Cytokine-dependent imatinib resistance in mouse BCR-ABL+, Arf-null lymphoblastic leukemia.
Genes Dev
; 21(18): 2283-7, 2007 Sep 15.
Article
de En
| MEDLINE
| ID: mdl-17761812
ABSTRACT
Retroviral transduction of the BCR-ABL kinase into primary mouse bone marrow cells lacking the Arf tumor suppressor rapidly generates polyclonal populations of continuously self-renewing pre-B cells, virtually all of which have leukemic potential. Intravenous infusion of 20 such cells into healthy syngeneic mice induces rapidly fatal, transplantable lymphoblastic leukemias that resist imatinib therapy. Introduction of BCR-ABL into Arf-null severe combined immunodeficient (SCID) bone marrow progenitors lacking the cytokine receptor common gamma-chain yields leukemogenic pre-B cells that exhibit greater sensitivity to imatinib in vivo. Hence, salutary cytokines in the hematopoietic microenvironment can facilitate leukemic proliferation and confer resistance to targeted therapy.
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Pipérazines
/
Pyrimidines
/
Cytokines
/
Protéines de fusion bcr-abl
/
Résistance aux médicaments antinéoplasiques
/
Inhibiteur p16 de kinase cycline-dépendante
/
Leucémie-lymphome lymphoblastique à précurseurs B et T
Limites:
Animals
Langue:
En
Journal:
Genes Dev
Sujet du journal:
BIOLOGIA MOLECULAR
Année:
2007
Type de document:
Article
Pays d'affiliation:
États-Unis d'Amérique