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Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders
Open accessAbstract
The analysis of rare chromosomal translocations in myeloproliferative disorders has highlighted the importance of aberrant tyrosine kinase signaling in the pathogenesis of these diseases. Here we have investigated samples from 679 patients and controls for the nonreceptor tyrosine kinase JAK2 V617F mutation. Of the 480 myeloproliferative disorder (MPD) samples, the proportion of positive cases per disease subtype was 30 (20%) of 152 for atypical or unclassified MPD, 2 of 134 (2%) for idiopathic hypereosinophilic syndrome, 58 of 72 (81%) for polycythemia vera, 24 of 59 (41%) essential thrombocythemia (ET), and 15 of 35 (43%) for idiopathic myelofibrosis. V617F was not identified in patients with systemic mastocytosis (n = 28), chronic or acute myeloid leukemia (n = 35), secondary erythrocytosis (n = 4), or healthy controls (n = 160). Homozygosity for V617F was seen in 43% of mutant samples and was closely correlated with chromosome 9p uniparental disomy. Homozygosity was significantly less common in ET compared with other MPD subtypes. In 53 cases analyzed, the median level of PRV1 expression was significantly higher in V617F-positive cases compared with cases without the mutation. We conclude that V617F is widespread in MPDs. Detection of this acquired mutation is likely to have a major impact on the way patients with MPD are diagnosed, as well as serving as an obvious target for signal transduction therapy.
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“Activation of JAK2 caused by this mutation leads to constitutive activation of STAT3 and is associated with reduced survival in idiopathic myelofibrosis.54,55”
From Critical analysis of the potential for targeting STAT3 in human malignancy (2013) · cites this paper as [52]
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Cited by
Sorted by citations
Items 601–700 of 762
Chen, Y., Zhao, H., Luo, J., Liao, Y.-P., Tan, K., & Hu, G.-Y. (2021) · Oncology Letters · doi:10.3892/ol.2021.12612 · Cited by 3
Trifa, A., Lighezan, D., Jucan, C., Tripon, F., Arbore, D. R., Bojan, A., Gligor-Popa, Ș., Pop, R., Dima, D., & Bănescu, C. (2020) · doi:10.2478/rrlm-2020-0025 · Cited by 3
“a tetra-primer PCR until 2015, or detected and quantified using a real-time PCR assay thereafter (23,24).”
MethodMousinho, F., Santos, P. S. E., Azevedo, A., Pereira, J., Lemos, R., Matos, S., Viana, J., & Lima, F. (2018) · Molecular and clinical oncology · doi:10.3892/mco.2018.1682 · Cited by 3
“MPNs represent a group of heterogeneous chronic conditions, in which the main picture is characterized by medullary proliferation of at least one myeloid lineage, and increased number of mostly mature elements in the peripheral blood (7).”
Chen, Y., Han, X., Wang, F., Bai, B.-B., & Wang, Y. (2017) · Internal medicine journal (Print) · doi:10.1111/imj.13407 · Cited by 3
The JAK2V617F mutation in normal individuals takes place in differentiating cells.
Krichevsky, S., Prus, E., Perlman, R., Fibach, E., & Ben-yehuda, D. (2017) · Blood Cells, Molecules & Diseases · doi:10.1016/j.bcmd.2017.01.001 · Cited by 3
Park, S., & Ha, J.-S. (2015) · International Journal of Laboratory Hematology · doi:10.1111/ijlh.12328 · Cited by 3
“The unique somatic point mutation, Janus kinase 2 (JAK2) V617F, was discovered in MPNs, and >95% PV cases and approximately 60% of ET and PMF patients harbor this JAK2 mutation, which affects the JAK-signal transducers and activators of transcription (STAT) signaling pathway [2].”
