{'fraction_non_alphanumeric': 0.023255813953488372, 'fraction_numerical': 0.0049833887043189366, 'mean_word_length': 5.409574468085107, '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}}
Serine biosynthesis: fuel for the melanoma cell growth engine

implications for the treatment of melanoma and other cancers. A variety of cancer cell types, including melanoma cells, can be induced to undergo senescence. In fact, it is now recognized that standard chemotherapy and ionizing radiation not only induce an expected apoptotic response but can also trigger senescence induction (Nardella et al., 2011). Reactivation of a senescence program therefore represents a potential therapeutic strategy for the treatment of melanoma, whose resistance to more traditional therapies – notably, those that induce apoptosis – limits the efficacy of current anti-melanoma drugs. However, a potential problem of senescence induction as a therapeutic strategy is that the senescent cells will secrete proteins that promote the tumorigenic properties of any neighboring transformed cells that have not undergone senescence or apoptosis. The results of Ohanna et al. hint at a potential solution to this conundrum. Targeted inhibition of the PNAS using, for example, NF-jB or PARP-1 inhibitors in conjunction with traditional chemotherapy may prevent the adverse consequence of senescence induction (Figure 1).