{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T09:36:30Z","timestamp":1787564190795,"version":"build-2736575974"},"reference-count":44,"publisher":"Akademiai Kiado Zrt.","issue":"23","license":[{"start":{"date-parts":[[2024,6,9]],"date-time":"2024-06-09T00:00:00Z","timestamp":1717891200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.akjournals.com"],"crossmark-restriction":true},"short-container-title":["OH"],"published-print":{"date-parts":[[2024,6,9]]},"abstract":"<jats:p>\n                    A JAK-kin\u00e1z m\u0171k\u00f6d\u00e9se egyes, sejtfelsz\u00edni receptorokhoz k\u00f6t\u00f6tt jel\u00e1tviteli\n                    \u00fatvonalak k\u00f6zponti eleme (JAK\/STAT \u00fatvonal), a fiziol\u00f3gi\u00e1s sejtaktiv\u00e1ci\u00f3\n                    k\u00f6zvet\u00edt\u0151je. K\u00f6zvet\u00edt\u0151 hat\u00e1sa a myeloid eredet\u0171 sejtekben, els\u0151sorban\n                    macrophagokban, neutrophil granulocyt\u00e1kban, illetve a thrombocyt\u00e1kban is\n                    sz\u00fcks\u00e9ges a nem specifikus gyullad\u00e1sos reakci\u00f3 elind\u00edt\u00e1s\u00e1hoz. A jel\u00e1tviteli\n                    \u00fatvonal k\u00f3ros aktiv\u00e1ci\u00f3ja a kr\u00f3nikus myeloproliferativ neoplasi\u00e1kban az egyik\n                    leggyakoribb genetikai elt\u00e9r\u00e9s \u00e9s a fokozott myelo- \u00e9s thrombopoesis egyik j\u00f3l\n                    ismert \u2019driver\u2019 mechanizmusa. A myeloproliferativ neoplasi\u00e1k diagnosztik\u00e1j\u00e1hoz a\n                    szerzett patog\u00e9n\n                    <jats:italic>JAK2<\/jats:italic>\n                    -mut\u00e1ci\u00f3k (els\u0151sorban a\n                    <jats:italic>V617F<\/jats:italic>\n                    vari\u00e1ns) kimutat\u00e1sa is hozz\u00e1tartozik. Ismertt\u00e9 v\u00e1lt\n                    ugyanakkor, hogy a g\u00e9nhiba \u2013 m\u00e1s, ritk\u00e1bb elt\u00e9r\u00e9sek mellett \u2013 ak\u00e1r hossz\u00fa ideig\n                    fenn\u00e1llhat jelent\u0151s hematol\u00f3giai elt\u00e9r\u00e9sek n\u00e9lk\u00fcl. Ezt az \u00e1llapotot klon\u00e1lis\n                    haemopoesisnek nevezik. A vari\u00e1ns\n                    <jats:italic>JAK2<\/jats:italic>\n                    \u00fajabb megfigyel\u00e9sek\n                    szerint a myeloid eredet\u0171 sejtek funkci\u00f3j\u00e1ra ebben a helyzetben is komoly\n                    aktiv\u00e1l\u00f3 hat\u00e1st fejthet ki, \u00e9s meggy\u0151z\u0151 \u00f6sszef\u00fcgg\u00e9seket mutattak ki a\n                    gyullad\u00e1sos h\u00e1tt\u00e9rrel rendelkez\u0151 cardiovascularis sz\u00f6v\u0151dm\u00e9nyekkel kapcsolatosan.\n                    A klon\u00e1lis\n                    <jats:italic>JAK2<\/jats:italic>\n                    -elt\u00e9r\u00e9s, valamint az ischaemi\u00e1s sz\u00edvbetegs\u00e9g,\n                    illetve a hasi aortaaneurysma kialakul\u00e1sa k\u00f6z\u00f6tt is jelent\u0151s \u00f6sszef\u00fcgg\u00e9sek\n                    m\u00e9rhet\u0151k. M\u00e1ra egy\u00e9rtelm\u0171, hogy az atheromak\u00e9pz\u0151d\u00e9s \u00e9s a k\u00f6vetkezm\u00e9nyes\n                    coronariasclerosis kialakul\u00e1sa egy komplex thromboinflammatoricus folyamat\n                    k\u00f6vetkezm\u00e9nye, \u00e9s jelent\u0151s m\u00e9rt\u00e9kben f\u00fcgg t\u00f6bbek k\u00f6z\u00f6tt a\n                    <jats:italic>JAK2<\/jats:italic>\n                    medi\u00e1lta sz\u00f6veti macrophag\u2013granulocyta interakci\u00f3kt\u00f3l. K\u00f6zlem\u00e9ny\u00fcnkben a\n                    fokozott kock\u00e1zat h\u00e1tter\u00e9ben h\u00faz\u00f3d\u00f3 mechanizmusokat \u00e9s a rendelkez\u00e9sre \u00e1ll\u00f3\n                    leg\u00fajabb ismereteket elemezz\u00fck. Orv Hetil. 2024; 165(23): 883\u2013890.