{'fraction_non_alphanumeric': 0.03594351732991014, 'fraction_numerical': 0.03337612323491656, 'mean_word_length': 5.39344262295082, '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}}
Challenges facing JAK inhibitor therapy for myeloproliferative neoplasms.

William Vainchenker discovered the gain-of-function mutation in the gene encoding Janus kinase (JAK) 2 (JAK2 V617F) in early 2004 (reported in 2005)1 and subsequently described its association with BCR-ABL1–negative myeloproliferative neoplasms and its ability to induce erythrocytosis in mice. At that time, many researchers hoped that a specific targeted agent would be developed for these neoplasms, similar to imatinib for chronic myeloid leukemia. This particular prospect was bolstered by the detection of other activating mutations that are relevant to JAK–signal transducer and activator of transcription (STAT) (e.g., MPL W515L and JAK2 K539L) in patients with JAK2 V617F–negative disease. . . .