BackgroundGorukmez, O., Sag, S., Görükmez, Ö., Ture, M., Topak, A., Sahinturk, S., Ozkaya, G., Gulten, T., Ali, R., & Yakut, T. (2015) · Genetic Testing and Molecular Biomarkers · doi:10.1089/gtmb.2014.0334 · Cited by 3
“Polycythemia vera (PV), essential thrombocytosis (ET), and primary myelofibrosis are the most common BCR-ABL fusion gene-negative myeloproliferative neoplasms (Jones et al. , 2005).”
Decreased expression of PIAS1 and PIAS3 in essential thrombocythemia patients.
Hsiao, H., Liu, Y.-C., Yang, M.-Y., Tsai, Y.-F., Liu, T.-C., Chang, C.-C., & Lin, S.-K. (2013) · Genetics and Molecular Research · doi:10.4238/2013.november.18.10 · Cited by 3
“The JAK2V617F mutation was identified by the amplification refractory mutation system (ARMS) (Jones et al., 2005).”
BackgroundMethodRole of Signaling Pathways in Acute Myeloid Leukemia
Abdullah, M., & Sem, Z. (2011) · InTech eBooks · doi:10.5772/39093 · Cited by 4
“(Jones et al., 2005).”
JAK2 mutations in myeloproliferative neoplasms
Gangat, N., & Tefferi, A. (2011) · doi:10.4267/2042/44548 · Cited by 3
“JAK2 exon 12 mutations A small proportion of patients with PV are JAK2V617F negative when tested by sensitive allelespecific assays (Jones et al., 2005).”
Kreft, A., Kindler, T., Springer, E., & Kirkpatrick, C. (2011) · Virchows Archiv · doi:10.1007/s00428-011-1154-2 · Cited by 3
“In contrast to bcr– abl, the JAK2 mutation does not result in a distinct entity or phenotype but can be detected in the three most common Ph-negative MPNs with different frequencies; as a constant finding in polycythemia vera (PV) and in about half of the patients with essential thrombocythaemia (ET) and primary myelo…”
BackgroundSpasovski, V., Tošić, N., Kostić, T., Pavlovic, S., & Čolović, M. (2010) · Srpski Arhiv za Celokupno Lekarstvo · doi:10.2298/sarh1010614s · Cited by 3
Molecular characterization of chronic myeloproliferative neoplasias in México
Ruiz-Argüelles, G., Garcés‐Eisele, J., Ortíz-López, R., Rivas-Llamas, R., Gómez-Almaguer, D., & Ruiz-Delgado, G. (2009) · Hematology · doi:10.1179/102453309x439836 · Cited by 3
Phenotype and genotype in the myeloproliferative disorders
Spivak, J. L. (2007) · European journal of haematology. Supplementum · doi:10.1111/j.1600-0609.2007.00936.x · Cited by 3
“These findings were consistent with other studies suggesting that JAK2 V617F is observed with the greatest frequency in PV (12).”
ResultTefferi, A. (2006) · Current Hematologic Malignancy Reports · doi:10.1007/s11899-006-0027-2 · Cited by 3
Quantification of clonal hematopoiesis in polycythemia vera
Siebolts, U., Ateş, M., Spitz, R., Thiele, J., & Wickenhauser, C. (2005) · Virchows Archiv · doi:10.1007/s00428-005-0047-7 · Cited by 3
Altomare, I., & Kessler, C. (2019) · Consultative Hemostasis and Thrombosis · doi:10.1016/b978-0-323-46202-0.00019-4 · Cited by 3
The Frequency Of JAK2 V617F Gen Mutation And Its Associations With Whole Blood Count Parameters
Ünal, K., Erdoğan, S., & Yilmaz, F. (2014) · doi:10.5505/tjb.2014.39206 · Cited by 3
“Daha önce yayınlanmış çalışmalarda, JAK2 V617F mutasyon sıklığı PV olan hastalar için % 95, ET ve PMF için % 40-50 olarak belirlenmiştir [11].”
