|
1
|
Kavalerchik E, Goff D and Jamieson CH:
Chronic myeloid leukemia stem cells. J Clin Oncol. 26:2911–2915.
2008. View Article : Google Scholar : PubMed/NCBI
|
|
2
|
Li S, Kralovics R, De Libero G,
Theocharides A, Gisslinger H and Skoda RC: Clonal heterogeneity in
polycythemia vera patients with JAK2 exon12 and JAK2-V617F
mutations. Blood. 111:3863–3866. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
3
|
Laibe S, Tadrist Z, Arnoulet C, Sainty D
and Mozziconacci MJ: A myeloproliferative disorder may hide another
one. Leuk Res. 33:1133–1136. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
4
|
Tam CS, Nussenzveig RM, Popat U,
Bueso-Ramos CE, Thomas DA, Cortes JA, Champlin RE, Ciurea SE,
Manshouri T, Pierce SM, et al: The natural history and treatment
outcome of blast phase BCR-ABL- myeloproliferative neoplasms.
Blood. 112:1628–1637. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
5
|
Abdel-Wahab O, Mullally A, Hedvat C,
Garcia-Manero G, Patel J, Wadleigh M, Malinge S, Yao J, Kilpivaara
O, Bhat R, et al: Genetic characterization of TET1, TET2, and TET3
alterations in myeloid malignancies. Blood. 114:144–147. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
6
|
Campbell PJ and Green AR: The
myeloproliferative disorders. N Engl J Med. 355:2452–2466. 2006.
View Article : Google Scholar : PubMed/NCBI
|
|
7
|
Baxter EJ, Scott LM, Campbell PJ, East C,
Fourouclas N, Swanton S, Vassiliou GS, Bench AJ, Boyd EM and Curtin
N: Cancer Genome Project: Acquired mutation of the tyrosine kinase
JAK2 in human myeloproliferative disorders. Lancet. 365:1054–1061.
2005. View Article : Google Scholar : PubMed/NCBI
|
|
8
|
Kralovics R, Passamonti F, Buser AS, Teo
SS, Tiedt R, Passweg JR, Tichelli A, Cazzola M and Skoda RC: A
gain-of-function mutation of JAK2 in myeloproliferative disorders.
N Engl J Med. 352:1779–1790. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
9
|
Levine RL, Wadleigh M, Cools J, Ebert BL,
Wernig G, Huntly BJ, Boggon TJ, Wlodarska I, Clark JJ, Moore S, et
al: Activating mutation in the tyrosine kinase JAK2 in polycythemia
vera, essential thrombocythemia, and myeloid metaplasia with
myelofibrosis. Cancer Cell. 7:387–397. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
10
|
Zhao R, Xing S, Li Z, Fu X, Li Q, Krantz
SB and Zhao ZJ: Identification of an acquired JAK2 mutation in
polycythemia vera. J Biol Chem. 280:22788–22792. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
11
|
James C, Ugo V, Le Couédic JP, Staerk J,
Delhommeau F, Lacout C, Garçon L, Raslova H, Berger R,
Bennaceur-Griscelli A, et al: A unique clonal JAK2 mutation leading
to constitutive signalling causes polycythaemia vera. Nature.
434:1144–1148. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
12
|
Pradhan A, Lambert QT, Griner LN and
Reuther GW: Activation of JAK2-V617F by components of heterodimeric
cytokine receptors. J Biol Chem. 285:16651–16663. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
13
|
Dahabreh IJ, Giannouli S, Zoi C, Zoi K,
Voulgarelis M and Moutsopoulos HM: Management of hypereosinophilic
syndrome: A prospective study in the era of molecular genetics.
Medicine (Baltimore). 86:344–354. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
14
|
Dahabreh IJ, Giannouli S, Zoi C, Zoi K,
Loukopoulos D and Voulgarelis M: Hypereosinophilic syndrome:
Another face of janus? Leuk Res. 32:1483–1485. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
15
|
Jones AV, Kreil S, Zoi K, Waghorn K,
Curtis C, Zhang L, Score J, Seear R, Chase AJ, Grand FH, et al:
Widespread occurrence of the JAK2 V617F mutation in chronic
myeloproliferative disorders. Blood. 106:2162–2168. 2005.
