{'fraction_non_alphanumeric': 0.03125, 'fraction_numerical': 0.02297794117647059, 'mean_word_length': 5.405882352941177, '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}}
p53 mutations in esophageal tumors from high‐incidence areas of China

Carcinomas of the upper digestive tract (squamous‐cell carcinoma of the esophagus, adenocarcinoma of the cardia) from 24 patients residing in Linxian (China) and near‐by high‐incidence areas were analyzed for mutations in exons 5–8 of the p53 tumor‐suppressor gene. Mutations were identified by polymerase chain reaction amplification and direct sequencing in 50% of the specimens. Eleven tumors harbored a single base‐pair substitution leading to either an amino‐acid substitution (8 tumors) or a chain‐termination signal (3 tumors), and one tumor revealed a 15‐bp deletion in exon 7 with a silent base substitution adjacent to the deletion site. Mutations occurred in all 4 exons examined, with a preponderance in exon 5. Of the 6 mutations identified among the 14 adenocarcinomas examined, 3 were G to T transversions, a mutation that has thus far been absent from reported mutations in Barrett's esophageal adenocarcinomas and dysplasias from patients residing in Europe and North America. © 1995 Wiley‐Liss, Inc.