members

Richard Van Etten, MD, PhD
Principal Investigator
Phone: 617-636-6449
Fax: 617-636-6127
Richard Van Etten

BS, Mathematics, M.I.T., Cambridge, MA
BS, Biology, M.I.T., Cambridge, MA
MD, Stanford University School of Medicine, Stanford, CA
PhD, Biophysics, Stanford University, Stanford, CA

Dr. Van Etten received an MD and PhD in Biophysics from Stanford University School of Medicine, where he worked with David Clayton on molecular genetics of mammalian mitochondrial DNA. After postgraduate training in internal medicine and hematology at Brigham & Women's Hospital in Boston, he was a postdoctoral fellow with David Baltimore at the Whitehead Institute. He was a faculty member in the Departments of Genetics and Medicine at Harvard Medical School until 2003, when he joined MORI as Professor of Medicine and Director of Hematologic Malignancies. The Van Etten lab studies the molecular pathogenesis of leukemia with an emphasis on dysregulated tyrosine kinases and mouse model systems. A new area of interest is oxidative stress and the role of the peroxiredoxin family of antioxidant enzymes in cell signaling and cancer.


Wayne W. Chan, BSE
MD/PhD Student in Cell and Molecular Physiology
617-636-6424
Wayne Chan

BSE, Chemical Engineering, Princeton University, NJ

My work is focused on defining the signaling pathways downstream of Bcr-Abl in the molecular pathogenesis of chronic myelogenous leukemia (CML). Our laboratory has shown that binding of the adaptor protein Grb2 at Tyr177 of the Bcr-Abl fusion protein is required for the induction of a CML-like myeloproliferative disease. However, these results do not exclude the binding of other SH2 domain containing proteins at Tyr177. In order to dissect the roles of other adaptor proteins in the pathogenesis of CML, we have taken a genetic approach and generated various Bcr-Abl mutants with different predicted binding specificities. I am currently testing these mutants to determine if they confer a different phenotype in our bone marrow transplant mouse model.


Alex Danilov
Hematology/Oncology Fellow
Alex Danilov

 

 

 

 

 

 


Darci Gaiotti
Clinical Fellow
617-636-6421
Darci Gaiotti

 

 

 

 


 

L. Cristina Gavrilescu, PhD
Postdoctoral Fellow
617-636-6425
L. Cristina Gavrilescu

Maitrise, Cellular Biology and Physiology, University Pierre and Marie Curie, Paris, France
MS, Biology, New York University, New York, NY
PhD, Immunology, Cornell University, Ithaca, NY

While CML is due to the Bcr-Abl translocation, many other human CML-like diseases have been identified in the last decade, and are induced by other translocations, in particular those involving the intracellular part of type II RTKs (Receptor Tyrosine kinases). I am particularly focusing on FGFR1 and its different fusion partners (ZNF198, FOP, etc) and PDGFRa and it’s fusion partners (Fip1L1, Bcr). These diseases take then the name of EMS (8p11 myeloproliferative syndrome) in cases involving the intracellular domain of FGFR1, or CEL (chronic eosinophilic leukemia) if the platelet-derived growth factor receptor alpha subunit (PDGFRa) is involved. I Myc-tagged a variety of ZNF1980FGFR1 point mutants for ease of study, reconstructed the patient-isolated Bcr-PDGFRa oncogene and created specific point-mutants, and am working on creating a lentiviral vector that would express at the same time both an siRNA and the oncogene of interest. Our laboratory developed a bone marrow transplant mouse model for leukemia/lymphoma, using retroviruses encoding the oncogenes of interest, that I am using it to carry out a preclinical testing of molecularly targeted therapeutic agents for the different growth-factor-receptor-derived oncogenes I study.



Mo-Ying Hsieh

Graduate Student
617-636-9539
Mo-Ying Hsieh

 


Nilamani Jena, PhD
Postdoctoral Fellow
617-636-3098
Nilamani Jena

BS, Orissa University of Agriculture and Technology, Bhubaneswar, India
MS, Madurai Kamaraj University, Madurai, India
PhD, Kimmel Cancer Center Thomas Jefferson, University, Philadelphia, PA

Deregulated cell proliferation or reduced cell death or both are inalienable components of tumor development. The BCR-ABL oncogene, which causes chronic myeloid leukemia, induces cellular proliferation and inhibits apoptosis. BCR-ABL activates several pathways leading to activation of the cell cycle machinery. The process of cell cycle is quite complex, and this complexity is amplified due to presence of redundancy in enzymes and their regulators. The objective of my research is to identify and characterize specific cell cycle modulators that are targets of BCR-ABL mediated cell proliferation signals. Previously, I have shown that, despite the redundancy in D-type Cyclins, Cyclin D2 is essential for BCR-ABL induced cell proliferation. At present, my goal is to identify the role of cyclin dependent kinase inhibitor p21 in BCR-ABL mediated cell proliferation.


Katherine Lazarides, BS
Research Assistant
617-636-0148
Katherine Lazarides

BS, University of Massachusetts, Amherst 



 

 

 

 


Juliana Lewis
Graduate Student
617-636-0148
Juliana Lewis

 

 


 

 

 


Yi-Fen Lu, PhD
Graduate Student
617-636-0148
Yi-Fen Lu

MS Immunology, National Taiwan University, Taiwan
PhD Candidate, Sackler School, Tufts University, Boston

My work is mainly focused on developing potential immunotherapy of relapse-phase CML. Despite the clinical success of treating patients with imatinib, the Abl kinase inhibitor is never curing. Allogeneic stem cell transplantation (allo-SCT) thus remains the only curative therapy. For patients having CML relapse after allo-SCT, donor leukocyte infusion (DLI) could induce remission in most of the patients; however, the mechanism is not fully understood. One part of my work seeks to understand the mechanism underlying this phenomenon. I am also developing the therapeutic mouse model that combines the use of imatinib and DLI on mixed chimera.


Marcos Salazar
Graduate Student
617-636-1107
Marcos Salazar

 

 

 

 


Christoph Walz, MD
Postdoctoral Fellow
617-636-6424
Christoph Walz

MD, University of Heidelberg

Chronic myeloproliferative disorders (CMPD) are clonal disorders of the myeloid stem cell. In a subset of patients with CMPD, acquired aberrations of certain protein molecules, so-called tyrosine kinases as ABL1 and JAK2, can be frequently identified. Using bone marrow transplantation models, we are trying to determine the impact of ABL1 and JAK2 downstream molecules for the molecular pathogenesis, in particular the role of Signal Transducers and Activators of Transcription (STAT5) proteins. In addition, we are investigating if and how JAK2 expression levels may alter the myeloproliferative disease phenotype in vivo.

 


Virginia Zaleskas, MD
Postdoctoral Fellow
617-636-1108
Virginia Zaleskas

MD, Tufts University School of Medicine

Our laboratory and others have demonstrated activation of the JAK/STAT signaling pathway by Bcr-Abl, the product of the Philadelphia chromosome in chronic myeloid leukemia (CML). However, the importance of this pathway to the pathogenesis of CML and its utility as a therapeutic target in treatment of CML are not known. My project focuses on the mechanism of activation of STAT proteins in CML cells and the role of this pathway in leukemogenesis by Bcr-Abl.

 

 

 


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