Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Science 8 May 1992:
Vol. 256. no. 5058, pp. 836 - 839
DOI: 10.1126/science.1375394

Articles

Science, Vol 256, Issue 5058, 836-839
Copyright © 1992 by American Association for the Advancement of Science


articles

Initiation of deregulated growth of multipotent progenitor cells by bcr-abl in vitro

ML Gishizky and ON Witte

Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024.

Expression of the bcr-abl oncogene in multipotent progenitor cells (MPPCs) is implicated as a key event in the development of chronic myelogenous leukemia. Bone marrow enriched for MPPCs was infected with a retrovirus that carried bcr-abl. The mixed-lineage colonies that resulted were responsive to growth factors and could differentiate. These cells later became growth factor-independent but, when injected into severe combined immunodeficient mice, were not leukemogenic. Thus, the presence of bcr-abl alone does not cause growth factor independence, although it initiates a stepwise process. This system may prove useful in the study of other oncogenes that cause leukemia.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
SHP-2 phosphatase is required for hematopoietic cell transformation by Bcr-Abl.
J. Chen, W.-M. Yu, H. Daino, H. E. Broxmeyer, B. J. Druker, and C.-K. Qu (2007)
Blood 109, 778-785
   Abstract »    Full Text »    PDF »
Src Family Kinases Phosphorylate the Bcr-Abl SH3-SH2 Region and Modulate Bcr-Abl Transforming Activity.
M. A. Meyn III, M. B. Wilson, F. A. Abdi, N. Fahey, A. P. Schiavone, J. Wu, J. M. Hochrein, J. R. Engen, and T. E. Smithgall (2006)
J. Biol. Chem. 281, 30907-30916
   Abstract »    Full Text »    PDF »
The age incidence of chronic myeloid leukemia can be explained by a one-mutation model.
F. Michor, Y. Iwasa, and M. A. Nowak (2006)
PNAS 103, 14931-14934
   Abstract »    Full Text »    PDF »
Kinase domain mutants of bcr-abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib..
I. J. Griswold, M. MacPartlin, T. Bumm, V. L. Goss, T. O'Hare, K. A. Lee, A. S. Corbin, E. P. Stoffregen, C. Smith, K. Johnson, et al. (2006)
Mol. Cell. Biol. 26, 6082-6093
   Abstract »    Full Text »    PDF »
BCR/ABL kinase induces self-mutagenesis via reactive oxygen species to encode imatinib resistance.
M. Koptyra, R. Falinski, M. O. Nowicki, T. Stoklosa, I. Majsterek, M. Nieborowska-Skorska, J. Blasiak, and T. Skorski (2006)
Blood 108, 319-327
   Abstract »    Full Text »    PDF »
Id1 transcription inhibitor-matrix metalloproteinase 9 axis enhances invasiveness of the breakpoint cluster region/abelson tyrosine kinase-transformed leukemia cells..
M. Nieborowska-Skorska, G. Hoser, L. Rink, M. Malecki, P. Kossev, M. A. Wasik, and T. Skorski (2006)
Cancer Res. 66, 4108-4116
   Abstract »    Full Text »    PDF »
The Jab1/COP9 signalosome subcomplex is a downstream mediator of Bcr-Abl kinase activity and facilitates cell-cycle progression.
K. Tomoda, J.-y. Kato, E. Tatsumi, T. Takahashi, Y. Matsuo, and N. Yoneda-Kato (2005)
Blood 105, 775-783
   Abstract »    Full Text »    PDF »
Combination of rapamycin and protein tyrosine kinase (PTK) inhibitors for the treatment of leukemias caused by oncogenic PTKs.
M. G. Mohi, C. Boulton, T.-L. Gu, D. W. Sternberg, D. Neuberg, J. D. Griffin, D. G. Gilliland, and B. G. Neel (2004)
