METHODS: EEP was obtained by maceration with absolute ethanol, then it was concentrated in rotaevaporator up to complete evaporation of the solvent. The crude extract was fractionated with hexane, ethyl acetate, chloroform and methanol and they were subjected to phytochemical screening and total phenolic compounds. Antioxidant activity of EEP and fractions was done by means of the 2,2-diphenyl-1-picryhydrazyl (DPPH) method. Biomarkers of red propolis were identified by LC-Orbitrap-FTMS. To assess cytotoxic activity of the extract, cells were exposed to EEP over 72 h. Cell viability was assessed by means of MTT assay. The percentage of cell growth inhibition (IC50) was analysed by means of non-linear regression, and the absorbance values of the various investigated concentrations were subjected to one-factor analysis of variance (ANOVA) followed by Tukey's or Tamhane's tests (α = 0.05).
RESULTS: The results obtained using phytochemical screening and LC-Orbitrap-FTMS indicated the presence of phlobaphene tannins, catechins, chalcones, aurones, flavonones, flavonols, xanthones, pentacyclic triterpenoids and guttiferones in Brazilian red propolis. EEP and its hexane, chloroform and ethyl acetate fractions obtained by liquid-liquid partitioning exhibited satisfactory antioxidant percentages. EEP (IC50
METHODS: We systematically searched for original research in PubMed, Cochrane Central Register of Controlled Studies, CINAHL Plus, EMBASE and HuGE Navigator from database inception until January 2018. Studies on association between polymorphism and antineoplastic-induced cardiovascular toxicity in patients treated for cancer of all antineoplastic agents were included except for anthracycline. Case reports, conference abstracts, reviews and non-patient studies were excluded. Data extracted by two independent reviewers were combined with random-effects model and reported according to PRISMA and MOOSE guidelines.
RESULTS: The 35 studies included examined a total of 219 SNPs in 80 genes, 11 antineoplastic and 5 types of cardiovascular toxicities. Meta-analyses showed that human epidermal growth factor receptor 2 (HER2) rs1136201, a risk variants (pooled OR: 2.43; 1.17-5.06, p = 0.018) is a potential predictors for trastuzumab-related cardiotoxicity. Gene dose effect analysis showed number of variant allele may contribute to the risk too.
CONCLUSIONS: This review found that HER2 rs1136201 can have the potential in predicting trastuzumab-related heart failure. As such, further studies are needed to confirm the validity of these results as well as determine the economic aspect of using SNPs prior to its implementation as a clinical practice.