Diverse underlying proliferation response to growth factors in imatinib-treated Philadelphia chromosome-positive leukemias

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 signali...

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Bibliographic Details
Published in:Leukemia research 2013-01, Vol.37 (1), p.93-101
Main Authors: Nemoto, Atsushi, Inukai, Takeshi, Uno, Kanako, Kiyokawa, Nobutaka, Miyagawa, Yoshitaka, Takahashi, Kazuya, Sato, Hiroki, Akahane, Koshi, Hirose, Kinuko, Honna-Oshiro, Hiroko, Goi, Kumiko, Kagami, Keiko, Nakazawa, Shinpei, Fujimoto, Junichiro, Inaba, Toshiya, Sugita, Kanji
Format: Article
Language:English
Subjects:
Antineoplastic Agents - pharmacology
BCR–ABL
Benzamides
Cell Line, Tumor
Cell proliferation
Cell Proliferation - drug effects
Gene expression
Granulocyte Colony-Stimulating Factor - pharmacology
Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology
Growth factor
Growth factors
Hematology, Oncology and Palliative Medicine
Human hematopoiesis
Humans
Imatinib
Imatinib Mesylate
Intercellular Signaling Peptides and Proteins - pharmacology
Interleukin 7
Interleukin-6 - pharmacology
Leukemia - drug therapy
Leukemia - genetics
Leukemia - pathology
Philadelphia Chromosome
Philadelphia chromosome-positive leukemia
Piperazines - pharmacology
Pyrimidines - pharmacology
Signal transduction
Transcription factors
Tumor cell lines
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Summary: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.
ISSN:0145-2126
1873-5835
DOI:10.1016/j.leukres.2012.10.001