PNAS 101, 3130-3135
   Abstract »    Full Text »    PDF »
Expression of BCR/ABL and BCL-2 in myeloid progenitors leads to myeloid leukemias.
S. Jaiswal, D. Traver, T. Miyamoto, K. Akashi, E. Lagasse, and I. L. Weissman (2003)
PNAS 100, 10002-10007
   Abstract »    Full Text »    PDF »
Induced Dendritic Cell Differentiation of Chronic Myeloid Leukemia Blasts Is Associated with Down-Regulation of BCR-ABL.
I. Lindner, M. A. Kharfan-Dabaja, E. Ayala, D. Kolonias, L. M. Carlson, Y. Beazer-Barclay, U. Scherf, J. H. Hnatyszyn, and K. P. Lee (2003)
J. Immunol. 171, 1780-1791
   Abstract »    Full Text »    PDF »
Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment.
R. Bhatia, M. Holtz, N. Niu, R. Gray, D. S. Snyder, C. L. Sawyers, D. A. Arber, M. L. Slovak, and S. J. Forman (2003)
Blood 101, 4701-4707
   Abstract »    Full Text »    PDF »
BCR/ABL-mediated Increased Expression of Multiple Known and Novel Genes That May Contribute to the Pathogenesis of Chronic Myelogenous Leukemia.
S. Salesse and C. M. Verfaillie (2003)
Mol. Cancer Ther. 2, 173-182
   Abstract »    Full Text »    PDF »
Direct Evidence That Bcr-Abl Tyrosine Kinase Activity Disrupts Normal Synergistic Interactions Between Kit Ligand and Cytokines in Primary Primitive Progenitor Cells.
A. Strife, D. Wisniewski, C. Liu, C. L. Lambek, Z. Darzynkiewicz, R. T. Silver, and B. Clarkson (2003)
Mol. Cancer Res. 1, 176-185
   Abstract »    Full Text »
Complementary functions of the antiapoptotic protein A1 and serine/threonine kinase pim-1 in the BCR/ABL-mediated leukemogenesis.
M. Nieborowska-Skorska, G. Hoser, P. Kossev, M. A. Wasik, and T. Skorski (2002)
Blood 99, 4531-4539
   Abstract »    Full Text »    PDF »
Functional Cooperation among Ras, STAT5, and Phosphatidylinositol 3-Kinase Is Required for Full Oncogenic Activities of BCR/ABL in K562 Cells.
J. Sonoyama, I. Matsumura, S. Ezoe, Y. Satoh, X. Zhang, Y. Kataoka, E. Takai, M. Mizuki, T. Machii, H. Wakao, et al. (2002)
J. Biol. Chem. 277, 8076-8082
   Abstract »    Full Text »    PDF »
The BCR/ABL Transgene Causes Abnormal NK Cell Differentiation and Can Be Found in Circulating NK Cells of Advanced Phase Chronic Myelogenous Leukemia Patients.
H. Nakajima, R. Zhao, T. C. Lund, J. Ward, M. Dolan, B. Hirsch, and J. S. Miller (2002)
J. Immunol. 168, 643-650
   Abstract »    Full Text »    PDF »
Clonal analysis of differentiating embryonic stem cells reveals a hematopoietic progenitor with primitive erythroid and adult lymphoid-myeloid potential.
R. C. R. Perlingeiro, M. Kyba, and G. Q. Daley (2001)
Development 128, 4597-4604
   Abstract »    Full Text »    PDF »
A model of human p210bcr/ABL-mediated chronic myelogenous leukemia by transduction of primary normal human CD34+ cells with a BCR/ABL-containing retroviral vector.
R. C. Zhao, Y. Jiang, and C. M. Verfaillie (2001)
Blood 97, 2406-2412
   Abstract »    Full Text »    PDF »
Nucleophosmin-anaplastic lymphoma kinase associated with anaplastic large-cell lymphoma activates the phosphatidylinositol 3-kinase/Akt antiapoptotic signaling pathway.
R.-Y. Bai, T. Ouyang, C. Miething, S. W. Morris, C. Peschel, and J. Duyster (2000)
Blood 96, 4319-4327
   Abstract »    Full Text »    PDF »
Molecular Abnormalities in Chronic Myeloid Leukemia: Deregulation of Cell Growth and Apoptosis.