View Article : Google Scholar : PubMed/NCBI
|
|
16
|
Steensma DP, Dewald GW, Lasho TL, Powell
HL, McClure RF, Levine RL, Gilliland DG and Tefferi A: The JAK2
V617F activating tyrosine kinase mutation is an infrequent event in
both ‘atypical myeloproliferative disorders and myelodysplastic
syndromes. Blood. 106:1207–1209. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
17
|
Tefferi A and Vardiman JW: Classification
and diagnosis of myeloproliferative neoplasms: The 2008 World
Health Organization criteria and point-of-care diagnostic
algorithms. Leukemia. 22:14–22. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
18
|
Baker SJ, Rane SG and Reddy EP:
Hematopoietic cytokine receptor signaling. Oncogene. 26:6724–6737.
2007. View Article : Google Scholar : PubMed/NCBI
|
|
19
|
Morgan KJ and Gilliland DG: A role for
JAK2 mutations in myeloproliferative diseases. Annu Rev Med.
59:213–222. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
20
|
Wernig G, Mercher T, Okabe R, Levine RL,
Lee BH and Gilliland DG: Expression of Jak2V617F causes a
polycythemia vera-like disease with associated myelofibrosis in a
murine bone marrow transplant model. Blood. 107:4274–4281. 2006.
View Article : Google Scholar : PubMed/NCBI
|
|
21
|
Lacout C, Pisani DF, Tulliez M, Gachelin
FM, Vainchenker W and Villeval JL: JAK2V617F expression in murine
hematopoietic cells leads to MPD mimicking human PV with secondary
myelofibrosis. Blood. 108:1652–1660. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
22
|
Tiedt R, Hao-Shen H, Sobas MA, Looser R,
Dirnhofer S, Schwaller J and Skoda RC: Ratio of mutant JAK2-V617F
to wild-type Jak2 determines the MPD phenotypes in transgenic mice.
Blood. 111:3931–3940. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
23
|
Shide K, Shimoda HK, Kumano T, Karube K,
Kameda T, Takenaka K, Oku S, Abe H, Katayose KS, Kubuki Y, et al:
Development of ET, primary myelofibrosis and PV in mice expressing
JAK2 V617F. Leukemia. 22:87–95. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
24
|
Steensma DP, McClure RF, Karp JE, Tefferi
A, Lasho TL, Powell HL, DeWald GW and Kaufmann SH: JAK2 V617F is a
rare finding in de novo acute myeloid leukemia, but STAT3
activation is common and remains unexplained. Leukemia. 20:971–978.
2006. View Article : Google Scholar : PubMed/NCBI
|
|
25
|
Vizmanos JL, Ormazábal C, Larráyoz MJ,
Cross NC and Calasanz MJ: JAK2 V617F mutation in classic chronic
myeloproliferative diseases: A report on a series of 349 patients.
Leukemia. 20:534–535. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
26
|
Akada H, Yan D, Zou H, Fiering S,
Hutchison RE and Mohi MG: Conditional expression of heterozygous or
homozygous Jak2V617F from its endogenous promoter induces a
polycythemia vera-like disease. Blood. 115:3589–3597. 2010.
View Article : Google Scholar : PubMed/NCBI
|
|
27
|
Choi S-E, Hong SW and Yoon SO: Proposal of
an appropriate decalcification method of bone marrow biopsy
specimens in the era of expanding genetic molecular study. J Pathol
Transl Med. 49:236–242. 2015. View Article : Google Scholar : PubMed/NCBI
|
|
28
|
Dziaman T, Ludwiczak H, Ciesla JM,
Banaszkiewicz Z, Winczura A, Chmielarczyk M, Wisniewska E,
Marszalek A, Tudek B and Olinski R: PARP-1 expression is increased
in colon adenoma and carcinoma and correlates with OGG1. PLoS One,.
