{'fraction_non_alphanumeric': 0.015209125475285171, 'fraction_numerical': 0.0028517110266159697, 'mean_word_length': 5.420731707317073, '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}}
Isozyme patterns of pyruvate kinase in various primary liver tumors induced during the process of hepatocarcinogenesis.

Hepatic nodular hyperplasia and highly, well, and poorly differentiated hepatomas and a cholangioma were produced in liver of rats fed N -fluorenylacetamide and N -nitrosomorpholin. The isozyme patterns of these primary liver tumors were studied both quantitatively with the use of antiserum to rat muscle pyruvate kinase and qualitatively by means of electrophoresis on polyacrylamide gel.

Both nodular hyperplasia and highly differentiated hepatomas showed total activities similar to that of normal liver, while the proportion of M2-type activity was found to increase with statistical significance. Well-differentiated hepatomas have a markedly low level of L-type and about the same level of M2-type activity as found in both nodular hyperplasia and highly differentiated hepatoma. Poorly differentiated hepatomas and a cholangioma have extraordinarily high activity of the M2 type and low activity of L-type pyruvate kinase.