title: 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 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.
authors.affiliation: Department of Pediatrics, School of Medicine, University of Yamanashi, Yamanashi 409-3898, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Nemoto
authors.forename: Takeshi
authors.initials: T
authors.lastname: Inukai
authors.forename: Kanako
authors.initials: K
authors.lastname: Uno
authors.forename: Nobutaka
authors.initials: N
authors.lastname: Kiyokawa
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Miyagawa
authors.forename: Kazuya
authors.initials: K
authors.lastname: Takahashi
authors.forename: Hiroki
authors.initials: H
authors.lastname: Sato
authors.forename: Koshi
authors.initials: K
authors.lastname: Akahane
authors.forename: Kinuko
authors.initials: K
authors.lastname: Hirose
authors.forename: Hiroko
authors.initials: H
authors.lastname: Honna-Oshiro
authors.forename: Kumiko
authors.initials: K
authors.lastname: Goi
authors.forename: Keiko
authors.initials: K
authors.lastname: Kagami
authors.forename: Shinpei
authors.initials: S
authors.lastname: Nakazawa
authors.forename: Junichiro
authors.initials: J
authors.lastname: Fujimoto
authors.forename: Toshiya
authors.initials: T
authors.lastname: Inaba
authors.forename: Kanji
authors.initials: K
authors.lastname: Sugita
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D001549:Benzamides; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D006801:Humans; D000068877:Imatinib Mesylate; D036341:Intercellular Signaling Peptides and Proteins / Q000494:pharmacology*; D015850:Interleukin-6 / Q000494:pharmacology; D007938:Leukemia / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D010677:Philadelphia Chromosome; D010879:Piperazines / Q000494:pharmacology*; D011743:Pyrimidines / Q000494:pharmacology*
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6; D010879:Piperazines; D011743:Pyrimidines; D016179:Granulocyte Colony-Stimulating Factor; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D000068877:Imatinib Mesylate