{'fraction_non_alphanumeric': 0.025573192239858905, 'fraction_numerical': 0.006172839506172839, 'mean_word_length': 5.135135135135135, '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}}
Does Cancer Solve an Optimization Problem?

Many cancers are characterized by a high degree of aneuploidy, which isbelieved to be a result of chromosomal instability (CIN). The precise role of CIN incancer is still the matter of a heated debate. We present a quantitative framework forexamining the selection pressures acting on populations of cells and weigh the \pluses"and \minuses" of CIN from the point of view of a sel¯sh cell. We calculate the optimalrate of chromosome loss assuming that cancer is initiated by inactivation of a tumorsuppressor gene followed by a clonal expansion. The resulting rate, p* ~ ¼ 10-2 per celldivision per chromosome, is similar to that obtained experimentally by Lengauer et al(1997). Our analysis further suggests that CIN does not arise simply because it allowsa faster accumulation of carcinogenic mutations. Instead, CIN must arise because ofalternative reasons, such as environmental factors, epigenetic events, or as a directconsequence of a tumor suppressor gene inactivation. The increased variability aloneis not a su±cient explanation for the presence of CIN in the majority of cancers.