Brain tumors are challenging to handle and cause severe mortality and morbidity. The primary therapy for brain tumors, a combination of radiotherapy, chemotherapy (i.e temozolomide), and corticosteroids, is considered inadequate to improve patients' clinical conditions and associated with many adverse effects. There is an urgent need for new compounds or repurposing of existing therapies, which could improve brain tumor patients' prognosis. Metformin, commonly used for type 2 diabetes medication, has been examined for its protective action in cancer, reducing cancer risk and cancer-related mortality. However, its effect on cancer is still in rigorous debate. This study examines recent studies on the effects of metformin in primary brain tumor patients through systematic reviews. The literature search was performed on PubMed, ScienceDirect, and SpringerLink databases for articles published between 2013 and 2020. We selected clinical studies comparing the therapeutic outcomes of brain tumor therapy with and without metformin. The clinical benefits of the drug were assessed through the overall survival (OS) and progression-free survival (PFS) of brain tumor patients. Those studies demonstrated that the combination of metformin with temozolomide given post-radiotherapy resulted in better OS and PFS . Nonetheless, the efficacy and safety of metformin need further clinical testing in the wider population.
Aim: This study aim to determine the prevalence of Type 2 diabetes mellitus (T2DM) in primary brain tumor (BT) subjects and to assess the relationship between mutant p53 serum and HbA1c and insulin. Background: T2DM is known to increase the risk of various types of cancer, which are thought to be caused by hyperglycemia, hyperinsulinemia, and inflammation. A cohort study that looked at more than 500,000 subjects with DM over 11 years showed an increased risk in different types of cancer, including brain tumors. However, several recent studies have shown the opposite. One of the important pathways in the pathogenesis of brain tumors is the p53 pathway, in which mutations in the TP53 gene can cause brain cell growth abnormalities. Objective: The first stage involved taking subject data for the period January 2017-November 2020 from the medical records of the RSUPN dr. Cipto Mangunkusumo to assess the prevalence of T2DM in BT subjects. The second stage was an observational study with a cross-sectional design which collected primary data on subjects (n=86) to assess the relationship between mutant p53 serum and HbA1c and insulin. Methods: The analysis of mutant p53 serum and insulin was made using the ELISA method, while measurement of HbA1c was made using the boronate affinity method. Results: The results show that the prevalence of T2DM in BT subjects at dr. Cipto Mangunkusumo was relatively low (9%). Serum mutant p53 levels in T2DM (1.53 ng/mL ± 0.60) were significantly higher than in BT+T2DM and BT (P < 0.001). The HbA1c value was significantly lower in BT (5.15% ± 0.44) compared to BT+T2DM and T2DM (P < 0.001), while T2DM insulin levels (39.54 IU/mL ± 19.1) were significantly higher than BT+T2DM and BT (P < 0.001). There was no correlation between mutant serum p53 levels and HbA1c and insulin in the three groups. Conclusion: The study concludes that the prevalence of BT with T2DM is relatively low (9%) and that serum levels of mutant p53 in T2DM subjects are higher than subjects with BT, but there is no correlation between serum mutant p53 levels and HbA1c and insulin values. Further research needs to be conducted by analyzing p53 mutants from other specimens, such as brain tumor tissue.
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