Nf1 deficiency causes Ras-mediated granulocyte/macrophage colony stimulating factor hypersensitivity and chronic myeloid leukaemia

Nature Genetics

Volumn 12, Issue 2, 1996, Pages 137-143

  Largaespada, David A ^a   Brannan, Camilynn I ^a,b   Jenkins, Nancy A ^a   Copeland, Neal G ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b UNIVERSITY OF FLORIDA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

GRANULOCYTE MACROPHAGE COLONY STIMULATING FACTOR; GUANOSINE TRIPHOSPHATASE ACTIVATING PROTEIN; RAS PROTEIN;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CHRONIC MYELOID LEUKEMIA; CONTROLLED STUDY; GENETIC SCREENING; HEMATOPOIETIC STEM CELL; MOUSE; NEUROFIBROMATOSIS; NONHUMAN; ONCOGENE RAS; POINT MUTATION; PRIORITY JOURNAL; SIGNAL TRANSDUCTION;

ACUTE DISEASE; ANIMALS; BONE MARROW; CELL DIFFERENTIATION; CELL LINE, TRANSFORMED; CROSSES, GENETIC; DISEASE MODELS, ANIMAL; DISEASE PROGRESSION; FEMALE; GENES, NEUROFIBROMATOSIS 1; GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR; GUANOSINE TRIPHOSPHATE; HEMATOPOIETIC STEM CELL TRANSPLANTATION; HEMATOPOIETIC STEM CELLS; HUMANS; LEUKEMIA, MYELOID; LEUKEMIA, MYELOID, CHRONIC; LIVER; MALE; MICE; MICE, INBRED C57BL; RAS PROTEINS; SIGNAL TRANSDUCTION;

EID: 0030045594     PISSN: 10614036     EISSN: None     Source Type: Journal    
DOI: 10.1038/ng0296-137     Document Type: Article

References (35)

