The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Nf1 deficiency causes Ras-Dediated granulocyte/macrophage colony stimulating factor hypersensitivity and chronic myeloid leukaemia
Abstract
The Ras signal transduction pathway is often deregulated in human myeloid leukaemia. For example, activating point mutations in RAS genes are found in some patients with juvenile chronic myelogenous leukaemia (JCML), while other patients with JCML show loss of the neurofibromatosis type 1 (NF1) gene, a Ras GTPase activating protein. By generating mice whose haematopoietic system is reconsituted with Nf1 deficient haematopoietic stem cells we show that Nf1 gene loss, by itself, is sufficient to produce the myeloproliferative symptoms associated with human JCML. We also provide evidence to indicate that Nf1 gene loss induces myeloproliferative disease through a Ras-mediated hypersensitivity to granulocyte/macrophage-colony stimulating factor (GM-CSF). Finally, we describe a genetic screen for identifying genes that cooperate with Nf1 gene loss during progression to acute myeloid leukaemia.
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“and juvenile myelomonocytic leukemia (6).”
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Cites
Neurofibromatosis, Phenotype, Natural History, and Pathogenesis
Riccardi, V. M., & Smirniotopoulos, J. G. (1992) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/00005072-199211000-00009 · Cited by 897
Tumour predisposition in mice heterozygous for a targeted mutation in Nf1
Jacks, T., Shih, T. S., Schmitt, E. M., Bronson, R. T., Bernards, A., & Weinberg, R. A. (1994) · Nature Genetics · doi:10.1038/ng0794-353 · Cited by 780
Aberrant regulation of ras proteins in malignant tumour cells from type 1 neurofibromatosis patients
Basu, T. N., Gutmann, D. H., Fletcher, J. A., Glover, T. W., Collins, F. S., & Downward, J. (1992) · Nature · doi:10.1038/356713a0 · Cited by 669
Pendergast, A. M., Quilliam, L. A., Cripe, L. D., Bassing, C. H., Dai, Z., Li, N., Batzer, A., Rabun, K. M., Der, C. J., Schlessinger, J., et al. (1993) · Cell · doi:10.1016/s0092-8674(05)80094-7 · Cited by 657
Brannan, C. I., Perkins, A. S., Vogel, K. S., Ratner, N., Nordlund, M. L., Reid, S. W., Buchberg, A. M., Jenkins, N. A., Parada, L. F., & Copeland, N. G. (1994) · Genes & Development · doi:10.1101/gad.8.9.1019 · Cited by 641
Self-citationDeClue, J. E., Papageorge, A. G., Fletcher, J. A., Diehl, S. R., Ratner, N., Vass, W. C., & Lowy, D. R. (1992) · Cell · doi:10.1016/0092-8674(92)90407-4 · Cited by 580
Characterization and regulation of RB6-8C5 antigen expression on murine bone marrow cells
Hestdal, K., Ruscetti, F. W., Ihle, J. N., Jacobsen, S. E. W., Dubois, C. M., Kopp, W. C., Longo, D., & Keller, J. R. (1991) · The Journal of Immunology · doi:10.4049/jimmunol.147.1.22 · Cited by 464
Shannon, K., O'Connell, P., Martin, G. A., Paderanga, D., Olson, K., Dinndorf, P. A., & McCormick, F. P. (1994) · New England Journal of Medicine · doi:10.1056/nejm199403033300903 · Cited by 440
Bcr‐Abl oncoproteins bind directly to activators of the Ras signalling pathway.
Puil, L. J., Liu, J., Gish, G., Mbamalu, G., Bowtell, D. D. L., Pelicci, P. G., Arlinghaus, R. B., & Pawson, T. J. (1994) · The EMBO Journal · doi:10.1002/j.1460-2075.1994.tb06319.x · Cited by 438
Receptors for granulocyte-macrophage colony-stimulating factor, interleukin-3, and interleukin-5
Miyajima, A., Mui, A. L.-F., Ogorochi, T., & Sakamaki, K. (1993) · Blood · doi:10.1182/blood.v82.7.1960.bloodjournal8271960 · Cited by 414
Research works printed but not linked: 2
- Hope, D.G. & Mulvihill, J.J. Malignancy in neunofibromatosis. Adv. Neurol. 29, 33–56 (1981).
- Gonda, T.J. Molecular and cellular activities of Myb: regulation in normal hemopoiesis and transformation. Seminars in virology 2, 351–361 (1991).
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Transcription Factors, Normal Myeloid Development, and Leukemia
Tenen, D. G., Hromas, R., Licht, J. D., & Zhang, D.-E. (1997) · Blood · doi:10.1182/blood.v90.2.489 · Cited by 735
Germline KRAS mutations cause Noonan syndrome
Schubbert, S., Zenker, M., Rowe, S. L., Böll, S., Klein, C., Bollag, G., van der Burgt, I., Musante, L., Kalscheuer, V., Wehner, L.-E., et al. (2006) · Nature Genetics · doi:10.1038/ng1748 · Cited by 730
Mutations in PTPN11 implicate the SHP-2 phosphatase in leukemogenesis
Loh, M. L. (2003) · Blood · doi:10.1182/blood-2003-09-3287 · Cited by 422
Niemeyer, C. M., Aricò, M., Basso, G., Biondi, A., Rajnoldi, A. C., Creutzig, U., Haas, O. A., Harbott, J., Hasle, H., Kerndrup, G. B., et al. (1997) · PubMed · doi:10.1182/blood.v89.10.3534 · Cited by 405
The tyrosine phosphatase Shp2 (PTPN11) in cancer
Chan, G., Kalaitzidis, D., & Neel, B. G. (2008) · Cancer and Metastasis Reviews · doi:10.1007/s10555-008-9126-y · Cited by 392
Metadata
- Authors
- Largaespada, D. A., Brannan, C. I., Jenkins, N. A., & Copeland, N. G.
- Affiliations
- Frederick National Laboratory for Cancer Research (US)
- University of Florida (US)
- Venue
- Nature Genetics
- Published
- 1996-02
- Volume
- 12
- Issue
- 2
- Pages
- 137-143
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- OpenAlex
- W2087533846
- Cited by
- 284
- References
- 33
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 6 · 2018: 4 · 2017: 3 · 2016: 8 · 2015: 4 · 2014: 4 · 2013: 6 · 2012: 14
- FWCI
- 15.71
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Neurofibromatosis and Schwannoma Cases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- neurofibromatosis type 1, NF1 deficiency, Ras signaling, GM-CSF, GM-CSF hypersensitivity, chronic myeloid leukemia, myeloproliferative neoplasms, hematopoietic stem cells, genetic screen, Ras GTPase-activating protein
- MeSH terms
- Acute Disease, Animals, Bone Marrow, Cell Differentiation, Cell Line, Transformed, Crosses, Genetic, Disease Models, Animal, Female, Guanosine Triphosphate, Hematopoietic Stem Cells, Humans, Leukemia, Myeloid, Liver, Male, Mice, Inbred C57BL, Signal Transduction, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Granulocyte-Macrophage Colony-Stimulating Factor, Genes, Neurofibromatosis 1, Hematopoietic Stem Cell Transplantation, Disease Progression, ras Proteins, Mice
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