Signaling in leukemia: which messenger to kill?
Open Access
- 15 February 2000
- journal article
- editorial
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 105 (4) , 419-422
- https://doi.org/10.1172/jci9461
Abstract
No abstract availableKeywords
This publication has 19 references indexed in Scilit:
- The Grb2 binding site is required for the induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase.2000
- Fatal myeloproliferation, induced in mice by TEL/PDGFβR expression, depends on PDGFβR tyrosines 579/581Journal of Clinical Investigation, 2000
- Lessons learned from the development of an Abl tyrosine kinase inhibitor for chronic myelogenous leukemiaJournal of Clinical Investigation, 2000
- Diverse Signaling Pathways Activated by Growth Factor Receptors Induce Broadly Overlapping, Rather Than Independent, Sets of GenesCell, 1999
- The P190, P210, and P230 Forms of the BCR/ABL Oncogene Induce a Similar Chronic Myeloid Leukemia–like Syndrome in Mice but Have Different Lymphoid Leukemogenic ActivityThe Journal of Experimental Medicine, 1999
- The TEL/platelet-derived growth factor β receptor (PDGFβR) fusion in chronic myelomonocytic leukemia is a transforming protein that self-associates and activates PDGFβR kinase-dependent signaling pathwaysProceedings of the National Academy of Sciences, 1996
- Alternative signals to RAS for hematopoietic transformation by the BCR-ABL oncogeneCell, 1995
- Chromosomal translocations in human cancerNature, 1994
- Tyr-716 in the platelet-derived growth factor beta-receptor kinase insert is involved in GRB2 binding and Ras activation.Molecular and Cellular Biology, 1994
- t(5;12)(q31;p12) A clinical entity with features of both myeloid leukemia and chronic myelomonocytic leukemiaCancer Genetics and Cytogenetics, 1993