1. Riccardi, V. M. In Neurofibromatosis: phenotype, natural history, and pathogenesis. (Johns Hopkins Press, Baltimore, 1992).
2. Bader, J.L. Neurofibromatosis and cancer. Ann. N. Y. Acad. Sci. 486, 56-65 (1986).
3. Hope, D.G. & Mulvihill, J.J. Malignancy in neurofibromatosis. Adv. Neurol. 29, 33-56 (1981).
4. Bader, J.L. & Miller, R.W. Neurofibromatosis and childhood leukemia. J. Pediat. 92, 925-929 (1978).
5. Gutmann, D.H. & Collins, F.S. The neurofibromatosis type 1 gene and its protein product, neurofibromin. Neuron 10, 335-343 (1993).
6. Barbacid, M. Ras oncogenes: their role in neoplasia. Eur. J. Clin. Invest. 20, 225-235 (1990).
7. Johnson, M.R., Look, A.T., DeClue, J.E., Valentine, M.B. & Lowy, D.R. Inactivation of the NF1 gene in human melanoma and neuroblastoma cell lines without impaired regulation of GTP-Ras. Proc. Natl. Acad. Sci. USA 90, 5539-5543 (1993).
8. Johnson, M.R. et al. Neuroflbromin can inhibit ras-dependent growth by a mechanism independent of its GTPase-accelerating function. Molec. cell. Biol. 14, 641-645 (1994).
9. Shannon, K.M. et al. Loss of the normal NF1 altele from the bone marrow of children with type 1 neurofibromatosis and malignant myeloid disorders. New Engl. J. Med. 330, 597-601 (1994).
10. Jacks, T. et al. Tumor predisposition in mice heterozygous for a targeted mutation in Nf1. Nature Genet 7, 353-361 (1994).
11. Buchberg, A.M., Bedigian, H.G., Jenkins, N.A. & Copeland, N.G. Evi-2, a common integration site involved in murine myeloid leukemogenesis. Molec. Cell. Bol. 10, 4658-4666 (1990).
12. Largaespada, D.A., Shaughnessy, J.D., Jenkins, N.A. & Copeland, N.G. Retroviral insertion at the Evi-2 locus in BXH-2 myeloid leukemia cell lines disrupts Hn expression without changes in steady state ras-GTP levels. J. Virol. 69, 5095-5102 (1995).
13. Kalra, R., Paderanga, D.C., Olson, K. & Shannon, K.M. Genetic analysis is consistent with the hypothesis that NF1 limits myeloid growth through p21 ras. Blood 84, 3435-3439 (1994).
14. Brannan, C.I. et al. Targeted disruption of the neurofibromatosis type-1 gene leads to developmental abnormalities in heart and various neural crest-derived tissues. Genes Dev. 8, 1019-1029 (1994).
15. Moore, M. A. S., McNeill, T. A., & Haskill, J. S. Density distribution analysis of in vivo and in vitro colony forming cells in developing fetal liver. J. Cell. Physiol. 75, 181-192 (1970).
16. Dunn, A.R. et al. In Biological characterization of regulators encoded by cloned hemopoietic growth factor gene sequences. (Cold Spring Harbor Laboratory, New York, 1985).
17. Emanuel, P.D., Bates, L.J., Castleberry, R.B., Gualtieri, R.J. & Zuckerman, K.S. Selective hypersensitivity to granulaocyte-macrophage colony-stimulating factor by juvenile chronic myeloid leukemia hematopoietic progenitors. Blood 77, 925-929 (1991).
18. Miyajima, A., Mui, A.L., Ogorochi, T. & Sakamaki, K. Receptors for granulocyte-macrophage colony-stimulating factor, interleukin-3, and interleukin-5. Blood 82, 1960-1974 (1993).
19. Castro-Malaspina, H. et al. Subacute and chronic myelomonocytic leukemia in children (Juvenile CML): Clinical and hematologic observations, and identification of prognostic factors. Cancer 54, 675-686 (1984).
20. Hestdal, K. et al. Characterization and regulation of RB6-8C5 antigen expression on murine bone marrow cells. J. Immunol. 147, 22-28 (1991).
21. Lang, R.A. et al. Transgenic mice expressing a hemopoietic growth factor gene (GM-CSF) develop accumulations of macrophages, blindness, and a fatal syndrome of tissue damage. Cell 51, 675-686 (1987).
22. Johnson, G.R., Gonda, T.J., Metcalf, D., Hariharan, I.K. & Cory, S. A lethal myeloproliferative syndrome in mice transplanted with bone marrow cells infected with a retrovirus expressing granulocyle-macrophage colony stimulating factor. EMBO J. 8, 441-448 (1989).
23. Satoh, T., Nakafuku, M., Miyajima, A. & Kaziro, Y. Involvement of ras p21 protein in signal-transduction pathways from interleukin 2, interleukin 3, and granulocyte/macrophage colony-stimulating factor, but not from interleukin 4. Proc. Natl. Acad. Sci. USA 88, 3314-3318 (1991).
24. DeClue, J.E. et al. Abnormal regulation of mammalian p21 ras contrinutes to malignant tumor growth in von Recklinghausen (Type 1) neurofibromatosis. Cell 68, 265-273 (1992).
25. Basu, T.N. et al. Aberrant regulation of ras proteins in malignant tumor cells from type 1 neurofibromatosis patients. Nature 356, 713-715 (1992).
26. Gonda, T.J., E. M. Macmillan, Townsend, P.V. & Hapel, A.J. Differentiation state and responses to hematopoietic growth factors of murine myeloid cells transformed by myb. Blood 82, 2813-2822 (1993).
27. Gonda, T. J. Molecular and cellular activities of Myb: regulation in normal hemopoiesis and transformation. Seminars in Virology 2, 351-361 (1991).
28. Janssen, J.W.G. et al. RAS gene mutations in acute and chronic myelocytic leukemias, chronic myeloproliferative disorders, and myelodysplastic syndromes. Proc. Natl. Acad. Sci. USA 84, 9228-9232 (1987).
29. The, I. et al. Neurofibromatosis type 1 gene mutations in neuroblastoma. Nature Genet. 3, 62-66 (1993).
30. Bedigian, H.G., Johnson, D.A., Jenkins, N.A., Copeland, N.G. & Evans, R. Spontaneous and induced leukemias of myeloid origin in recombinant inbred BXH-2 mice. J. Virol. 51, 586-594 (1984).
31. Jenkins, N.A., Copeland, N.G., Taylor, B.A., Bedigian, H.G. & Lee, B.K. Ecotropic murine leukemia virus DNA content of normal and lymphomalous tissues of BXH-2 recombinant inbred mice. J. Virol. 42, 379-388 (1982).
32. von Lohuizen, M. & Berns, A. Tumorigenesis by slow transforming retroviruses - an update. Biochim. Biophys. Acta. 1032 (2-3), 213-235 (1990).
33. Peters, G. Oncogenes at viral integration sites. Cell. Growth Differ. 1, 503-510 (1990).
34. Puil, L. et al. Bcr-abl oncoproteins bind directly to activators of the ras signalling pathway. EMBO J. 13, 764-773 (1994).
35. Pendergast, A. M. et at. BCR-ABL-induced oncogenesis is mediated by direct interaction of the SH2 domain of the GRB-2 adaptor protein. Cell 75, 175-185 (1993).