Papers by Philippe Clézardin
Bone, Dec 1, 2012
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Supplementary Methods from The HIF-1–Inducible Lysyl Oxidase Activates HIF-1 via the Akt Pathway ... more Supplementary Methods from The HIF-1–Inducible Lysyl Oxidase Activates HIF-1 via the Akt Pathway in a Positive Regulation Loop and Synergizes with HIF-1 in Promoting Tumor Cell Growth
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Encyclopedia of Endocrine Diseases, 2019
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Blood, 1992
Osteonectin is a 32-Kd phosphoglycoprotein originally described in bone but also found in platele... more Osteonectin is a 32-Kd phosphoglycoprotein originally described in bone but also found in platelets. Platelet and bone osteonectin are different both structurally and immunologically. We have previously shown that platelet osteonectin, by binding to thrombospondin, is involved in the secretion-dependent phase of the platelet aggregation process. In this study, we used antiosteonectin antibodies in combination with immunogold labeling to investigate by electron microscopy the fine localization of osteonectin within normal and gray platelets. Using both a polyclonal and monoclonal antibody ON3, osteonectin was specifically located at the internal face of alpha- granule membranes within normal platelets. Osteonectin was not distributed within all alpha-granules, probably because of its low platelet content. In addition, using immunofluorescence, osteonectin could also be detected in immature and mature megakaryocytes with a granular pattern of staining, suggesting that osteonectin is s...
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VIIIth International Congress on Thrombosis and Haemostasis, 1981
The binding of 125I-labelled lectins to major and minor platelet glycoproteins (GP) and their sub... more The binding of 125I-labelled lectins to major and minor platelet glycoproteins (GP) and their subunits has been investigated. Human platelets were isolated, washed, solubilized in sodium dodecyl sulphate (SDS) under non-reducing conditions and separated on 5, 7.5 and 10 % non-reduced/reduced 2-D polyacrylamide gels. The gels were incubated with 125I-labelled lectins; Lens culinaris lectin (LCL), concanavalin A (ConA) wheat germ agglutinin (WGA) or Ricinus communis agglutinin (RCA-120), then washed extensively dried and exposed to X-ray film by indirect autoradiography. Surface-labelled platelets were similarly separated. WGA and RCA bound predominantly to GPIbα but also to two minor bands above and below it which were affected by neuraminidase treatment. One of them bound two 125I-lectins (LCL and ConA) while GPIbα did not. Additional GP bands were detected by lectin binding and by surface-labelling beneath GPIIIβ (IV). With platelets labelled by the neuraminidase/galactose oxidase/...
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European Urology Supplements, 2003
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European Journal of Cancer Supplements, 2010
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Bone Cancer, 2010
Publisher Summary This chapter focuses on the mechanisms that draw metastatic cells to colonize b... more Publisher Summary This chapter focuses on the mechanisms that draw metastatic cells to colonize bone. It also discusses the possible contribution of osteoblastic and vascular stem cell niches in the early development of bone metastases. Several factors expressed by metastatic cells and other cells from the bone marrow microenvironment (CXCR4/CXCL-12, RANK/RANKL, E-selectin, integrins, proteases, Runx2) have been identified as being capable of mediating the early development of bone metastases. Undoubtedly, these factors provide attractive new targets for cancer therapeutics. However, cancer (stem) cells and bone marrow stem cells use overlapping molecular features to interact with the vascular endothelium, and invade and thrive in the bone marrow, suggesting that therapies targeting some of these factors expressed by cancer cells could also have detrimental effects on bone marrow cells.
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Bulletin du cancer, 2013
Bone metastases are common complications of cancers. These skeletal lesions are usually osteolyti... more Bone metastases are common complications of cancers. These skeletal lesions are usually osteolytic (excess of bone destruction), osteosclerostic (excess of bone formation) or mixed. Metastatic cancer cells residing in the bone marrow alter the functions of bone-resorbing (osteoclasts) and bone-forming (osteoblasts) cells and hijack signals coming from the bone matrix. In this review, we first described cellular and molecular mechanisms that drive cancer cells to colonize the bone marrow. We next show how cancer cells alter bone remodelling to promote the formation of osteolytic or osteosclerotic lesions.
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IBMS BoneKEy, 2011
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IBMS BoneKEy, 2011
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IBMS BoneKEy, 2011
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IBMS BoneKEy, 2011
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European Journal of Biochemistry, 1989
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Clinical & Experimental Metastasis, 2007
Advanced cancers are prone to metastasize. Visceral metastases are more likely to be fatal, while... more Advanced cancers are prone to metastasize. Visceral metastases are more likely to be fatal, while patients with only metastases to bone can survive up to 10 years or more. However, effective treatments for bone metastases are not yet available and bisphosphonates improve the quality of life with no life-prolonging benefits. Bone metastases are classified as osteolytic, osteosclerotic or mixed lesions according to the bone cell types more prominently involved. Either conditions induce high morbidity and dramatically increase the risk of pathological fractures. Several molecular mechanisms bring about cancer cells to metastasize to bone, and osteotropic cancer cells are believed to acquire bone cell-like properties which improve homing, adhesion, proliferation and survival in the bone microenvironment. The acquisition of a bone cell pseudo-phenotype, denominated osteomimicry, is likely to rely on expression of osteoblastic and osteoclastic genes, thus requiring a multigenic programme. Several microenvironmental factors improve the ability of cancer cells to develop at skeletal sites, and a reciprocal deleterious stimulation generates a vicious cycle between the tumour cells and the cells residing in the bone environment. The impact of the stem cell niche in the development of bone metastases and in the phenomenon of tumour dormancy, that allows tumour cells to remain quiescent for decades before establishing overt lesions, is at present only speculative. However, the osteoblast niche, known to maintain the haematopoietic stem cell population in a quiescent status, is likely to be involved in the development of bone metastases and this promising research field is rapidly expanding.
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Cellular and Molecular Life Sciences (CMLS), 1998
Integrins have been repeatedly found involved in cancer metastasis. The past two years have seen ... more Integrins have been repeatedly found involved in cancer metastasis. The past two years have seen considerable evolution in our knowledge on the role of these integrins in tumour cells. This includes the elucidation of different signalling pathways by which integrins dictate the anchorage-independent growth, survival and motility of tumour cells. Moreover, integrins may have a more complex role in cancer metastasis as they cooperate with serine proteases and metalloproteases to promote tumour cell invasion and angiogenesis. Finally, integrins favour tumor cell extravasation.
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Bone, 2006
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Bone, 1995
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Bone, 2009
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Bone, 2011
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Papers by Philippe Clézardin