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Imatinib independent aberrant methylation of NOV/CCN3 in chronic myelogenous leukemia patients: a mechanism upstream of BCR-ABL1 function?

Abstract Background The NOV gene product, CCN3, has been reported in a diverse range of tumors to serve as a negative growth regulator, while acting as a tumor suppressor in Chronic Myelogenous Leukemia (CML). However, the precise mechanism of its silencing in CML is poorly understood. In the curren...

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Автори: Mousa Vatanmakanian, Mahmood Tavallaie, Shirin Ghadami
Формат: Artigo
Мова:Inglês
Опубліковано: BMC 2019-04-01
Серія:Cell Communication and Signaling
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Онлайн доступ:http://link.springer.com/article/10.1186/s12964-019-0350-6
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