Retroviral transduction models of Ph+ leukemia: Advantages and limitations for modeling human hematological malignancies in mice

Blood Cells, Molecules, and Diseases

Volumn 27, Issue 1, 2001, Pages 201-205

  Van Etten, Richard A ^a  

^a HARVARD MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BCR ABL PROTEIN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BONE MARROW CANCER; BONE MARROW TRANSPLANTATION; CONTROLLED STUDY; GENE EXPRESSION; HEMATOPOIETIC STEM CELL; KNOCKOUT MOUSE; LEUKEMIA; LEUKEMOGENESIS; MOLECULAR CLONING; MOUSE; NONHUMAN; ONCOGENE; PHILADELPHIA 1 CHROMOSOME; PRIORITY JOURNAL; PROVIRUS; RETROVIRUS; SIGNAL TRANSDUCTION; TRANSGENIC MOUSE;

MUS MUSCULUS; RETROVIRAL PROVIRUS;

EID: 0035052161     PISSN: 10799796     EISSN: None     Source Type: Journal    
DOI: 10.1006/bcmd.2000.0370     Document Type: Article

References (21)

1. Animal models of Philadelphia-positive leukemia
2. bcr/abl gene of the Philadelphia chromosome
3. The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity
4. Efficient and rapid induction of a chronic myelogenous leukemia-like myeloproliferative disease in mice receiving P210 bcr/abl-transduced bone marrow
5. Bcr-Abl efficiently induces a myeloproliferative disease and production of excess interleukin-3 and granulocyte-macrophage colony-stimulating factor in mice: A novel model for chronic myelogenous leukemia
6. Blast crisis in a murine model of chronic myelogenous leukemia
7. Efficient transplantation of BCR-ABL-induced chronic myelogenous leukemia-like syndrome in mice
8. The Src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase
9. p190 fusion gene made by homologous recombination causes B-cell acute lymphoblastic leukemias in chimeric mice with independence of the endogenous bcr product
10. BCR/ABL P210 and P190 cause distinct leukemia in transgenic mice
11. Bcr-Abl with an SH3 deletion retains the ability to induce a myeloproliferative disease in mice, yet c-Abl activated by an SH3 deletion induces only lymphoid malignancy
12. The Grb2 binding site is required for induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase
13. Reduced oncogenicity of p190 Bcr/Abl F-actin-binding domain mutants
14. Bcr/Abl associated leukemogenesis in bcr null mutant mice
15. Interleukin-3 and granulocyte-macrophage colony-stimulating factor are not required for induction of chronic myeloid leukemia-like myeloproliferative disease in mice by BCR/ABL
16. The cytostatic function of c-Abl is controlled by multiple nuclear localization signals, and requires the p53 and Rb tumor suppressor gene products
17. Human bcr-abl gene has a lethal effect on embryogenesis
18. A bcr-v-abl oncogene induces lymphomas in transgenic mice
19. Reversibility of acute B-cell leukaemia induced by BCR-ABL1
20. Clonal development and karyotype evolution during leukemogenesis of BCR/ABL transgenic mice
21. A primitive hematopoietic cell is the target for the leukemic transformation in human Philadelphia-positive acute lymphoblastic leukemia