Research Topics
Species | Ruibao RenSummaryAffiliation: Brandeis University Country: USA Publications
Research Grants
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Detail Information
Publications
Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenous leukaemiaRuibao Ren
Rosenstiel Basic Medical Sciences Research Center, MS029, Brandeis University, 415 South Street, Waltham, Massachusetts 02454 9110, USA
Nat Rev Cancer 5:172-83. 2005..What have clinical trials of imatinib and studies using mouse models for BCR-ABL leukaemogenesis taught us about the functions of BCR-ABL beyond its kinase activity, and how these functions contribute to CML pathogenesis?..- Dissecting the molecular mechanism of chronic myelogenous leukemia using murine modelsRuibao Ren
Leuk Lymphoma 43:1549-61. 2002.... - The molecular mechanism of chronic myelogenous leukemia and its therapeutic implications: studies in a murine modelRuibao Ren
Rosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts 02454 9110, USA
Oncogene 21:8629-42. 2002..The in vivo studies of leukemogenesis will help to advance mechanism-based therapies for CML, as well as to understand fundamental rules of leukemogenesis and hematopoiesis... - Modeling the dosage effect of oncogenes in leukemogenesisRuibao Ren
Rosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, MA 02454 9110, USA
Curr Opin Hematol 11:25-34. 2004.... 
Oncogenic NRAS, KRAS, and HRAS exhibit different leukemogenic potentials in miceChaitali Parikh
Rosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, MA 02454, USA
Cancer Res 67:7139-46. 2007..The models established here provide a system for further studying the molecular mechanisms in the pathogenesis of myeloid malignancies and for testing targeted therapies...
Mouse model for NRAS-induced leukemogenesisChaitali Parikh
Rosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts, USA
Methods Enzymol 439:15-24. 2008..This model provides a system for further studying the molecular mechanisms in the pathogenesis of myeloid malignancies and for testing targeted therapies...- IRF-4 functions as a tumor suppressor in early B-cell developmentJaime Acquaviva
Rosenstiel Basic Medical Sciences Research Center and Department of Biology, Brandeis University, Waltham, MA 02454 9110, USA
Blood 112:3798-806. 2008..The context dependent roles of IRF-4 in oncogenesis should be an important consideration in developing cancer therapies targeting IRF-4... - Cooperation between deficiencies of IRF-4 and IRF-8 promotes both myeloid and lymphoid tumorigenesisSeung Hee Jo
Rosenstiel Basic Medical Sciences Research Center and Department of Biology, Brandeis University, Waltham, MA, USA
Blood 116:2759-67. 2010..Combined losses of IRF-4 and IRF-8 therefore can cooperate in the development of both myeloid and lymphoid tumors... - IRF-4 suppresses BCR/ABL transformation of myeloid cells in a DNA binding-independent mannerSeung Hee Jo
Rosenstiel Basic Medical Sciences Research Center and Department of Biology, Brandeis University, Waltham, Massachusetts 02454, USA
J Biol Chem 287:1770-8. 2012..However, IRF-4 tumor suppressor activity is lost in IRF association domain (IAD) deletion mutants. These results demonstrate that IRF-4 suppresses BCR/ABL transformation by a novel cytoplasmic function involving its IAD domain... - Palmitoylation of oncogenic NRAS is essential for leukemogenesisBenjamin Cuiffo
Rosenstiel Basic Medical Sciences Research Center and Department of Biology, Brandeis University, Waltham, MA, USA
Blood 115:3598-605. 2010.... - Targeted degradation of the AML1/MDS1/EVI1 oncoprotein by arsenic trioxideDavid Shackelford
Rosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts 02454-9110, USA
Cancer Res 66:11360-9. 2006..Our results suggest that ATO could be used as a part of targeted therapy for AME-, AML1/MDS1-, MDS1/EVI1-, and EVI1-positive human cancers... - Effect of Ras inhibition in hematopoiesis and BCR/ABL leukemogenesisKarina J Baum
Rosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, MA 02454, USA
J Hematol Oncol 1:5. 2008..These results suggest that Ras activation is essential for the development of lymphoid and erythroid cells but not myeloid cells and that Ras is a critical target of BCR/ABL in the pathogenesis of CML, but not B-ALL... - Oncogenic NRAS rapidly and efficiently induces CMML- and AML-like diseases in miceChaitali Parikh
Rosenstiel Basic Medical Sciences Research Center, MS029, Brandeis University, Waltham, MA 02454-9110, USA
Blood 108:2349-57. 2006..The mouse model for NRAS leukemogenesis established here provides a system for further studying the molecular mechanisms in the pathogenesis of myeloid malignancies and for testing relevant therapies... - Both AML1 and EVI1 oncogenic components are required for the cooperation of AML1/MDS1/EVI1 with BCR/ABL in the induction of acute myelogenous leukemia in miceGrace M Cuenco
Rosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, MA 02454-9110, USA
Oncogene 23:569-79. 2004..The results indicate that both the AML1 and EVI1 oncogenic components are required for the leukemogenic potential of AME and for the cooperation of AME and BCR/ABL in the induction of AML... - The coiled-coil domain and Tyr177 of bcr are required to induce a murine chronic myelogenous leukemia-like disease by bcr/ablYiping He
Department of Pathology and Laboratory Medicine, Institute for Medicine and Engineering, University of Pennsylvania, Philadelphia, USA
Blood 99:2957-68. 2002..These results show that both the bcr coiled-coil domain and Tyr177 are required for MPD induction by bcr/abl and provide the basis for investigating downstream signaling pathways that lead to CML... - c-CBL is not required for leukemia induction by Bcr-Abl in miceDaniela M Dinulescu
Department of Cell and Developmental Biology, OR, USA
Oncogene 22:8852-60. 2003..Most importantly, in a transplantation model of CML, Bcr-Abl was capable of inducing fatal leukemia in mice in the absence of c-Cbl protein. Our results indicate that c-Cbl is dispensable for Bcr-Abl-induced leukemogenesis in mice... - Localization of BCR-ABL to F-actin regulates cell adhesion but does not attenuate CML developmentJason A Wertheim
Department of Pathology and Laboratory Medicine, University of Pennsylvania, 611 BRB II/III, 421 Curie Blvd, Philadelphia, PA 19104-6160
Blood 102:2220-8. 2003..Together, our results suggest that F-actin localization may play a pivotal role in modulating adhesion but that it is dispensable for the development of CML...
Research Grants
- Ras signaling in leukemogenesisRuibao Ren; Fiscal Year: 2010..The ultimate goal of these studies is to identify critical molecular events in Ras leukemogenesis, allowing therapeutic interventions of leukemias involving Ras. ..
- IDENTIFICATION OF TARGETS OF BCR ABL IN THE LEUKEMOGENICRuibao Ren; Fiscal Year: 2005..These studies will help to further design rational therapeutic interventions for CML and to understand the mechanisms involved in leukemogenesis in general. ..
- REGULATION OF IMMUNOGLOBULIN GENE EXPRESSION IN B CELLSRuibao Ren; Fiscal Year: 2003..The rules of combinatorial transcription activation will also allow the design of novel transcription regulatory sequences to direct therapeutic expression of exogenous genes in selected cells. ..
- BCR-ABL TARGET IDENTIFICATION IN THE LEUKEMOGENIC PATHWARuibao Ren; Fiscal Year: 2000....
- Ras signaling in leukemogenesisRuibao Ren; Fiscal Year: 2009..The ultimate goal of these studies is to identify critical molecular events in Ras leukemogenesis, allowing therapeutic interventions of leukemias involving Ras. ..