Philippe Clézardin

ORCID: 0000-0003-0149-4463
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About
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Research Areas
  • Bone health and treatments
  • Radiopharmaceutical Chemistry and Applications
  • Medical Imaging and Pathology Studies
  • Bone Metabolism and Diseases
  • Cell Adhesion Molecules Research
  • Angiogenesis and VEGF in Cancer
  • Cancer Diagnosis and Treatment
  • Microbial metabolism and enzyme function
  • MicroRNA in disease regulation
  • HER2/EGFR in Cancer Research
  • Cancer, Hypoxia, and Metabolism
  • Monoclonal and Polyclonal Antibodies Research
  • Prostate Cancer Treatment and Research
  • Management of metastatic bone disease
  • Protease and Inhibitor Mechanisms
  • Platelet Disorders and Treatments
  • Cancer Cells and Metastasis
  • Sphingolipid Metabolism and Signaling
  • Circular RNAs in diseases
  • Bone health and osteoporosis research
  • Bone and Joint Diseases
  • Inflammatory mediators and NSAID effects
  • Glycosylation and Glycoproteins Research
  • Aldose Reductase and Taurine
  • Alkaline Phosphatase Research Studies

Université Claude Bernard Lyon 1
2015-2024

Pathophysiology, Diagnosis and Treatment of Bone Diseases
2005-2024

Inserm
2015-2024

University of Sheffield
2019-2024

Dana-Farber Cancer Institute
2019

Hôpital Orthopédique de la Suisse Romande
2016

Hospices Civils de Lyon
2016

Università Campus Bio-Medico
2013

Institut Curie
2013

Weston Park Cancer Centre
2012

The role of lysophosphatidic acid (LPA) in cancer is poorly understood. Here we provide evidence for a LPA the progression breast bone metastases. receptors LPA1, LPA2, and LPA3 were expressed human primary tumors series cell lines. inducible overexpression LPA1 MDA-BO2 cells specifically sensitized these to mitogenic action vitro. In vivo, enhanced growth subcutaneous tumor xenografts promoted metastasis formation mice by increasing both skeletal destruction. This suggested that endogenous...

10.1172/jci22123 article EN Journal of Clinical Investigation 2004-12-15

The role of lysophosphatidic acid (LPA) in cancer is poorly understood. Here we provide evidence for a LPA the progression breast bone metastases. receptors LPA1, LPA2, and LPA3 were expressed human primary tumors series cell lines. inducible overexpression LPA1 MDA-BO2 cells specifically sensitized these to mitogenic action vitro. In vivo, enhanced growth subcutaneous tumor xenografts promoted metastasis formation mice by increasing both skeletal destruction. This suggested that endogenous...

10.1172/jci200422123 article EN Journal of Clinical Investigation 2004-12-15

Bisphosphonates exhibit direct antitumor activity in animal models, but only at high doses that are incompatible with the clinical dosing regimens approved for treatment of cancer patients skeletal metastases. We compared effects bisphosphonates zoledronic acid and clodronate a mouse model bone metastasis. Mice (n = 6–10 per group) were treated acid, clodronate, or vehicle starting before (preventive protocols) after (treatment intravenous injection human B02/GFP.2 breast cells, which...

10.1093/jnci/djk054 article EN JNCI Journal of the National Cancer Institute 2007-02-20

The reasons why tumor cells metastasize to bone remain obscure. There is some evidence support the theory that integrins (acting as cell surface adhesion receptors) play a role in mediating metastasis certain organs. Here, we report overexpression of functionally active integrin alpha(v)b3 Chinese hamster ovary (CHO) drastically increased incidence, number, and area metastases nude mice compared with those observed mock-transfected CHO (CHO dhfr+) or expressing inactive beta3Delta744)....

10.1096/fj.01-0911fje article EN The FASEB Journal 2002-06-21

Platelet-derived lysophosphatidic acid (LPA) supports the progression of breast and ovarian cancer metastasis to bone. The mechanisms through which LPA promotes bone formation are, however, unknown. Here we report that silencing type 1 receptor (LPA(1)) in cells blocks production tumor-derived cytokines are potent activators osteoclast-mediated destruction significantly reduces osteolytic metastases. Moreover, functional blockade action on its cognate LPA(1) using a pharmacological...

