The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Mice Defective in Two Apoptosis Pathways in the Myeloid Lineage Develop Acute Myeloblastic Leukemia
Open accessAbstract
Fas-deficient (Fas(lpr/lpr)) mice constitutively expressing Bcl-2 in myeloid cells by the hMRP8 promoter often develop a fatal disease analogous to human acute myeloblastic leukemia (AML-M2). Hematopoietic cells from leukemic Fas(lpr/lpr)hMRP8bcl-2 animals form clonogenic blast colonies in vitro and can transfer disease to wild-type mice. In vitro ligation of Fas on Fas+/+ hMRP8bcl-2 marrow cells depletes approximately 50% of myeloid progenitor activity, demonstrating that Bcl-2 can only partially block Fas-mediated death signals in myelomonocytic progenitors. In addition, Fas(lpr/lpr) marrow contains greatly increased numbers of myeloid colony-forming cells as compared to Fas+/+ controls. Taken together, these data suggest that Fas has a novel role in the regulation of myelopoiesis and that Fas may act as a tumor suppressor to control leukemogenic transformation in myeloid progenitor cells.
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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
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The AML1/ETO fusion protein activates transcription of BCL-2
Klampfer, L., Zhang, J., Zelenetz, A. O., Uchida, H., & Nimer, S. D. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.24.14059 · Cited by 182
Cited by
Stem cells, cancer, and cancer stem cells
Reya, T., Morrison, S. J., Clarke, M. F., & Weissman, I. L. (2001) · Nature · doi:10.1038/35102167 · Cited by 9,738
Self-citationExtrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy
Fulda, S., & Debatin, K.-M. (2006) · Oncogene · doi:10.1038/sj.onc.1209608 · Cited by 2,312
Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML
Jamieson, C. H. M., Ailles, L. E., Dylla, S. J., Muijtjens, M., Jones, C., Zehnder, J. L., Gotlib, J., Li, K., Manz, M. G., Keating, A., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040258 · Cited by 1,485
Passegué, E., Jamieson, C. H. M., Ailles, L. E., & Weissman, I. L. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2034201100 · Cited by 686
Self-citationFulda, S. (2009) · International Journal of Cancer · doi:10.1002/ijc.24064 · Cited by 615
Metadata
- Authors
- Traver, D., Akashi, K., Weissman, I. L., & Lagasse, E.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 1998-07
- Volume
- 9
- Issue
- 1
- Pages
- 47-57
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W1967007700
- Cited by
- 173
- References
- 7
- FWCI
- 3.71
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Mice Defective in Two Apoptosis Pathways in the Myeloid Lineage Develop Acute Myeloblastic Leukemia. https://app.cochat.ai/papers/10.1016/s1074-7613(00)80587-7
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- Traver, D., Akashi, K., Weissman, I. L., & Lagasse, E. (1998). Mice Defective in Two Apoptosis Pathways in the Myeloid Lineage Develop Acute Myeloblastic Leukemia. Immunity. https://doi.org/10.1016/s1074-7613(00)80587-7
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