A. Di Bacco, K. Keeshan, S. L. McKenna, and T. G. Cotter (2000)
Oncologist 5, 405-415
   Abstract »    Full Text »
Regulated expression of P210 Bcr-Abl during embryonic stem cell differentiation stimulates multipotential progenitor expansion and myeloid cell fate.
T. Era and O. N. Witte (2000)
PNAS 97, 1737-1742
   Abstract »    Full Text »    PDF »
BCR-ABL and v-SRC tyrosine kinase oncoproteins support normal erythroid development in erythropoietin receptor-deficient progenitor cells.
S. Ghaffari, H. Wu, M. Gerlach, Y. Han, H. F. Lodish, and G. Q. Daley (1999)
PNAS 96, 13186-13190
   Abstract »    Full Text »    PDF »
Posttranslational Processing of the Thrombopoietin Receptor Is Impaired in Polycythemia Vera.
A. R. Moliterno and J. L. Spivak (1999)
Blood 94, 2555-2561
   Abstract »    Full Text »    PDF »
Chronic Myeloid Leukemia.
C. L. Sawyers (1999)
N. Engl. J. Med. 340, 1330-1340
   Full Text »    PDF »
BCR/ABL-mediated leukemogenesis requires the activity of the small GTP-binding protein Rac.
T. Skorski, P. Wlodarski, L. Daheron, P. Salomoni, M. Nieborowska-Skorska, M. Majewski, M. Wasik, and B. Calabretta (1998)
PNAS 95, 11858-11862
   Abstract »    Full Text »    PDF »
Inhibition of BCR-ABL Expression With Antisense Oligodeoxynucleotides Restores beta 1 Integrin-Mediated Adhesion and Proliferation Inhibition in Chronic Myelogenous Leukemia Hematopoietic Progenitors.
R. Bhatia and C. M. Verfaillie (1998)
Blood 91, 3414-3422
   Abstract »    Full Text »    PDF »
Gene Therapy for Chronic Myelogenous Leukemia (CML): A Retroviral Vector That Renders Hematopoietic Progenitors Methotrexate-Resistant and CML Progenitors Functionally Normal and Nontumorigenic In Vivo.
R. C.H. Zhao, R. S. McIvor, J. D. Griffin, and C. M. Verfaillie (1997)
Blood 90, 4687-4698
   Abstract »    Full Text »    PDF »
Oncogenic Transcription Factors in the Human Acute Leukemias.
A. T. Look (1997)
Science 278, 1059-1064
   Abstract »    Full Text »
Retrovirus-Mediated Gene Transfer of NPM-ALK Causes Lymphoid Malignancy in Mice.
M. U. Kuefer, A. T. Look, K. Pulford, F. G. Behm, P. K. Pattengale, D. Y. Mason, and S. W. Morris (1997)
Blood 90, 2901-2910
   Abstract »    Full Text »    PDF »
Distribution of ABL and BCR Genes in Cell Nuclei of Normal and Irradiated Lymphocytes.
S. Kozubek, L. Ryznar, M. Kozubek, R.D. Govorun, E.A. Krasavin, and G. Horneck (1997)
Blood 89, 4537-4545
   Abstract »    Full Text »    PDF »
Blastic transformation of p53-deficient bone marrow cells by p210bcr/abl tyrosine kinase.
T. Skorski, M. Nieborowska-Skorska, P. Wlodarski, D. Perrotti, R. Martinez, M. A. Wasik, and B. Calabretta (1996)
PNAS 93, 13137-13142
   Abstract »    Full Text »    PDF »
v-Abl-mediated Apoptotic Suppression Is Associated with SHC Phosphorylation without Concomitant Mitogen-activated Protein Kinase Activation.
P. J. Owen-Lynch, A. K. Y. Wong, and A. D. Whetton (1995)
J. Biol. Chem. 270, 5956-5962
   Abstract »    Full Text »    PDF »
Oncology and Hematology.
J. E. Karp and S. Broder (1994)
JAMA 271, 1693-1695
   Abstract »    PDF »
The Molecular Basis of Leukemia.
M. J. Cline (1994)
N. Engl. J. Med. 330, 328-336
   Full Text »



To Advertise     Find Products


Science. ISSN 0036-8075 (print), 1095-9203 (online)