BackgroundInfluentialMolecular Testing in Hematologic Malignancies
Behdad, A., Betz, B. L., Lim, M. S., & Bailey, N. G. (2014) · Springer eBooks · doi:10.1007/978-1-4899-8050-2_10 · Cited by 1
The Role of Janus Kinase 2 (JAK2) in the Pathologenesis of Myeloproliferative Disorders
Gari, M. A. (2009) · Journal of King Abdulaziz University-Medical Sciences · doi:10.4197/med.16-1.1 · Cited by 2
“Although, most patients with PV are JAK2 V617F are positive when assessed using appropriately sensitive allele-specific assays, a small proportion of patients with PV are negative for the JAK2 V617F allele([10,19,20,52]).”
BackgroundOncogenic signals as treatment targets in classic myeloproliferative neoplasms.
Tefferi, A., Levine, R., & Kantarjian, H. (2009) · Biology of Blood and Marrow Transplantation · doi:10.1016/j.bbmt.2008.10.010 · Cited by 3
“Subsequently, the mutation has also described in other myeloid neoplasms [65,66].”
BackgroundSyeed, N. (2019) · Asian Pacific Journal of Cancer Prevention · doi:10.31557/apjcp.2019.20.12.3611 · Cited by 2
Naumann, N., Dangelo, V., Lübke, J., Bresser, J., Hagen, V. A., Dengler, J. B., Metzgeroth, G., Kreil, S., Hockenberger, T., Hofmann, W., et al. (2025) · Scientific Reports · doi:10.1038/s41598-025-11096-6 · Cited by 2
“Initial cytogenetic and/or FISH analysis revealed a typical t(9;22)(q34;q11) in 2/5 patients (#4, #5) and an atypical karyotype in 3/5 patients (#1: 46,XX[31]; #2: 46,XY,−5,+mar[2]/46,XY[15]; #3: 46,XY, der(11)t(9;11)(p21;p15)[7]/46,XY[8]).”
Khazeem, M., & Alwan, A. F. (2025) · Journal of Applied Hematology · doi:10.4103/joah.joah_42_25 · Cited by 2
Khazeem, M., & Alwan, A. F. (2024) · Iraqi Journal of Hematology · doi:10.4103/ijh.ijh_46_24 · Cited by 2
Carretta, C., Parenti, S., Bertesi, M., Rontauroli, S., Badii, F., Tavernari, L., Genovese, E., Malerba, M., Papa, E., Sperduti, S., et al. (2024) · Leukemia · doi:10.1038/s41375-024-02373-w · Cited by 2
Safavi, M., Monabati, A., Safaei, A., Mirtalebi, M., & Faghih, M. (2021) · Iranian Journal of Pathology · doi:10.30699/ijp.2021.136458.2495 · Cited by 2
“MPL is the receptor of thrombopoietin and has a pivotal role in megakaryopoiesis and platelet production (1-5).”
BackgroundOptimization of a Low-Cost, Sensitive PNA Clamping PCR Method for JAK2 V617F Variant Detection.
Francia, R. D., Crisci, S., Muto, T., Giancola, C., Petriccone, L., Catapano, O., Cummarro, A., Pinto, A., & Frigeri, F. (2020) · The Journal of Applied Laboratory Medicine · doi:10.1093/jalm/jfaa041 · Cited by 2
Chatterjee, T., & Ahuja, A. (2018) · Indian Journal of Hematology and Blood Transfusion · doi:10.1007/s12288-017-0913-x · Cited by 2
Hipk is required for JAK/STAT activity and promotes hemocyte-derived tumorigenesisPreprint
Blaquiere, J., Wray, N., & Verheyen, E. (2016) · bioRxiv · doi:10.1101/058156 · Cited by 2
“Dysregulation of the JAK/STAT pathway has been linked to leukemia, myeloproliferative neoplasms, and solid tumors in flies and vertebrates (Amoyel et al., 2014; Dearolf, 1998; Jones et al., 2005; Lacronique, 1997; Levine et al., 2005).”
