{'fraction_non_alphanumeric': 0.036101083032490974, 'fraction_numerical': 0.02888086642599278, 'mean_word_length': 5.0, '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}}
Manifestations of cancer cachexia induced by colon 26 adenocarcinoma are not fully ascribable to interleukin‐6

In order to further clarify the role of interleukin 6 (IL‐6) in the pathogenesis of cachexia, recombinant human IL‐6 (hIL‐6) was administered s.c. by osmotic pump for 9 days at a dose of 1 or 10 μg/day into CDFI mice inoculated with a non‐cachexia‐inducing subclone of colon 26 adenocarcinoma (clone 5), or with a cachexia‐inducing subclone (clone 20) of this malignancy. The serum level of IL‐6 in non‐cachectic mice with clone‐5 tumors was 35% lower than in cachectic mice bearing clone 20 of colon 26 adenocarcinoma on the 19th day after tumor inoculation. IL‐6 administration induced anemia, thrombocytosis and visceral organ hypertrophy not only in mice with clone‐5 tumors but also in control mice with no tumor burden. Lipolysis and proteolysis became conspicuous when a large dose (10 μg/day) of IL‐6 was infused into mice with clone‐5 tumors. However, IL‐6 supplementation did not induce loss of body weight, a decline in food intake or lymphocytopenia, which were characteristically observed in cachectic mice with clone‐20 tumors. In conclusion, IL‐6 appears to be a permissive factor for the development of cachexia but, while it can induce some of the symptoms typical of cachexia, it cannot in itself induce the full cachectic syndrome. © 1995 Wiley‐Liss Inc.