{'fraction_non_alphanumeric': 0.01957831325301205, 'fraction_numerical': 0.009789156626506024, 'mean_word_length': 5.611940298507463, '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}}
From this month's Histopathology

The burgeoning of gastrointestinal endoscopy and greater awareness of the precursor lesions of adenocarcinoma have contributed to the increasing importance of the reliable assessment of dysplasia in biopsies particularly from the lower oesophagus and the colorectum. Geboes & Van Eyken (p. 99) review the criteria and methods for diagnosing dysplasia and malignancy in biopsies from Barrett's oesophagus. They highlight the difficulties of distinguishing between reactive or regenerative atypia and dysplasia, and appraise critically whether dysplasia should be subjected to a three-tier classification or a clinically more applicable classification distinguishing only between highand low-grade dysplasia. Geboes & Van Eyken also question the role of ancillary techniques such as staining for mucins or p53; although these have the potential to increase the objectivity of the assessment of cancer risk, histological assessment of cytological and architectural features remains the preferred method. Turning to the assessment of ulcerative colitis-related dysplasia, Wong et al. (p. 108) report their experience with Ki67 and p53 immunostaining. The distribution of Ki67 staining is helpful because, if confined to the basal third of the crypts, it appears to exclude a diagnosis of dysplasia.