Role of JAK2 in the pathogenesis and therapy of myeloproliferative disorders

被引：431

作者：

Levine, Ross L.

Pardanani, Animesh

Tefferi, Ayalew

Gilliland, D. Gary

机构：

[1] Mayo Clin, Div Hematol, Rochester, MN 55905 USA

[2] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dana Farber Canc Inst, Boston, MA 02155 USA

[3] Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA

[4] Harvard Univ, Sch Med, Harvard Stem Cell Inst, Boston, MA 02115 USA

[5] Broad Inst Harvard, Boston, MA 02115 USA

[6] MIT, Cambridge Ctr 7, Boston, MA 02115 USA

来源：

NATURE REVIEWS CANCER | 2007年 / 7卷 / 09期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1038/nrc2210

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The myeloproliferative disorders polycythaemia vera (PV), essential thombocythaemia (ET), and primary myelofibrosis (PMF) are clonal disorders of multipotent haematopoietic progenitors. The genetic cause of these diseases was not known until 2005, when several independent groups demonstrated that most patients with PV, ET and PMF acquire a single point mutation in the cytoplasmic tyrosine kinase JAK2 ( JAK2V617F). These discoveries have changed the landscape for diagnosis and classification of PV, ET and PMF, and show the ability of genomic technologies to identify new molecular targets in human malignancies with pathogenetic, diagnostic and therapeutic significance.

引用

页码：673 / 683

页数：11

共 112 条

[81] Samuelsson J, 2006, HAEMATOLOGICA, V91, P1281
[82] CIS3/SOCS-3 suppresses erythropoietin (EPO) signaling by binding the EPO receptor and JAK2
Sasaki, A
Yasukawa, H
Shouda, T
Kitamura, T
Dikic, I
Yoshimura, A
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (38) : 29338 - 29347
[83] Germline KRAS mutations cause Noonan syndrome
Schubbert, S
Zenker, M
Rowe, SL
Böll, SB
Klein, C
Bollag, G
van der Burgt, I
Musante, L
Kalscheuer, V
Wehner, LE
Nguyen, H
West, B
Zhang, KYJ
Sistermans, E
Rauch, A
Niemeyer, CM
Shannon, K
Kratz, CP
[J]. NATURE GENETICS, 2006, 38 (03) : 331 - 336
[84] Stat5 is essential for the myelo- and lymphoproliferative disease induced by TEL/JAK2
Schwaller, J
Parganas, E
Wang, DM
Cain, D
Aster, JC
Williams, IR
Lee, CK
Gerthner, R
Kitamura, T
Frantsve, J
Anastasiadou, E
Loh, ML
Levy, DE
Ihle, JN
Gilliland, DG
[J]. MOLECULAR CELL, 2000, 6 (03) : 693 - 704
[85] JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis
Scott, Linda M.
Tong, Wei
Levine, Ross L.
Scott, Mike A.
Beer, Philip A.
Stratton, Michael R.
Futreal, P. Andrew
Erber, Wendy N.
McMullin, Mary Frances
Harrison, Claire N.
Warren, Alan J.
Gilliland, D. Gary
Lodish, Harvey F.
Green, Anthony R.
[J]. NEW ENGLAND JOURNAL OF MEDICINE, 2007, 356 (05) : 459 - 468
[86] Progenitors homozygous for the V617F mutation occur in most patients with polycythemia vera, but not essential thrombocythemia
Scott, Linda M.
Scott, Mike A.
Campbell, Peter J.
Green, Anthony R.
[J]. BLOOD, 2006, 108 (07) : 2435 - 2437
[87] The V617F JAK2 mutation is uncommon in cancers and in myeloid malignancies other than the classic myeloproliferative disorders
Scott, LM
Campbell, PJ
Baxter, EJ
Todd, T
Stephens, P
Edkins, S
Wooster, R
Stratton, MR
Futreal, PA
Green, AR
[J]. BLOOD, 2005, 106 (08) : 2920 - 2921
[88] Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia
Shah, NP
Nicoll, JM
Nagar, B
Gorre, ME
Paquette, RL
Kuriyan, J
Sawyers, CL
[J]. CANCER CELL, 2002, 2 (02) : 117 - 125
[89] Overriding imatinib resistance with a novel ABL kinase inhibitor
Shah, NP
Tran, C
Lee, FY
Chen, P
Norris, D
Sawyers, CL
[J]. SCIENCE, 2004, 305 (5682) : 399 - 401
[90] Expression of Bcl-x in erythroid precursors from patients with polycythemia vera
Silva, M
Richard, C
Benito, A
Sanz, C
Olalla, I
Fernández-Luna, JL
[J]. NEW ENGLAND JOURNAL OF MEDICINE, 1998, 338 (09) : 564 - 571

← 3 4 5 6 7 8 9 10 11 12 →