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Peter V. Hauschka, PhD

Associate Professor, Department of Orthopaedic surgery, Harvard Medical School

Senior Research Associate, Orthopaedic Surgery, Boston Children's Hospital

Contact Info

Peter Hauschka
Boston Children's Hospital
300 Longwood Avenue
Boston, MA, 02115
Mailstop: Enders 1007
Phone: 617-919-2950
Fax: 617-919-2952
peter.hauschka@childrens.harvard.edu

Assistant

Not Available.

DF/HCC Program Affiliation

Breast Cancer
Angiogenesis, Invasion and Metastasis

Research Abstract

Osteolytic Tumors in Bone: Metastatic breast adenocarcinoma and multiple myeloma cause morbidity and death because of tumor cell interference and "takeover" of the normal regulatory pathways involving bone marrow stromal cells, osteoblasts, and resorptive osteoclasts. We are investigating human breast cancer cells, testing the hypothesis that mimicry of the osteoblast phoneotype provides survival advantages in skeletal metastatic sites. Interaction of breast adnocarcinoma cells with normal bone marrow stromal cells in the metatstatic site stimulates osteoclast dvelopment and bone destruction. We are testing whether the osteolytic reaction to breast adenocarcinoma cells is achieved by upregulation of the osteoclast differentiation receptor, RANK, or its ligand (RANKL), or downregulation of the protective decoy receptor osteoprotegerin (OPG). The identical receptor (RANK) and ligand (RANKL) determine the survival of dendritic cells (antigen-presenting cells) for the continued instruction of T-cells.


Osteolytic Tumors in Bone: Metastatic breast adenocarcinoma and multiple myeloma cause morbidity and death because of tumor cell interference and "takeover" of the normal regulatory pathways involving bone marrow stromal cells, osteoblasts, and resorptive osteoclasts. Interaction of breast adenocarcinoma cells with normal bone marrow stromal cells in the metastatic site stimulates osteoclast development and bone destruction. We are investigating human breast cancer cells, testing two hypotheses: 1) does breast cancer mimicry of the osteoblast phenotype provide survival advantages in skeletal metastatic sites? and 2) is the osteolytic reaction to breast adenocarcinoma cells is achieved by upregulation of the osteoclast differentiation receptor, RANK, or its ligand RANKL, or downregulation of the protective decoy receptor osteoprotegerin OPG? The identical RANK-RANKL receptor-ligand pair determine the survival of dendritic cells (antigen-presenting cells) for the continued instruction of T-cells.

Publications

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