1. Diverse underlying proliferation response to growth factors in imatinib-treated Philadelphia chromosome-positive leukemias
- Author
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K Uno, Toshiya Inaba, Shinpei Nakazawa, Kazuya Takahashi, Koshi Akahane, Nobutaka Kiyokawa, Junichiro Fujimoto, Kinuko Hirose, Atsushi Nemoto, Hiroki Sato, Kanji Sugita, Takeshi Inukai, Yoshitaka Miyagawa, Keiko Kagami, Kumiko Goi, and Hiroko Honna-Oshiro
- Subjects
Cancer Research ,medicine.medical_treatment ,Antineoplastic Agents ,Biology ,Philadelphia chromosome ,Piperazines ,Immunophenotyping ,hemic and lymphatic diseases ,Cell Line, Tumor ,Granulocyte Colony-Stimulating Factor ,medicine ,Humans ,Philadelphia Chromosome ,Cell Proliferation ,ABL ,Leukemia ,Interleukin-6 ,Growth factor ,Granulocyte-Macrophage Colony-Stimulating Factor ,Imatinib ,Hematology ,medicine.disease ,Imatinib mesylate ,Pyrimidines ,Oncology ,Cell culture ,Benzamides ,Cancer research ,Imatinib Mesylate ,Intercellular Signaling Peptides and Proteins ,medicine.drug - 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.
- Published
- 2012