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Ansetzen am JAK-STAT-Signalweg in bösartigen und gutartigen Zellen in myeloproliferativen Neoplasmen
Date:6/14/2013

STOCKHOLM, June 14, 2013 /PRNewswire/ --

Dr. Ross Levine wird die Ergebnisse einer Studie zu einem Ansetzen am JAK-STAT-Signalweg in myeloproliferativen Neoplasmen vorstellen.

Myeloproliferative Neoplasmen (MPN) sind klonale Bluterkrankungen, die sich durch eine übermäßige Produktion reifer Blutzellen auszeichnen. Patienten zeigen eine vergrößerte Milz, systemische Symptome und hohe Werte zirkulierender inflammatorischer Zytokine. Die Identifizierung somatischer Mutationen in JAK2, MPL und LNK bei der Mehrheit der MPN-Patienten führte zur Entwicklung von JAK-Kinase-Inhibitoren. JAK1/2-Inhibitoren verbessern die Splenomegalie- und systemischen Symptome; allerdings ist der Mechanismus, wodurch dies in den Patienten geschieht, bislang nicht geklärt. Um in PMF veränderte Zytokine zu identifizieren, haben wir die Zytokinwerte von MPN-Mäusen und Kontrollmäusen gemessen. Wir haben festgestellt, dass eine Gruppe von Zytokinen im Serum erkrankter Mäuse verglichen mit den Kontrollmäusen auffällig hoch war; besonders relevant ist dabei, dass viele genau dieser Zytokine auch bei MPN-Patienten in großen Mengen vorhanden sind. Außerdem normalisierte der JAK1/2-Inhibitor Ruxolitinib ungewöhnliche Zytokinwerte bei PMF-Mäusen, was mit der entzündungshemmenden Wirkung von Ruxolitinib im klinischen Umfeld übereinstimmt. Wichtig ist, dass wir demonstriert haben, dass Ruxolitnib die Signalisierung sowohl von mutanten als auch nicht-mutanten Zellen unterdrücken muss, was auf einen neuartigen Wirkungsmechanismus hinweist, durch den JAK-Inhibitoren klinisch vorteilhaft sind. Wir demonstrieren, dass Nebensignaleffekte zwischen mutanten und nicht-mutanten Populationen ein wichtiges Merkmal von MPNs sind. Schließlich unterstützen unsere Studien den Gedanken, dass JAK-Kinaseinhibition in b
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SOURCE European Hematology Association
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