BackgroundGenetically Engineered In Vitro Erythropoiesis
Geiler, C., Andrade, I., Clayton, A., & Greenwald, D. R. (2016) · International Journal of Stem Cells · doi:10.15283/ijsc.2016.9.1.53 · Cited by 3
“Patients with PV have a homozygous JAK2 V617F mutation, and patients with ET have a heterozygous mutation, indicating the dose dependent effect of the mutation (34).”
BackgroundBenguella-Benmansour, M., Boucherit, K., Benchikh, N., Mesli, N., Chabni, N., Messaoudi, A., Bekadja, A., Boucherit, Z., & Mozziconacci, M. (2014) · doi:10.1007/s12558-014-0304-7 · Cited by 2
Characteristics of the four subtypes of myelodysplastic/myeloproliferative neoplasms
Wu, H.-L., Bian, S., Chu, J., Zhong, X., Sun, H., Zhang, B.-C., & Lu, Z.-M. (2013) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2013.975 · Cited by 2
“as being positive in <20% of MDS/MPN patients (17); however, in this study, only one case was positive for the JAK2 gene among the five MDS/MPN cases.”
MGMT Gene Promoter Methylation Analysis by Pyrosequencing of Brain Tumour
Kim, Y. Z., Song, Y.-J., Kim, K. U., & Kim, D. C. (2011) · doi:10.4132/koreanjpathol.2011.45.5.455 · Cited by 2
JAK2 46/1 haplotype seems not to be associated with lower limb deep venous thrombosis.
Trifa, A., Criṣan, S., Popp, R., Cucuianu, A., & Buzoianu, A. (2010) · Blood Cells, Molecules & Diseases · doi:10.1016/j.bcmd.2010.07.004 · Cited by 2
Politou, M., Zoi, C., Dahabreh, I., Rallidis, L., Gialeraki, A., Loukopoulos, D., & Zoi, K. (2009) · Leukemia · doi:10.1038/leu.2008.368 · Cited by 2
“The JAK2 V617F mutation was detected using a tetra-primer amplification refractory mutation system (ARMS) polymerase chain reaction (PCR) assay with a sensitivity of 1p”
MethodSpanoudakis, E., Margaritis, D., Kotsianidis, I., Georgiou, G., Tripsianis, G., Anastasiadis, A., Karakolios, A., Pantelidou, D., Panayiotidis, P., Bourikas, G., et al. (2008) · Leukemia research : a Forum for Studies on Leukemia and Normal Hemopoiesis · doi:10.1016/j.leukres.2008.01.013 · Cited by 2
Manola, K., Stavropoulou, C., Georgakakos, V. N., Zoi, K., Fisfis, M., Evmorfiadis, I., Zoi, C., Pantelias, G., Stefanoudaki, K., & Sambani, C. (2007) · Leukemia research : a Forum for Studies on Leukemia and Normal Hemopoiesis · doi:10.1016/j.leukres.2006.11.014 · Cited by 2
Update on the treatment of polycythemia vera with recombinant interferon alfa or imatinib mesylate
Silver, R. (2007) · Current Hematologic Malignancy Reports · doi:10.1007/s11899-007-0006-2 · Cited by 2
“The recent finding of a molecular abnormality, the JAK2 V617F mutation, in more than 95% of patients with PV suggests that this mutation may be exploited in order to measure the response to rIFNB or imatinib of patients with PV, particularly those who have responded clinically [ 24 ].”
BackgroundChapter 25 – Molecular Hematopathology
Cook, J. (2009) · doi:10.1016/b978-044306901-7.50030-4 · Cited by 2
Germline predisposition in myeloproliferative neoplasms.
