups and according to genotype. RESULTS: Mean age was 40.1-yo (±12.3), 50% of the pts were male, mean lesion diameter was 41.7 mm (±17.2 mm) and histological distribution was 61.9%, 25.4% and 12.7% for AD, OD and OA, respectively. Surgical resection was total in 47.6%, subtotal in 31.7% and biopsy was performed in 20.6% of the cases. Alterations in IDH1/2 were found in 57.1%, pMGMT+ in 65.1%, overexpression of p53 and Olig2 in 30.2% and 44.4%, and 1p19q codeletion in 34.9%. The presence of alterations in ATRX was analysed in 25 patients, being positive in 16% (all IDH1 + /1p19q-). Median follow-up was 15.8 months (95%CI 7.6-42.0), OS was 39.2 months (95%CI 1.3-114) and the variables positively modifying OS were pMGMT+ (p = 0.004), 1p19q codeletion (p = 0.015), the extension of surgical intervention (p = 0.011) and the number of lobes involved (p = 0.021). Multivariate analysis showed that pMGMT and 1p19q codeletion modified the OS in our population (p = 0.039 and 0.047, respectively). CONCLUSIONS: This is the first study which has evaluated the molecular profile in LGG pts from Latin-America. Our findings confirmed the prognostic relevance of pMGMT and 1p19q codeletion, without finding a positive relation for IDH1/2 mutations. This finding could have been explained by sample size and selection bias. Alterations in ATRX are limited to the population of pts having AD/OA and IDH1 + /1p19q-.