作者: Dongguang Li , Yaoyu Chen , Shaoguang Li , Cong Peng
DOI: 10.18632/ONCOTARGET.100603
关键词:
摘要: Received: May 5, 2010 , Accepted: 18, Published: June 7, // Chronic myeloid leukemia (CML) is initiated from the BCR-ABL-expressing stem cells (LSCs). These LSCs are highly resistant to BCR-ABL kinase inhibitors, imatinib, dasantinib and nilotinib, methods for eradication of still not available. It critical identify genes that play roles in survival proliferation LSCs. We recently discovered tumor suppressor gene Pten downregulated CML mice. By genetic deletion or overexpression Pten, we confirmed functions as a CML, consistent with role acute (AML) progenitor T-ALL progenitors. Functional enhancement pathway provides therapeutic strategy targeting