Chernoff, M., & Drazer, M. (2026) · Seminars in hematology (Print) · doi:10.1053/j.seminhematol.2026.06.006 · Cited by 1
Aci, R., Keskin, A., Sezer, Ö., Karakaya, T., Semiz, S., & Kızılet, H. (2025) · Scandinavian Journal of Clinical and Laboratory Investigation · doi:10.1080/00365513.2025.2502945 · Cited by 1
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Khazeem, M., & Alwan, A. F. (2024) · Journal of Applied Hematology · doi:10.4103/joah.joah_72_24 · Cited by 1
Crișan, A., Tripon, F., Bogliș, A., Crauciuc, G., Trifa, A., Lázár, E., Macarie, I., Gabor, M., & Bănescu, C. (2024) · Medicina · doi:10.3390/medicina60030506 · Cited by 1
“JAK2 V617F and CALR mutations were performed as presented in previous papers [7,49,50].”
MethodLigia, S., Scalzulli, E., Carmosino, I., Palumbo, G., Molinari, M. C., Poggiali, R., Costa, A., Bisegna, M., Martelli, M., & Breccia, M. (2024) · Frontiers in Oncology · doi:10.3389/fonc.2023.1338417 · Cited by 1
“Canonical JAK2 V617F and exon 12 mutations in MPNs are well described (1, 2).”
BackgroundA novel germline hyperactivating JAK2 mutation L604F
Dvořáček, L., Marková, J., Holoubek, A., Grebeňová, D., Kundrát, D., Kuželová, K., & Schwarz, J. (2023) · Annals of Hematology · doi:10.1007/s00277-023-05423-y · Cited by 1
Naseem, S., Binota, J., Varma, N., Satyarthi, P., Rana, P., & Malhotra, P. (2021) · Journal of Hematopathology · doi:10.1007/s12308-021-00462-8 · Cited by 1
“JAK2V617F mutation status was tested in all samples by amplification refractory mutation system PCR (ARMSPCR) [17].”
MethodKurtović-Kozarić, A., Islamagić, E., Ašić, A., Mehinovic-Cavcic, L., Bešić, L., Sahinbegovic, H., Komic, H., Kurtovic, S., & Burazerović, L. (2021) · Acta Medica Academica · doi:10.5644/ama2006-124.334 · Cited by 1
“(2005) involves two outer control primers (FO and RO) which are complementary to the region flanking exon 14 of the JAK2 gene, while the inner primers are complementary to the region flanking the G (in case of a wild-type sequence) or the T (in case of a mutation) (83).”
BackgroundPrevalence of JAK2 V617F Mutation in Iranian Patients with Myeloproliferative Neoplasms
Hamid, M., & Shahbazi, Z. (2020) · doi:10.22037/amls.v6.32758 · Cited by 1
“JAK2 V617F is occasionally detected in leukemia or other bone marrow disorders and related disease (7).”
BackgroundAtere, M., Al-Zakhari, R., Collins, J., Rotatori, F., & Muzangwa, L. (2020) · Case Reports in Oncological Medicine · doi:10.1155/2020/9654048 · Cited by 1
Khatamianfar, S., Akbari, M., Karizi, S. Z., & Deilamani, F. K. (2019) · doi:10.5812/jhgg.88293 · Cited by 1
Kajikawa, N., Seki, Y., Fujio, T., Okoshi, Y., Hori, M., Saito, H., Iijima, T., & Kojima, H. (2018) · Internal medicine · doi:10.2169/internalmedicine.1093-18 · Cited by 1
“The discovery of the JAK2 V617F mutation, which is detectable in more than 95% of patients with PV, has clarified the molecular pathogenesis of this disorder (1-5).”
BackgroundTefferi, A. (2017) · Holland‐Frei Cancer Medicine · doi:10.1002/9781119000822.hfcm123 · Cited by 2
Xu, N., Porter-Morgan, H., Doran, N., & Keller, C. (2016) · doi:10.5430/ijhe.v5n4p122 · Cited by 1
Estimate of JAK 2 V617F Mutation and Activity of Catalase Enzyme in Myeloproliferative Neoplasm
Abdullah, H., Saifullah, P., Shebib, Z. A., & Abdullah, A. (2016) · doi:10.22401/jnus.19.3.01 · Cited by 1
“& Amy; who found JAK2 V617F mutation are present (81%), (<90%) and (82%) in PV patients Consecutive [8],[16],[17].”