9:e1155582014. View Article : Google Scholar
|
|
29
|
Burduk PK, Bodnar M, Sawicki P, Szylberg
Ł, Wiśniewska E, Kaźmierczak W, Martyńska M and Marszałek A:
Expression of metalloproteinases 2 and 9 and tissue inhibitors 1
and 2 as predictors of lymph node metastases in oropharyngeal
squamous cell carcinoma. Head Neck. 37:418–422. 2015. View Article : Google Scholar : PubMed/NCBI
|
|
30
|
Remmele W and Stegner HE: Recommendation
for uniform definition of an immunoreactive score (IRS) for
immunohistochemical estrogen receptor detection (ER-ICA) in breast
cancer tissue. Pathologe. 8:138–140. 1987.(In German). PubMed/NCBI
|
|
31
|
Pfaffl MW: A new mathematical model for
relative quantification in real-time RT-PCR. Nucleic Acids Res.
29:e452001. View Article : Google Scholar : PubMed/NCBI
|
|
32
|
Sidon P, El Housni H, Dessars B and
Heimann P: The JAK2V617F mutation is detectable at very low level
in peripheral blood of healthy donors. Leukemia. 20:16222006.
View Article : Google Scholar : PubMed/NCBI
|
|
33
|
Scott LM, Tong W, Levine RL, Scott MA,
Beer PA, Stratton MR, Futreal PA, Erber WN, McMullin MF, Harrison
CN, et al: JAK2 exon 12 mutations in polycythemia vera and
idiopathic erythrocytosis. N Engl J Med. 356:459–468. 2007.
View Article : Google Scholar : PubMed/NCBI
|
|
34
|
Pikman Y, Lee BH, Mercher T, McDowell E,
Ebert BL, Gozo M, Cuker A, Wernig G, Moore S, Galinsky I, et al:
MPLW515L is a novel somatic activating mutation in myelofibrosis
with myeloid metaplasia. PLoS Med. 3:e2702006. View Article : Google Scholar : PubMed/NCBI
|
|
35
|
Pardanani A, Lasho TL, Finke C, Hanson CA
and Tefferi A: Prevalence and clinicopathologic correlates of JAK2
exon 12 mutations in JAK2V617F-negative polycythemia vera.
Leukemia. 21:1960–1963. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
36
|
Pardanani AD, Levine RL, Lasho T, Pikman
Y, Mesa RA, Wadleigh M, Steensma DP, Elliott MA, Wolanskyj AP,
Hogan WJ, et al: MPL515 mutations in myeloproliferative and other
myeloid disorders: A study of 1182 patients. Blood. 108:3472–3476.
2006. View Article : Google Scholar : PubMed/NCBI
|
|
37
|
Chaligné R, Tonetti C, Besancenot R, Roy
L, Marty C, Mossuz P, Kiladjian JJ, Socié G, Bordessoule D, Le
Bousse-Kerdilès MC, et al: New mutations of MPL in primitive
myelofibrosis: Only the MPL W515 mutations promote a G1/S-phase
transition. Leukemia. 22:1557–1566. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
38
|
Beer PA, Campbell PJ, Scott LM, Bench AJ,
Erber WN, Bareford D, Wilkins BS, Reilly JT, Hasselbalch HC, Bowman
R, et al: MPL mutations in myeloproliferative disorders: Analysis
of the PT-1 cohort. Blood. 112:141–149. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
39
|
Boyd EM, Bench AJ, Goday-Fernández A,
Anand S, Vaghela KJ, Beer P, Scott MA, Bareford D, Green AR, Huntly
B, et al: Clinical utility of routine MPL exon 10 analysis in the
diagnosis of essential thrombocythaemia and primary myelofibrosis.
