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Items: 1 to 20 of 126

1.

Cardiac hypertrophy associated with myeloproliferative neoplasms in JAK2V617F transgenic mice.

Shi K, Zhao W, Chen Y, Ho WT, Yang P, Zhao ZJ.

J Hematol Oncol. 2014 Mar 19;7:25. doi: 10.1186/1756-8722-7-25.

2.

Thrombosis in myeloproliferative neoplasms with JAK2V617F mutation.

Sun T, Zhang L.

Clin Appl Thromb Hemost. 2013 Jul-Aug;19(4):374-81. doi: 10.1177/1076029612453761. Review.

PMID:
22826442
3.

Depletion of Jak2V617F myeloproliferative neoplasm-propagating stem cells by interferon-α in a murine model of polycythemia vera.

Mullally A, Bruedigam C, Poveromo L, Heidel FH, Purdon A, Vu T, Austin R, Heckl D, Breyfogle LJ, Kuhn CP, Kalaitzidis D, Armstrong SA, Williams DA, Hill GR, Ebert BL, Lane SW.

Blood. 2013 May 2;121(18):3692-702. doi: 10.1182/blood-2012-05-432989.

4.

Clinical and laboratory significance of defective P2Y(12) pathway function in patients with myeloproliferative neoplasms: a pilot study.

Chang H, Shih LY, Michelson AD, Dunn P, Frelinger AL, Wang PN, Kuo MC, Lin TL, Wu JH, Tang TC.

Acta Haematol. 2013;130(3):181-7. doi: 10.1159/000348413.

PMID:
23751441
5.

Oncogenic JAK2V617F requires an intact SH2-like domain for constitutive activation and induction of a myeloproliferative disease in mice.

Gorantla SP, Dechow TN, Grundler R, Illert AL, Zum Büschenfelde CM, Kremer M, Peschel C, Duyster J.

Blood. 2010 Nov 25;116(22):4600-11. doi: 10.1182/blood-2009-07-236133.

6.

The clinical significance of JAK2V617F mutation for Philadelphia-negative chronic myeloproliferative neoplasms in patients with splanchnic vein thrombosis.

Yonal I, Pinarbası B, Hindilerden F, Hancer VS, Nalcaci M, Kaymakoglu S, Diz-Kucukkaya R.

J Thromb Thrombolysis. 2012 Oct;34(3):388-96.

PMID:
22569900
7.

The thrombopoietin receptor, MPL, is critical for development of a JAK2V617F-induced myeloproliferative neoplasm.

Sangkhae V, Etheridge SL, Kaushansky K, Hitchcock IS.

Blood. 2014 Dec 18;124(26):3956-63. doi: 10.1182/blood-2014-07-587238.

8.

JAK2V617F-positive endothelial cells contribute to clotting abnormalities in myeloproliferative neoplasms.

Etheridge SL, Roh ME, Cosgrove ME, Sangkhae V, Fox NE, Chen J, López JA, Kaushansky K, Hitchcock IS.

Proc Natl Acad Sci U S A. 2014 Feb 11;111(6):2295-300. doi: 10.1073/pnas.1312148111.

9.

Hypoxia inhibits JAK2V617F activation via suppression of SHP-2 function in myeloproliferative neoplasm cells.

Mitsumori T, Nozaki Y, Kawashima I, Yamamoto T, Shobu Y, Nakajima K, Morishita S, Komatsu N, Kirito K.

Exp Hematol. 2014 Sep;42(9):783-92.e1. doi: 10.1016/j.exphem.2014.05.007.

PMID:
24860972
10.

[Progress of study on JAK2V617F mutation in myeloproliferative neoplasm].

Chen YX, Li Y, Zhang LY, Liu B.

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2011 Oct;19(5):1329-33. Review. Chinese.

PMID:
22040998
11.

Co-targeting the PI3K/mTOR and JAK2 signalling pathways produces synergistic activity against myeloproliferative neoplasms.

Bartalucci N, Tozzi L, Bogani C, Martinelli S, Rotunno G, Villeval JL, Vannucchi AM.

J Cell Mol Med. 2013 Nov;17(11):1385-96. doi: 10.1111/jcmm.12162.

12.

JAK2V617F somatic mutation in the general population: myeloproliferative neoplasm development and progression rate.

Nielsen C, Bojesen SE, Nordestgaard BG, Kofoed KF, Birgens HS.

Haematologica. 2014 Sep;99(9):1448-55. doi: 10.3324/haematol.2014.107631.

13.

Tyrosine 201 is required for constitutive activation of JAK2V617F and efficient induction of myeloproliferative disease in mice.

Yan D, Hutchison RE, Mohi G.

Blood. 2012 Aug 30;120(9):1888-98. doi: 10.1182/blood-2011-09-380808.

14.

JAK2 and MPL mutations in myeloproliferative neoplasms.

Koppikar P, Levine RL.

Acta Haematol. 2008;119(4):218-25. doi: 10.1159/000140634. Review.

PMID:
18566540
15.

Deletion of Stat3 enhances myeloid cell expansion and increases the severity of myeloproliferative neoplasms in Jak2V617F knock-in mice.

Yan D, Jobe F, Hutchison RE, Mohi G.

Leukemia. 2015 Oct;29(10):2050-61. doi: 10.1038/leu.2015.116.

16.

How does JAK2V617F contribute to the pathogenesis of myeloproliferative neoplasms?

Chen E, Mullally A.

Hematology Am Soc Hematol Educ Program. 2014 Dec 5;2014(1):268-76. doi: 10.1182/asheducation-2014.1.268. Review.

PMID:
25696866
17.

Loss of wild-type Jak2 allele enhances myeloid cell expansion and accelerates myelofibrosis in Jak2V617F knock-in mice.

Akada H, Akada S, Hutchison RE, Mohi G.

Leukemia. 2014 Aug;28(8):1627-35. doi: 10.1038/leu.2014.52.

18.

Absence of JAK2V617F mutation in Chinese deep vein thrombosis patients without myeloproliferative neoplasms.

Dong B, Zhang Y, Fu X, Wang G.

Thromb Res. 2012 May;129(5):664-5. doi: 10.1016/j.thromres.2011.12.018. No abstract available.

PMID:
22197451
19.

Loss of TET2 has dual roles in murine myeloproliferative neoplasms: disease sustainer and disease accelerator.

Kameda T, Shide K, Yamaji T, Kamiunten A, Sekine M, Taniguchi Y, Hidaka T, Kubuki Y, Shimoda H, Marutsuka K, Sashida G, Aoyama K, Yoshimitsu M, Harada T, Abe H, Miike T, Iwakiri H, Tahara Y, Sueta M, Yamamoto S, Hasuike S, Nagata K, Iwama A, Kitanaka A, Shimoda K.

Blood. 2015 Jan 8;125(2):304-15. doi: 10.1182/blood-2014-04-555508.

20.

Myeloproliferative neoplasm induced by constitutive expression of JAK2V617F in knock-in mice.

Marty C, Lacout C, Martin A, Hasan S, Jacquot S, Birling MC, Vainchenker W, Villeval JL.

Blood. 2010 Aug 5;116(5):783-7. doi: 10.1182/blood-2009-12-257063.

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