BackgroundInfluentialAdvances in the Diagnosis of Myeloproliferative Neoplasms
Jang, M.-A., & Choi, C. (2016) · doi:10.3904/kjm.2016.90.4.281 · Cited by 1
The Prevalence of JAK2-V617F Mutation in Sudanese Patients with Chronic Myeloproliferative Neoplasms
Abkar, H., Mohamed, B., & Hassan, F. (2016) · doi:10.9734/bjmmr/2016/24741 · Cited by 1
Melting curve アッセイとamplification refractory mutation system (ARMS)法によるJAK2 V617F変異の検出感度の比較
福塚, 勝., 竹岡, 加., 林田, 雅., 前川, ふ., 中村, 文., & 大野, 仁. (2013) · doi:10.12936/tenrikiyo.16-014 · Cited by 1
Effects of imatinib mesylate in patients with polycythemia vera: results of a phase II study
Merx, K., Fabarius, A., Erben, P., Griesshammer, M., Reiter, A., Hofmann, W., Hehlmann, R., Hochhaus, A., & Lengfelder, E. (2013) · Annals of Hematology · doi:10.1007/s00277-013-1725-1 · Cited by 1
Sholl, L., & Longtine, J. (2010) · Current Protocols in Human Genetics · doi:10.1002/0471142905.hg1004s67 · Cited by 1
“Because the V617F mutation is present in the vast majority of cases, it is amenable to targeted analysis using a simple and sensitive PCR approach (Jones et al., 2005)–amplification refractory mutation system (ARMS), a form of allele-specific PCR. NOTE: IPSOGEN (Marseilles, France) has developed a…”
BackgroundMethodBars, H. L., Boulland, M.-L., Bareau, B., Grosbois, B., Corolleur, M., Lamy, T., & Fardel, O. (2010) · International Journal of Laboratory Hematology · doi:10.1111/j.1751-553x.2010.01209.x · Cited by 1
“…status was initially assessed on peripheral blood granulocyte DNA using the qualitative amplification refractory mutation system PCR assay (Jones et al., 2005); diagnosis was available for 50 of these 58 patients (polycythemia vera, n = 31; essential thrombocythemia, n = 17; primary…”
MethodRole of IL12 Family in Regulation of Antitumor Immune Response
Dibra, D., & Li, S. (2009) · Springer eBooks · doi:10.1007/978-1-4419-0170-5_1
Myeloproliferative and Myelodysplastic/Myeloproliferative Neoplasms and Related Conditions
MBBS, F. B. J. B., Clark, M. D. M., & DM, B. S. W. (2009) · Bone Marrow Pathology · doi:10.1002/9781444309782.ch5 · Cited by 2
Melis, S., Vellinga, S., Zachée, P., Sierens, A., & Schouwer, P. D. (2009) · Acta Clinica Belgica · doi:10.1179/acb.2009.070 · Cited by 1
“Prior splenectomy In 2005, several groups described the presence of an acquired point mutation in the pseudokinase domain of Janus kinase 2 gene (JAK2 V617F) in patients suffering a myeloproliferative disorder(13-18).”
BackgroundMethodChronische Myeloproliferative Erkrankungen (CMPE)
Rechberger, E., Webersinke, G., & Petzer, A. (2008) · doi:10.1007/s11812-008-0036-2 · Cited by 1
Vaughan, B., Scott, M., Nacheva, E. P., & Howard, J. (2007) · Cancer Genetics and Cytogenetics · doi:10.1016/j.cancergencyto.2007.02.001 · Cited by 1
Myelodysplastic/Myeloproliferative Disorder Overlap Syndrome: How Should it be Approached?
