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Osteoporosis: HELP
Articles by Philippe Clézardin
Based on 3 articles published since 2010
(Why 3 articles?)

Between 2010 and 2020, P. Clézardin wrote the following 3 articles about Osteoporosis.
+ Citations + Abstracts
1 Review Adjuvant bisphosphonates in early breast cancer: consensus guidance for clinical practice from a European Panel. 2016

Hadji, P / Coleman, R E / Wilson, C / Powles, T J / Clézardin, P / Aapro, M / Costa, L / Body, J-J / Markopoulos, C / Santini, D / Diel, I / Di Leo, A / Cameron, D / Dodwell, D / Smith, I / Gnant, M / Gray, R / Harbeck, N / Thurlimann, B / Untch, M / Cortes, J / Martin, M / Albert, U-S / Conte, P-F / Ejlertsen, B / Bergh, J / Kaufmann, M / Holen, I. ·Department of Bone Oncology, Endocrinology and Reproductive Medicine, Philipps-University of Marburg, Frankfurt, Germany. · Academic Unit of Clinical Oncology, Weston Park Hospital, University of Sheffield, Sheffield r.e.coleman@sheffield.ac.uk. · Academic Unit of Clinical Oncology, Weston Park Hospital, University of Sheffield, Sheffield. · Cancer Centre London, Wimbledon, UK. · INSERM, Research Unit UMR403, University of Lyon, School of Medicine Lyon-Est, Lyon, France. · Breast Center of the Multidisciplinary Oncology Institute, Genolier, Switzerland. · Hospital de Santa Maria & Lisbon School of Medicine, Institute of Molecular Biology, Lisbon, Potugal. · CHU Brugmann, Université Libre de Bruxelles (ULB), Brussels, Belgium. · Medical School, National University of Athens, Athens, Greece. · Medical Oncology, University Campus Bio-medico, Rome, Italy. · Institute for Gynaecological Oncology, Centre for Comprehensive Gynecology, Mannheim, Germany. · Sandro Pitigliani Medical Oncology Unit, Department of Oncology, Hospital of Prato, Prato, Italy. · University of Edinburgh Cancer Research Centre, Western General Hospital, Edinburgh. · Institute of Oncology, Bexley Wing, St James Hospital Leeds, Leeds. · The Royal Marsden Hospital and Institute of Cancer Research, London, UK. · Department of Surgery and Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria. · Clinical Trials and Epidemiological Unit, University of Oxford, Oxford, UK. · Breast Center, Department of Obstetrics and Gynaecology, University of Munich, Munich, Germany. · Kantonsspital St Gallen, Breast Center, St Gallen, Switzerland. · Interdisciplinary Breast Cancer Center HELIOS Klinikum Berlin-Buch Germany, Gynecologic Oncology and Obstetrics, Berlin, Germany. · Department of Oncology, Vall d'Hebron Institute of Oncology (VHIO), Barcelona. · Department of Medical Oncology, Institute of Investigation Sanitaria Gregorio Marañón, University Complutense, Madrid, Spain. · Department of Surgery, Oncology and Gastroenterology, University of Padova, Padova, Italy. · Danish Breast Cancer Cooperative Group Statistical Center Department of Oncology Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. · Karolinska Institute and University Hospital, Stockholm, Sweden. · Institute for Obstetrics and Gynaecology, Goethe University, Frankfurt, Germany. ·Ann Oncol · Pubmed #26681681.

ABSTRACT: Bisphosphonates have been studied in randomised trials in early breast cancer to investigate their ability to prevent cancer treatment-induced bone loss (CTIBL) and reduce the risk of disease recurrence and metastasis. Treatment benefits have been reported but bisphosphonates do not currently have regulatory approval for either of these potential indications. This consensus paper provides a review of the evidence and offers guidance to breast cancer clinicians on the use of bisphosphonates in early breast cancer. Using the nominal group methodology for consensus, a systematic review of the literature was augmented by a workshop held in October 2014 for breast cancer and bone specialists to present and debate the available pre-clinical and clinical evidence for the use of adjuvant bisphosphonates. This was followed by a questionnaire to all members of the writing committee to identify areas of consensus. The panel recommended that bisphosphonates should be considered as part of routine clinical practice for the prevention of CTIBL in all patients with a T score of <-2.0 or ≥2 clinical risk factors for fracture. Compelling evidence from a meta-analysis of trial data of >18,000 patients supports clinically significant benefits of bisphosphonates on the development of bone metastases and breast cancer mortality in post-menopausal women or those receiving ovarian suppression therapy. Therefore, the panel recommends that bisphosphonates (either intravenous zoledronic acid or oral clodronate) are considered as part of the adjuvant breast cancer treatment in this population and the potential benefits and risks discussed with relevant patients.

