{'fraction_non_alphanumeric': 0.02543859649122807, 'fraction_numerical': 0.01929824561403509, 'mean_word_length': 5.069148936170213, '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}}
Blocking KRAS Signaling for the Treatment of Lung Cancer: Mission Possible?

━━ The three RAS oncogenes with high homology, considered to be undruggable, are the most fre-quently (approximately 25%) mutated gene family in human cancer. Missense mutations of the KRAS gene occur predominantly at codons 12, 13 or 61 and are observed in 30% of patients with lung adenocarcinoma in North American populations and 10% of those in Japanese populations. Although comprehensive efforts to develop therapeutic strategies to block the mutant RAS function, which is involved in the growth and development of cancer, have been made, clinically effective anti-RAS therapies have remained elusive for more than 30 years since the discovery of the RAS oncogenes in the 1980s. Therefore, in 2013, the National Cancer Institute (NCI) launched an RAS initiative to develop drugs that target the cell signaling pathway controlled by the RAS oncogenes. With research in progress, there is hope that mutant RAS can finally be conquered in the near future. In the present manuscript, I will describe the history of and recent advances in these research efforts.