Litzow, M. (2006) · doi:10.3816/clk.2006.n.014 · Cited by 1
Marie, I., & Hervé, F. (2006) · doi:10.1016/j.revmed.2006.02.011 · Cited by 1
V617F “JAKs” up myeloproliferative signal
Tefferi, A. (2005) · doi:10.1182/blood-2005-08-3352 · Cited by 1
Importance of molecular confirmation in the diagnosis of myeloproliferative disorders
Slater, D., Ronski, K., Delach, J. A., Benn, P., & Fang, M. (2005) · doi:10.1016/s1548-5315(11)70616-7 · Cited by 1
Molecular Testing in Myeloproliferative Neoplasms
Furtado, L. V., & Betz, B. (2017) · doi:10.1016/b978-0-12-800886-7.00034-0 · Cited by 1
Tuchayi, A. M., Sheth, S., & Smith, R. E. (2016) · doi:10.13188/2380-6842.1000014 · Cited by 1
“The JAK2 V617F point mutation has been reported in more than 90% of patients with polycythemia vera (PV) and approximately half of patients with primary myelofibrosis (PMF) and essential thrombocythemia (ET) [2-5].”
BackgroundPark, S., Kim, K., Lee, W., Ha, J., Ryoo, N., Jeon, D., Kim, J. R., Ham, J., Jang, S.-S., & Kim, Y. K. (2015) · doi:10.3343/lmo.2015.5.1.1 · Cited by 1
Bain, B. (2013) · doi:10.1002/9781444318470.ch5 · Cited by 1
Molecular Methods in Myeloproliferative Neoplasms
Leszczyńska, A., Prejzner, W., Bieniaszewska, M., & Hellmann, A. (2012) · Principles and practice · doi:10.1007/978-3-642-29467-9_28 · Cited by 1
“The most commonly used method in the routine laboratory setting is amplification refractory mutation system polymerase chain reaction (ARMS-PCR) (Jones et al. 2005; Chen et al. 2007).”
MethodPrinciples of Classification of Myeloid Neoplasms
Arber, D., & Vardiman, J. (2011) · doi:10.1016/b978-0-7216-0040-6.00043-5 · Cited by 1
Grützmann, R., & Pilarsky, C. (2010) · Methods in Molecular Biology · doi:10.1007/978-1-59745-545-9 · Cited by 1
The role of FasR/FasL system in pathogenesis of myeloprolyferative neoplasms
Spasovski, V., Tos̆ić, N., Kostić, T., Zukić, B., Stojiljković, M., Čolović, M., & Pavlović, S. (2010) · Archives of Biological Sciences · doi:10.2298/abs1002223s · Cited by 1
Mori, N., Yoshinaga, K., Tada, M., Wang, Y.-H., Shiseki, M., & Motoji, T. (2008) · doi:10.1590/s1415-47572008000300006 · Cited by 1
“Other recent studies found a similar incidence of the V617F mutation: 0/17 (Jones et al., 2005), 5/90 (6%) (Scott et al.”
BackgroundPolycythemia vera and other polycythemia syndromes.
Silver, R. (2008) · Cancer treatment and research · doi:10.1007/978-0-387-73744-7_1 · Cited by 1
Guru, S. A., Sumi, M. P., Mir, R., Waza, A. A., Bhat, M. A., Zuberi, M., Lali, P., & Saxena, A. (2020) · Human Cell · doi:10.1007/s13577-020-00370-6 · Cited by 16
S, M., H., Š., & M, P. (2014) · Balkan Journal of Medical Genetics · doi:10.2478/bjmg-2014-0026
Huang, J., Yin, X., Shi, X., Xiu-di, Y., Li, R., Zhang, X., Zhang, Y., Tong, H., Jin, J., & Huang, J. (2026) · Biomarker Research · doi:10.1186/s40364-026-01003-0
“Janus kinase 2 ( JAK2 ) driver mutations, especially JAK2 V617F , constitute a major molecular basis for MPNs [1–3].”