Br J Haematol. 149:250–257. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
40
|
Michiels JJ, Valster F, Wielenga J,
Schelfout K and De Raeve H: European vs 2015-World Health
Organization clinical molecular and pathological classification of
myeloproliferative neoplasms. World J Hematol. 4:16–53. 2015.doi:
10.5315/wjh.v4.i3.16. View Article : Google Scholar
|
|
41
|
Pasquier F, Cabagnols X, Secardin L, Plo I
and Vainchenker W: Myeloproliferative neoplasms: JAK2 signaling
pathway as a central target for therapy. Clin Lymphoma Myeloma
Leuk. 14:(Suppl). S23–S35. 2014. View Article : Google Scholar : PubMed/NCBI
|
|
42
|
Ihle JN and Gilliland DG: Jak2: Normal
function and role in hematopoietic disorders. Curr Opin Genet Dev.
17:8–14. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
43
|
Ihle JN: STATs: Signal transducers and
activators of transcription. Cell. 84:331–334. 1996. View Article : Google Scholar : PubMed/NCBI
|
|
44
|
Pircher TJ, Flores-Morales A, Mui AL,
Saltiel AR, Norstedt G, Gustafsson JA and Haldosén LA:
Mitogen-activated protein kinase kinase inhibition decreases growth
hormone stimulated transcription mediated by STAT5. Mol Cell
Endocrinol. 133:169–176. 1997. View Article : Google Scholar : PubMed/NCBI
|
|
45
|
Pircher TJ, Petersen H, Gustafsson JA and
Haldosén LA: Extracellular signal-regulated kinase (ERK) interacts
with signal transducer and activator of transcription (STAT) 5a.
Mol Endocrinol. 13:555–565. 1999. View Article : Google Scholar : PubMed/NCBI
|
|
46
|
Verstovsek S, Manshouri T, Quintás-Cardama
A, Harris D, Cortes J, Giles FJ, Kantarjian H, Priebe W and Estrov
Z: WP1066, a novel JAK2 inhibitor, suppresses proliferation and
induces apoptosis in erythroid human cells carrying the JAK2 V617F
mutation. Clin Cancer Res. 14:788–796. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
47
|
Aboudola S, Murugesan G, Szpurka H,
Ramsingh G, Zhao X, Prescott N, Tubbs RR, Maciejewski JP and Hsi
ED: Bone marrow phospho-STAT5 expression in non-CML chronic
myeloproliferative disorders correlates with JAK2 V617F mutation
and provides evidence of in vivo JAK2 activation. Am J Surg Pathol.
31:233–239. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
48
|
Nyga R, Pecquet C, Harir N, Gu H,
Dhennin-Duthille I, Régnier A, Gouilleux-Gruart V, Lassoued K and
Gouilleux F: Activated STAT5 proteins induce activation of the PI
3-kinase/Akt and Ras/MAPK pathways via the Gab2 scaffolding
adapter. Biochem J. 390:359–366. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
49
|
Rosa Santos SC, Dumon S, Mayeux P,
Gisselbrecht S and Gouilleux F: Cooperation between STAT5 and
phosphatidylinositol 3-kinase in the IL-3-dependent survival of a
bone marrow derived cell line. Oncogene. 19:1164–1172. 2000.
View Article : Google Scholar : PubMed/NCBI
|
|
50
|
Gibson SE, Schade AE, Szpurka H, Bak B,
Maciejewski JP and Hsi ED: Phospho-STAT5 expression pattern with
the MPL W515L mutation is similar to that seen in chronic
myeloproliferative disorders with JAK2 V617F. Hum Pathol.
39:1111–1114. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
51
|
Grimwade LF, Happerfield L, Tristram C,
McIntosh G, Rees M, Bench AJ, Boyd EM, Hall M, Quinn A, Piggott N,
et al: Phospho-STAT5 and phospho-Akt expression in chronic
myeloproliferative neoplasms. Br J Haematol. 147:495–506. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
52
|
Levy DE and Darnell JE Jr: Stats:
Transcriptional control and biological impact. Nat Rev Mol Cell
Biol. 3:651–662. 2002. View
Article : Google Scholar : PubMed/NCBI
|
