c-KIT expression enhances the leukemogenic potential of 32D cells.

Q Hu; M Trevisan; Y Xu; W Dong; S A Berger; S D Lyman; M D Minden

doi:10.1172/JCI117954

Department of Medical Biophysics and Medicine, University of Toronto, Ontario, Canada.

Find articles by Hu, Q. in: JCI | PubMed | Google Scholar

Department of Medical Biophysics and Medicine, University of Toronto, Ontario, Canada.

Find articles by Trevisan, M. in: JCI | PubMed | Google Scholar

Department of Medical Biophysics and Medicine, University of Toronto, Ontario, Canada.

Find articles by Xu, Y. in: JCI | PubMed | Google Scholar

Department of Medical Biophysics and Medicine, University of Toronto, Ontario, Canada.

Find articles by Dong, W. in: JCI | PubMed | Google Scholar

Department of Medical Biophysics and Medicine, University of Toronto, Ontario, Canada.

Find articles by Berger, S. in: JCI | PubMed | Google Scholar

Department of Medical Biophysics and Medicine, University of Toronto, Ontario, Canada.

Find articles by Lyman, S. in: JCI | PubMed | Google Scholar

Department of Medical Biophysics and Medicine, University of Toronto, Ontario, Canada.

Find articles by Minden, M. in: JCI | PubMed | Google Scholar

Published in Volume 95, Issue 6 on June 1, 1995
J Clin Invest. 1995;95(6):2530–2538. https://doi.org/10.1172/JCI117954.
© 1995 The American Society for Clinical Investigation

Published June 1, 1995 - Version history

The growth of human leukemic cells in culture and in vivo is dependent upon the presence of hematopoietic growth factors. Most populations of human leukemic acute myeloblastic leukemia (AML) cells express c-Kit on their surface and respond to Kit ligand (KL) in culture. To determine if this interaction was of potential significance in vivo we used a mouse model system. 32D cells, a murine IL-3-dependent myeloid cell line, were rendered KL responsive by transfection of the murine c-Kit. After injection of 32D or 32D-Kit cells into syngeneic hosts, animals bearing 32D-Kit cells, but not 32D cells, became moribund and were killed. These animals had circulating leukemic blast cells, infiltration of bone marrow, spleen, brain, liver, lung, and kidney. Cells recovered from some of the animals continued to be dependent upon IL-3 or KL for growth while in other cases the cells were factor independent. This model illustrates that the constitutive expression of c-Kit enhances the leukemic potential of 32D cells. The model will be useful for studying the progression of leukemia in vivo and testing whether interruption of the interaction of Kit and KL can affect the growth of leukemic cells.

Images.