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Jean-Jacques Body

Researcher at Université libre de Bruxelles

Publications -  397
Citations -  21506

Jean-Jacques Body is an academic researcher from Université libre de Bruxelles. The author has contributed to research in topics: Breast cancer & Zoledronic acid. The author has an hindex of 70, co-authored 384 publications receiving 19608 citations. Previous affiliations of Jean-Jacques Body include The Breast Cancer Research Foundation & University of California, San Francisco.

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Extracellular calcium downregulates estrogen receptor alpha and increases its transcriptional activity through calcium-sensing receptor in breast cancer cells.

TL;DR: Calcium released during the process of metastatic bone destruction could modulate the functions of the estrogen receptor, a key receptor involved in breast cancer cells growth and function, and thus participate in the pathogenesis of tumor-induced osteolysis.
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Rationale for the use of bisphosphonates in osteoblastic and osteolytic bone lesions.

Jean-Jacques Body
- 01 Aug 2003 - 
TL;DR: Zoledronic acid is the first bisphosphonate shown to have a direct clinical benefit in the treatment of osteoblastic bone metastases, reducing the number and rate of skeletal events in prostate cancer patients with metastatic bone disease.
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Efficacy and safety of the bisphosphonate Tiludronate for the treatment of tumor-associated hypercalcemia

TL;DR: Compared with aminobisphosphonates, tiludronate is not indicated for the treatment of tumor-associated hypercalcemia because of the need for high iv doses which are potentially nephrotoxic.
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Heterogeneity of metabolic response to systemic therapy in metastatic breast cancer patients.

TL;DR: Whole-body FDG-PET allows frequent heterogeneous responses after systemic therapy to be identified in bone-dominant metastatic breast cancer patients.
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Role of farnesoid X receptor (FXR) in the process of differentiation of bone marrow stromal cells into osteoblasts.

TL;DR: A new role for FXR is supported in the modulation of osteoblast/adipocyte balance: its activation stimulates RUNX2-mediated osteoblastic differentiation of BMSC, whereas its inhibition leads to an adipocyte-like phenotype.