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Lipid Nanocarriers for Oligonucleotide Delivery to the Brain
Published in Carla Vitorino, Andreia Jorge, Alberto Pais, Nanoparticles for Brain Drug Delivery, 2021
Andreia F. Jorge, Santiago Grijalvo, Alberto Pais, Ramón Eritja
One of the most exciting nucleic acid-based therapeutics used for downregulating gene expression is the ASO. In the late 1970s, Paul Zamecnick in a seminal work demonstrated that synthetic ASOs could be used therapeutically to inhibit protein translation [17]. ASOs are chemically modified single-stranded DNA (ssDNA) molecules, typically 12–30 nucleotides (nt) in length, which specifically bind to endogenous target mRNA by Watson-Crick base-pairing rules [18]. Following these rules, complementary base pairs are held together via specific hydrogen-bonding interactions and strengthened by the hydrophobic interactions arisen from purine-pyrimidine shape complementarity and base stacking. The chemical modification of ASOs is a requisite to guarantee stability in physiological conditions and to increase their potency and specificity to silence the mRNA target [19]. The most remarkable advance made towards the use of ASOs as therapeutic agents was the introduction of the phosphorothioate (PS) backbone modification, disclosed in 1970, which largely extends the half-lives of ASOs in serum and facilitates cellular uptake [20]. Equally relevant was the introduction of 2’-O-methyl (2’-O-Me; Fig. 8.1) modified ODNs which dramatically increased the resistance of ASOs to nucleases [21].
Mutation patterns of epidermal growth factor receptor gene in non-small cell lung cancer among Egyptian patients
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Wafaa H. Elmetnawy, Mona Qenawi, Salwa Sabet, Heba Bassiony
All EGFR mutations in the four exons; 18, 19, 20, 21; were assessed via allele-specific oligonucleotide Strip Assay. EGFR mutations were detected in 49 NSCLC samples (40.8%), where the occurrence incidence of mutations in each exon was 10.2%, 55.1%, 8.2%, and 26.5% of all the mutations, respectively. EGFR mutation status was correlated to the clinicopathological features of patients as shown in Table 3. There was no significant correlation between the age and the positivity to EGFR mutations (P = 0.709). Moreover, females exhibited non-significant higher mutated EGFR (35/49, 71.4%) than males (14/49, 28.6%) (P = 0.827). Although it was observed that nonsmokers showed higher incidence rate of EGFR mutations (30/49, 61.2%) compared to smokers (19/49, 38.8%); however, there is no significant correlation between EGFR mutations and smoking (P = 0.164). On the other hand, EGFR mutation positivity was significantly associated with advanced adenocarcinoma 43 (87.8%) (P = 0.000). Moreover, EGFR positive mutations were significantly associated with stage of tumor where 38 cases (77.6%) were at stage IV (P = 0.036). No significant difference was observed in tumor size between groups (Table 3).