Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2136969 | Leukemia Research | 2013 | 9 Pages |
Abstract
Since BCR–ABL plays an essential role in the growth factor-independent proliferation of Philadelphia chromosome (Ph)+ leukemia cells, imatinib treatment of Ph+ leukemia cells inactivates signaling pathways of BCR–ABL, and subsequent addition of growth factors (GFs) could restore the signaling pathways without reactivating BCR–ABL. Here we demonstrated that non-lymphoid Ph+ leukemia cell lines responded to diverse GFs depending on their immunophenotype and gene expression of transcription factors and GF receptors, while lymphoid Ph+ leukemia cell lines restrictively responded to flit3 ligand and interleukin-7, suggesting that GF sensitivity of imatinib-treated Ph+ leukemia cells could be powerful for specifying their distinctive lineage.
Keywords
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Authors
Atsushi Nemoto, Takeshi Inukai, Kanako Uno, Nobutaka Kiyokawa, Yoshitaka Miyagawa, Kazuya Takahashi, Hiroki Sato, Koshi Akahane, Kinuko Hirose, Hiroko Honna-Oshiro, Kumiko Goi, Keiko Kagami, Shinpei Nakazawa, Junichiro Fujimoto, Toshiya Inaba,