\n                  <\/jats:p>","DOI":"10.1556\/650.2024.33055","type":"journal-article","created":{"date-parts":[[2024,6,9]],"date-time":"2024-06-09T11:26:48Z","timestamp":1717932408000},"page":"883-890","update-policy":"https:\/\/doi.org\/10.1556\/policypage.crossmark.crossref.2","source":"Crossref","is-referenced-by-count":1,"title":["A JAK2 szomatikus g\u00e9nmut\u00e1ci\u00f3 lehets\u00e9ges betegs\u00e9gm\u00f3dos\u00edt\u00f3 hat\u00e1sa a cardiovascularis k\u00f3rk\u00e9pek kialakul\u00e1s\u00e1ban"],"prefix":"10.1556","volume":"165","author":[{"given":"Eszter","family":"Magyar","sequence":"first","affiliation":[{"name":"Debreceni Egyetem, \u00c1ltal\u00e1nos Orvostudom\u00e1nyi Kar, Patol\u00f3giai Int\u00e9zet Debrecen, Nagyerdei krt. 98., 4032 Magyarorsz\u00e1g"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anik\u00f3","family":"\u00dajfalusi","sequence":"additional","affiliation":[{"name":"Debreceni Egyetem, \u00c1ltal\u00e1nos Orvostudom\u00e1nyi Kar, Laborat\u00f3riumi Medicina Int\u00e9zet Budapest Magyarorsz\u00e1g"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marianna","family":"Czenke","sequence":"additional","affiliation":[{"name":"Debreceni Egyetem, \u00c1ltal\u00e1nos Orvostudom\u00e1nyi Kar, Patol\u00f3giai Int\u00e9zet Debrecen, Nagyerdei krt. 98., 4032 Magyarorsz\u00e1g"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G\u00e1bor","family":"M\u00e9hes","sequence":"additional","affiliation":[{"name":"Debreceni Egyetem, \u00c1ltal\u00e1nos Orvostudom\u00e1nyi Kar, Patol\u00f3giai Int\u00e9zet Debrecen, Nagyerdei krt. 98., 4032 Magyarorsz\u00e1g"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"425","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Vainchenker W, Constantinescu SN. 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Semin Diagn Pathol. 2023; 40:\n                    187\u2013194.","DOI":"10.1053\/j.semdp.2023.04.007"},{"key":"R8","unstructured":"Rajnai H, B\u00f6d\u00f6r Cs, Reiniger L, et al. Novel method in diagnosis of\n                    chronic myeloproliferative disorders \u2013 detection of JAK2\n                    mutation. [\u00daj lehet\u0151s\u00e9g a kr\u00f3nikus myeloproliferativ betegs\u00e9gek\n                    diagnosztik\u00e1j\u00e1ban \u2013 a JAK2 mut\u00e1ci\u00f3 kimutat\u00e1sa.] Orv Hetil.\n                    2006; 147: 2175\u20132179. [Hungarian]"},{"key":"R9","doi-asserted-by":"crossref","unstructured":"Andrikovics H, Szilv\u00e1si A, Meggyesi N, et al. Role of the activating\n                    mutation Val617Phe of Janus kinase 2 gene in myeloproliferative diseases and\n                    significance of its detection. [A 2-es t\u00edpus\u00fa Janus tirozin kin\u00e1z Val617Phe\n                    aktiv\u00e1l\u00f3 pontmut\u00e1ci\u00f3 szerepe \u00e9s kimutat\u00e1s\u00e1nak jelent\u0151s\u00e9ge myeloproliferat\u00edv\n                    szindr\u00f3m\u00e1ban.] Orv Hetil. 2007; 148: 203\u2013210. [Hungarian]","DOI":"10.1556\/OH.2007.27860"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Iv\u00e1nyi JL, Marton, E, Plander M. Significance of the\n                        JAK2V617F mutation in patients with chronic\n                    myeloproliferative neoplasia. [A JAK2V617F-mut\u00e1ci\u00f3\n                    jelent\u0151s\u00e9ge kr\u00f3nikus myeloproliferativ neoplasi\u00e1s betegeinkben.] Orv Hetil.\n                    2011; 152: 1795\u2013803. [Hungarian]","DOI":"10.1556\/OH.2011.29226"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Dombi P, Ill\u00e9s \u00c1, Demeter J, et al. Hungarian Philadelphia negative\n                    chronic myeloproliferative neoplasia registry. Evaluation of the polycythemia\n                    vera patients. [Philadelphia-negat\u00edv kr\u00f3nikus Myeloproliferativ Neoplasia\n                    Magyarorsz\u00e1gi Regiszter. Polycythaemia ver\u00e1s betegeink adatainak elemz\u00e9se.] Orv\n                    Hetil. 2017; 158: 901\u2013909. [Hungarian]","DOI":"10.1556\/650.2017.30766"},{"key":"R12","doi-asserted-by":"crossref","unstructured":"Perner F, Perner C, Ernst T, et al. Roles of JAK2\n                    in aging, inflammation, hematopoiesis and malignant transformation. Cells 2019;\n                    8: 854.","DOI":"10.3390\/cells8080854"},{"key":"R13","doi-asserted-by":"crossref","unstructured":"Satriotomo I, Bowen KK, Vemuganti R. JAK2 and STAT3 activation\n                    contributes to neuronal damage following transient focal cerebral ischemia. 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