2 Review Metastasis and bone loss: advancing treatment and prevention. 2010

Coleman, Robert E / Lipton, Allan / Roodman, G David / Guise, Theresa A / Boyce, Brendon F / Brufsky, Adam M / Clézardin, Philippe / Croucher, Peter I / Gralow, Julie R / Hadji, Peyman / Holen, Ingunn / Mundy, Gregory R / Smith, Matthew R / Suva, Larry J. ·Yorkshire Cancer Research Professor of Medical Oncology, Academic Unit of Clinical Oncology, Weston Park Hospital, Whitham Road, Sheffield S102SJ, UK. r.e.coleman@sheffield.ac.uk ·Cancer Treat Rev · Pubmed #20478658.

ABSTRACT: Tumor metastasis to the skeleton affects over 400,000 individuals in the United States annually, more than any other site of metastasis, including significant proportions of patients with breast, prostate, lung and other solid tumors. Research on the bone microenvironment and its role in metastasis suggests a complex role in tumor growth. Parallel preclinical and clinical investigations into the role of adjuvant bone-targeted agents in preventing metastasis and avoiding cancer therapy-induced bone loss have recently reported exciting and intriguing results. A multidisciplinary consensus conference convened to review recent progress in basic and clinical research, assess gaps in current knowledge and prioritize recommendations to advance research over the next 5 years. The program addressed three topics: advancing understanding of metastasis prevention in the context of bone pathophysiology; developing therapeutic approaches to prevent metastasis and defining strategies to prevent cancer therapy-induced bone loss. Several priorities were identified: (1) further investigate the effects of bone-targeted therapies on tumor and immune cell interactions within the bone microenvironment; (2) utilize and further develop preclinical models to study combination therapies; (3) conduct clinical studies of bone-targeted therapies with radiation and chemotherapy across a range of solid tumors; (4) develop biomarkers to identify patients most likely to benefit from bone-targeted therapies; (5) educate physicians on bone loss and fracture risk; (6) define optimal endpoints and new measures of efficacy for future clinical trials; and (7) define the optimum type, dose and schedule of adjuvant bone-targeted therapy.

3 Article Lysophosphatidic acid receptor type 1 (LPA1) plays a functional role in osteoclast differentiation and bone resorption activity. 2014

David, Marion / Machuca-Gayet, Irma / Kikuta, Junichi / Ottewell, Penelope / Mima, Fuka / Leblanc, Raphael / Bonnelye, Edith / Ribeiro, Johnny / Holen, Ingunn / Lopez Vales, Rùben / Jurdic, Pierre / Chun, Jerold / Clézardin, Philippe / Ishii, Masaru / Peyruchaud, Olivier. ·From the INSERM, UMR1033, UCB Lyon 1, Faculté de Médecine Lyon Est, 69732 Lyon, France. ·J Biol Chem · Pubmed #24429286.

ABSTRACT: Lysophosphatidic acid (LPA) is a natural bioactive lipid that acts through six different G protein-coupled receptors (LPA1-6) with pleiotropic activities on multiple cell types. We have previously demonstrated that LPA is necessary for successful in vitro osteoclastogenesis of bone marrow cells. Bone cells controlling bone remodeling (i.e. osteoblasts, osteoclasts, and osteocytes) express LPA1, but delineating the role of this receptor in bone remodeling is still pending. Despite Lpar1(-/-) mice displaying a low bone mass phenotype, we demonstrated that bone marrow cell-induced osteoclastogenesis was reduced in Lpar1(-/-) mice but not in Lpar2(-/-) and Lpar3(-/-) animals. Expression of LPA1 was up-regulated during osteoclastogenesis, and LPA1 antagonists (Ki16425, Debio0719, and VPC12249) inhibited osteoclast differentiation. Blocking LPA1 activity with Ki16425 inhibited expression of nuclear factor of activated T-cell cytoplasmic 1 (NFATc1) and dendritic cell-specific transmembrane protein and interfered with the fusion but not the proliferation of osteoclast precursors. Similar to wild type osteoclasts treated with Ki16425, mature Lpar1(-/-) osteoclasts had reduced podosome belt and sealing zone resulting in reduced mineralized matrix resorption. Additionally, LPA1 expression markedly increased in the bone of ovariectomized mice, which was blocked by bisphosphonate treatment. Conversely, systemic treatment with Debio0719 prevented ovariectomy-induced cancellous bone loss. Moreover, intravital multiphoton microscopy revealed that Debio0719 reduced the retention of CX3CR1-EGFP(+) osteoclast precursors in bone by increasing their mobility in the bone marrow cavity. Overall, our results demonstrate that LPA1 is essential for in vitro and in vivo osteoclast activities. Therefore, LPA1 emerges as a new target for the treatment of diseases associated with excess bone loss.