贺琪, 常春康 . JAKs通路在骨髓增殖性肿瘤发病机制中的作用及主要JAKs抑制剂的应用[J]. 诊断学理论与实践, 2020 , 19(02) : 111 -114 . DOI: 10.16150/j.1671-2870.2020.02.003
[1] | Arber DA, Orazi A, Hasserjian R, et al. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia[J]. Blood,2016, 127(20):2391-2405. |
[2] | Baxter EJ, Scott LM, Campbell PJ, et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloprolife-rative disorders[J]. Lancet, 2005, 365(9464):1054-1061. |
[3] | Pikman Y, Lee BH, Mercher T, et al. MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia[J]. PLoS Med, 2006, 3(7):e270. |
[4] | Nangalia J, Massie CE, Baxter EJ, et al. Somatic CALR mutations in myeloproliferative neoplasms with nonmuta-ted JAK2[J]. N Engl J Med, 2013, 369(25):2391-2405. |
[5] | Scott LM, Tong W, Levine RL, et al. JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis[J]. N Engl J Med, 2007, 356(5):459-468. |
[6] | Rampal R, Al-Shahrour F, Abdel-Wahab O, et al. Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis[J]. Blood, 2014, 123(22):e123-e133. |
[7] | Shuai K, Ziemiecki A, Wilks AF, et al. Polypeptide signalling to the nucleus through tyrosine phosphorylation of Jak and Stat proteins[J]. Nature,1993 Dec 9; 366(6455):580-583. |
[8] | O'Shea JJ, Murray PJ. Cytokine signaling modules in inflammatory responses[J]. Immunity, 2008, 28(4):477-487. |
[9] | Nishanth G, Wolleschak D, Fahldieck C, et al. Gain of function in Jak2V617F-positive T-cells[J]. Leukemia, 2017, 31(4):1000-1003. |
[10] | Prestipino A, Emhardt AJ, Aumann K, et al. Oncogenic JAK2V617F causes PD-L1 expression, mediating immune escape in myeloproliferative neoplasms[J]. Sci Transl Med, 2018, 10(429),pii:eaam7729. |
[11] | Hasselbalch HC. Perspectives on chronic inflammation in essential thrombocythemia, polycythemia vera, and myelofibrosis: is chronic inflammation a trigger and driver of clonal evolution and development of accelerated atherosclerosis and second cancer?[J]. Blood, 2012, 119(14):3219-3225. |
[12] | Fleischman AG, Aichberger KJ, Luty SB, et al. TNFα facilitates clonal expansion of JAK2V617F positive cells in myeloproliferative neoplasms[J]. Blood, 2011, 118(24):6392-6398. |
[13] | Boissinot M, Lippert E, Girodon F, et al. Latent myeloproliferative disorder revealed by the JAK2-V617F mutation and endogenous megakaryocytic colonies in patients with splanchnic vein thrombosis[J]. Blood, 2006, 108(9):3223-3224. |
[14] | Hobbs CM, Manning H, Bennett C, et al. JAK2V617F leads to intrinsic changes in platelet formation and reactivity in a knock-in mouse model of essential thrombocythemia[J]. Blood, 2013, 122(23):3787-3797. |
[15] | Leroy E, Constantinescu SN. Rethinking JAK2 inhibition: towards novel strategies of more specific and versatile Janus kinase inhibition[J]. Leukemia, 2017, 31(5):1023-1038. |
[16] | Verstovsek S, Mesa RA, Gotlib J, et al. A double-blind, placebo-controlled trial of ruxolitinib for myelofibrosis[J]. N Engl J Med, 2012, 366(9):799-807. |
[17] | Harrison C, Kiladjian JJ, Al-Ali HK, et al. JAK inhibition with ruxolitinib versus best available therapy for myelofibrosis[J]. N Engl J Med, 2012, 366(9):787-798. |
[18] | Vannucchi AM, Kiladjian JJ, Griesshammer M, et al. Ruxolitinib versus standard therapy for the treatment of polycythemia vera[J]. N Engl J Med, 2015, 372(5):426-435. |
[19] | Passamonti F, Saydam G, Lim L, et al. RESPONSE 2: a phase 3b study evaluating the efficacy and safety of ruxo-litinib in patients with hydroxyurea - resistant/intolerant polycytheinia vera versus best available therapy[J]. J Clin Oncol, 2014, 32:15. |
[20] | Harrison CN, Mead AJ, Panchal A, et al. Ruxolitinib vs best available therapy for ET intolerant or resistant to hydroxycarbamide[J]. Blood, 2017, 130(17):1889-1897. |
[21] | Harrison CN, Vannucchi AM, Platzbecker U, et al. Momelotinib versus best available therapy in patients with myelofibrosis previously treated with ruxolitinib(SIMPLIFY 2): a randomised, open-label, phase 3 trial[J]. Lancet Haematol, 2018, 5(2):e73-e81. |
[22] | Mesa RA, Vannucchi AM, Mead A, et al. Pacritinib versus best available therapy for the treatment of myelofibrosis irrespective of baseline cytopenias (PERSIST-1): an international, randomised, phase 3 trial[J]. Lancet Haematol, 2017, 4(5):e225-e236. |
[23] | Pardanani A, Harrison C, Cortes JE, et al. Safety and efficacy of fedratinib in patients with primary or secondary myelofibrosis: A randomized clinical trial[J]. JAMA Oncol, 2015, 1(5):643-651. |
[24] | Verstovsek S, Talpaz M, Ritchie E, et al. A phase I, open-label, dose-escalation, multicenter study of the JAK2 inhibitor NS-018 in patients with myelofibrosis[J]. Leukemia, 2017, 31(2):393-402. |
/
〈 |
|
〉 |