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Department of Medicine

Robert Wieder, M.D., Ph.D.


Provost, RBHS-Newark

Professor

Department of Medicine
wiederro@njms.rutgers.edu
 

Clinical Info

 

Hospital Affiliation

University Hospital, Newark

 

Insurance Participation

Insurance Participation: with Provider Number ( where applicable ) The information below is subject to change and should not be relied upon until after it is verified with the insurance company. In addition, psychiatric providers should be contacted directly for information on their participation with managed care and insurance companies.

Last Updated:

 

Biography

Overview

Awards & Achievements

Outstanding Breast Cancer Researcher Award, State of New Jersey Commission on Cancer Research, Clinical Sciences Faculty of the Year Award, UMDNJ-NJMS Faculty Association 2001

Lab Members

Robert Wieder, MD, PhD
Email: wiederro@umdnj.edu

Research: Our laboratory studies the mechanisms of dormancy and resistance to chemotherapy in breast cancer cells that metastasize to the bone marrow.

Tanya Dasgupta
Email: tdasgupt@umdnj.edu

Haiyan Lu
Email: luha@umdnj.edu

Samir Tivari
Email: tivarisa@umdnj.edu

Sri Harikrishna Vellanki, PhD
Email: vellans1@umdnj.edu

 

Education

M.D., 1983, Mount Sinai School of Medicine of New York
Ph.D., 1982, Mount Sinai School of Medicine of New York

 

Licensure & Certification

Medical Licensure
New Jersey

 

 

Current Research

Our laboratory studies the mechanisms of dormancy and resistance to chemotherapy in breast cancer cells that metastasize to the bone marrow. In a model of dormancy we demonstrated that well differentiated breast cancer cells that metastasize to the bone marrow are affected by growth factors present in the bone marrow stroma, that include basic fibroblast growth factor (FGF-2). FGF-2 induces a state of dormancy in well differentiated breast cancer cells that includes growth arrest in the G1 phase of the cell cycle and a change in the cellular integrin repertoire. Through an upregulated integrin alpha 5 beta 1, the cells receive specific survival signaling through a number of singaling pathways, that include the PI3K/Akt pathway. A number of other signaling pathways that engage in crosstalk contribute to the survival of these cells. Our current efforts are directed at understanding the mechanism of activation and crosstalk among a number of these pathways, with an emphasis on the small GTPase Rho.

Our interests also include understanding the mechanisms of cell death signaling by chemotherapy agents and the effects of retinoids and deltanoids in potentiating these cell death signaling pathways. These laboratory investigations are being translated into clinical trials.



 

 

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