10.1073/pnas.0600979103 article EN Proceedings of the National Academy of Sciences 2006-06-13

Abstract In breast cancer bone metastasis, tumor cells stimulate osteoclast-mediated resorption, and bone-derived growth factors released from resorbed growth. The αvβ3 integrin is an adhesion receptor expressed by osteoclasts. It implicated in cell invasion resorption. Here, we hypothesized that the therapeutic targeting of would prevent metastasis formation. We first showed that, compared with mock-transfected cells, i.v. inoculation αvβ3-overexpressing MDA-MB-231 animals increased...

10.1158/0008-5472.can-06-4499 article EN Cancer Research 2007-06-15

Abstract Bone morphogenetic protein 7 (BMP7) counteracts the physiological epithelial-to-mesenchymal transition (EMT), a process that is indicative of epithelial plasticity. Because EMT involved in cancer, we investigated whether BMP7 plays role breast cancer growth and metastasis. In this study, show decreased expression primary significantly associated with formation clinically overt bone metastases patients ≥10 years follow-up. line these clinical observations, inversely related to...

10.1158/0008-5472.can-06-2490 article EN Cancer Research 2007-09-15

Abstract Osteoclasts mediate bone destruction in breast cancer skeletal metastases. Cathepsin K is a proteinase that secreted by osteoclasts and degrades bone. Here, immunohistochemistry revealed cathepsin was expressed not only but also cells metastasize to Following intratibial injection with K–expressing human BT474 cells, tumor-bearing mice treated clinical dosing regimen of inhibitor (CKI; 50 mg/kg, twice daily) had osteolytic lesions were 79% smaller than those the vehicle. The effect...

10.1158/0008-5472.can-06-3940 article EN Cancer Research 2007-10-15

The aim of this study was to determine whether Dickkopf-1 (Dkk-1) expression in breast cancer associated with bone metastases. We first analysed Dkk-1 by human cell lines that induce osteolytic or osteoblastic lesions animals. levels were then measured the marrow aspirates hind limbs from eight NMRI mice inoculated cells induced metastases and 11 age-matched non-inoculated control Finally, serum 17 women complete remission, 19 metastases, 16 at non-bone sites healthy women. Only animals...

10.1038/sj.bjc.6603959 article EN cc-by-nc-sa British Journal of Cancer 2007-09-18

Receptor activator of NFkB (RANK), its ligand (RANKL) and the decoy receptor RANKL (osteoprotegerin, OPG) play a pivotal role in bone remodeling by regulating osteoclasts formation activity. stimulates migration RANK-expressing tumor cells vitro, conversely inhibited OPG.We examined mRNA expression levels RANKL/RANK/OPG publicly available microarray dataset 295 primary breast cancer patients. We next analyzed RANK immunohistochemistry an independent series 93 specimens investigated possible...

10.1371/journal.pone.0019234 article EN cc-by PLoS ONE 2011-04-29

miRNAs are master regulators of gene expression that play key roles in cancer metastasis. During bone metastasis, metastatic tumor cells must rewire their biology and express genes normally expressed by (a process called osteomimicry), which endow with full competence for outgrowth the marrow. Here, we establish miR-30 family members miR-30a, miR-30b, miR-30c, miR-30d, miR-30e as suppressors breast metastasis regulate multiple pathways, including osteomimicry. Low primary tumors from...

10.1158/0008-5472.can-17-3058 article EN Cancer Research 2018-07-24

Adaptation to hypoxia is a driving force for tumor progression that leads therapy resistance and poor clinical outcome. Hypoxic responses are mainly mediated by hypoxia-inducible transcription factor-1 (HIF-1). One critical HIF-1 target mediating lysyl oxidase (LOX), which catalyzes cross-linking of collagens elastin in the extracellular matrix, thereby regulating tissue tensile strength. Paradoxically, LOX has been reported be both upregulated downregulated cancer cells, especially...

10.1158/0008-5472.can-10-1516 article EN Cancer Research 2011-01-15
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