McCaul, N., Bingham, R. J., & Blann, A. D. (2026) · British Journal of Biomedical Science · doi:10.3389/bjbs.2025.14745
Research trends in essential thrombocythemia from 2001 to 2024: a bibliometric analysis
Pan, Y., Chen, L.-Y., Jiang, Q., Chen, D.-J., Wu, Y.-Q., Hou, L., Lang, H., & Yan, J. (2025) · Discover Oncology · doi:10.1007/s12672-025-02232-9
“Numerous groundbreaking studies have been featured in Blood , including but not limited to pivotal research on driver mutation [22, 23], key clinical data on ruxolitinib [24], and exploring best available therapies [25].”
Sayed, W. S., Al-bayati, A., Elzubair, L. G., Mohamed, S., & Alharthi, M. (2024) · Cureus · doi:10.7759/cureus.74401
Pai, U. K. N., Sankarankutti, R. T., Rafi, A., John, M. C., Raj, S., Earali, J., & Raveendran, S. (2024) · The Egyptian Journal of Haematology · doi:10.4103/ejh.ejh_63_24
Exogenous Janus Kinase 617 Codon Influences Small Noncoding RNAs and Gene Expression in Ba/F3 Cells.
Chen, Y.-Y., Wang, Y.-H., Chen, C.-C., Huang, C.-E., Hsu, C.-C., Hsiao, S.-H., & Leu, Y. (2024) · Journal of physiological investigation · doi:10.4103/ejpi.ejpi-d-24-00047
Sobieralski, P., Bieniaszewska, M., Bołkun, Ł., Sacha, T., Muzalewska-Wolska, M., Homenda, W., Bartkowiak, Ł. K., Smith, J., Rymko, M., Jachalska, A., et al. (2024) · Advances in Clinical and Experimental Medicine · doi:10.17219/acem/182857
Clinical significance of low level JAK2 V617F in peripheral blood testing
Rubic, M., Lee, L., & STEVENSON, W. C. (2024) · Pathology · doi:10.1016/j.pathol.2023.10.026
Erkal, O., Paksoy, B., & Patır, P. (2024) · Kocatepe Tıp Dergisi · doi:10.18229/kocatepetip.1254047
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“More than 95% of patients with PV and more than 50% of patients with ET and IMF have this mutation [10-13].”
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Elbager, S., Bayoumi, M., Tohit, E., Dowd, A., & Lai, M. (2020) · doi:10.21608/jbaar.2020.128502
“A. S., TEO, S. S., TIEDT, R., PASSWEG, J. R., TICHELLI, A., CAZZOLA, M. & SKODA, R. C. 2005.”
Cytogenetic evolution in myeloproliferative neoplasms with different molecular abnormalities.
Kim, S. Y., Koo, M., Park, Y., Kim, H., Choi, Q., Song, I., Jo, D., Kim, J., Kwon, G., & Koo, S. (2019) · Blood Cells, Molecules & Diseases · doi:10.1016/j.bcmd.2019.04.007
Metadata
- Authors
- Jones, A. V.
- Affiliations
- Cornell University (US)
- Corresponding author
- Jones, A. V.
- ORCID
- Jones, A. V.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2005-09-15
- Volume
- 106
- Issue
- 6
- Pages
- 2162-2168
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2126665281
- Cited by
- 843
- References
- 0
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 17 · 2023: 22 · 2022: 12 · 2021: 19 · 2020: 21 · 2019: 30 · 2018: 15 · 2017: 21 · 2016: 32 · 2015: 47 · 2014: 38 · 2013: 46 · 2012: 40
- FWCI
- 43.05
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Myeloproliferative Neoplasms: Diagnosis and Treatment
- Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- JAK2 V617F mutation, myeloproliferative neoplasms, polycythemia vera, essential thrombocythemia, primary myelofibrosis, idiopathic hypereosinophilic syndrome, tyrosine kinase signaling, mutation prevalence
- MeSH terms
- Chronic Disease, Female, Homozygote, Humans, Male, Myeloproliferative Disorders, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Signal Transduction, Prevalence, Case-Control Studies, Molecular Epidemiology, Microsatellite Repeats, Mutation, Missense, Janus Kinase 2
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