{'fraction_non_alphanumeric': 0.019461077844311378, 'fraction_numerical': 0.01122754491017964, 'mean_word_length': 5.490291262135922, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Detection of Phase‐1 Drug‐Metabolizing Epoxide Hydrolases in Glioblastoma Cells

Glioblastoma Multiforme (GBM) is a devastating prognosis for human brain tumors known for rapid proliferation, tumor invasiveness, cell migration, and drug resistance. Angiogenesis appears to be the main contributor of Glioblastoma's aggressive tumor growth. Epoxide Hydrolases (EH's) constitute an important class of drug metabolizing enzymes mainly distributed in liver and other extrahepatic tissues, including the brain. SEH substrates are responsible for vasoactive proliferation which may be an important contributor to angiogenesis and drug resistance. Previous studies have used sEH inhibitors to detect sEH activity in glioma cell lines U251 and U87 by fluorescence assay. In this Pilot study we report the expression of mEH and sEH's in GBM‐derived U118MG cell lines. The expression of mEH and sEH was determined by immunocytochemical staining ad western blotting analyses. Our results show that U118MG cells stained positive for both EH's and these results were confirmed by western blot analysis. These results demonstrate that mEH and sEH are coexpressed in GBM U118MG cells. Future goal is to further elucidate the possible roles of sEH in tumor cell proliferation by use of sEH inhibitors to reuce Glioblastoma's resistance to drug therapy.