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Yves A. DeClerck

Bio: Yves A. DeClerck is an academic researcher from Children's Hospital Los Angeles. The author has contributed to research in topics: Neuroblastoma & Matrix metalloproteinase. The author has an hindex of 55, co-authored 133 publications receiving 9642 citations. Previous affiliations of Yves A. DeClerck include Catholic University of Leuven & Amgen.


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Journal ArticleDOI
Ayuko Hoshino1, Ayuko Hoshino2, Han Sang Kim3, Han Sang Kim1, Linda Bojmar4, Linda Bojmar1, Linda Bojmar5, Kofi Ennu Gyan1, Michele Cioffi1, Jonathan M. Hernandez6, Jonathan M. Hernandez7, Jonathan M. Hernandez1, Constantinos P. Zambirinis6, Constantinos P. Zambirinis1, Gonçalo Rodrigues1, Gonçalo Rodrigues8, Henrik Molina9, Søren Heissel9, Milica Tesic Mark9, Loïc Steiner10, Loïc Steiner1, Alberto Benito-Martin1, Serena Lucotti1, Angela Di Giannatale1, Katharine Offer1, Miho Nakajima1, Caitlin Williams1, Laura Nogués11, Laura Nogués1, Fanny A. Pelissier Vatter1, Ayako Hashimoto2, Ayako Hashimoto1, Ayako Hashimoto12, Alexander E. Davies13, Daniela Freitas8, Daniela Freitas1, Candia M. Kenific1, Yonathan Ararso1, Weston Buehring1, Pernille Lauritzen1, Yusuke Ogitani1, Kei Sugiura12, Kei Sugiura2, Naoko Takahashi2, Maša Alečković14, Kayleen A. Bailey1, Joshua S. Jolissant1, Joshua S. Jolissant6, Huajuan Wang1, Ashton Harris1, L. Miles Schaeffer1, Guillermo García-Santos1, Guillermo García-Santos15, Zoe Posner1, Vinod P. Balachandran6, Yasmin Khakoo6, G. Praveen Raju16, Avigdor Scherz17, Irit Sagi17, Ruth Scherz-Shouval17, Yosef Yarden17, Moshe Oren17, Mahathi Malladi6, Mary Petriccione6, Kevin C. De Braganca6, Maria Donzelli6, Cheryl Fischer6, Stephanie Vitolano6, Geraldine P. Wright6, Lee Ganshaw6, Mariel Marrano6, Amina Ahmed6, Joe DeStefano6, Enrico Danzer6, Michael H.A. Roehrl6, Norman J. Lacayo18, Theresa C. Vincent19, Theresa C. Vincent5, Martin R. Weiser6, Mary S. Brady6, Paul A. Meyers6, Leonard H. Wexler6, Srikanth R. Ambati6, Alexander J. Chou6, Emily K. Slotkin6, Shakeel Modak6, Stephen S. Roberts6, Ellen M. Basu6, Daniel Diolaiti19, Benjamin A. Krantz6, Benjamin A. Krantz19, Fatima Cardoso20, Amber L. Simpson6, Michael F. Berger6, Charles M. Rudin6, Diane M. Simeone19, Maneesh Jain21, Cyrus M. Ghajar22, Surinder K. Batra21, Ben Z. Stanger23, Jack D. Bui24, Kristy A. Brown1, Vinagolu K. Rajasekhar6, John H. Healey6, Maria de Sousa1, Maria de Sousa8, Kim Kramer6, Sujit Sheth1, Jeanine Baisch1, Virginia Pascual1, Todd E. Heaton6, Michael P. La Quaglia6, David J. Pisapia1, Robert E. Schwartz1, Haiying Zhang1, Yuan Liu6, Arti Shukla25, Laurence Blavier26, Yves A. DeClerck26, Mark A. LaBarge27, Mina J. Bissell28, Thomas C. Caffrey21, Paul M. Grandgenett21, Michael A. Hollingsworth21, Jacqueline Bromberg6, Jacqueline Bromberg1, Bruno Costa-Silva20, Héctor Peinado11, Yibin Kang14, Benjamin A. Garcia23, Eileen M. O'Reilly6, David P. Kelsen6, Tanya M. Trippett6, David R. Jones6, Irina Matei1, William R. Jarnagin6, David Lyden1 
20 Aug 2020-Cell
TL;DR: EVP proteins can serve as reliable biomarkers for cancer detection and determining cancer type, and a panel of tumor-type-specific EVP proteins in TEs and plasma are defined, which can classify tumors of unknown primary origin.

565 citations

Journal Article
TL;DR: Down-regulation of metalloproteinase activity has a striking effect on local invasion and partially suppresses hematogenous metastasis in mice treated with MI/TIMP-2.
Abstract: The balance between levels of metalloproteinases and their corresponding inhibitors is a critical factor in tumor invasion and metastasis. Down-regulation of the activity of these proteases was achieved by transfection of invasive and metastatic rat cells with the complementary DNA for metalloproteinase inhibitor/tissue inhibitor of metalloproteinase 2 (MI/TIMP-2), a novel inhibitor of metalloproteinases recently described. (Y. A. DeClerk et al., J. Biol. Chem., 264: 17445–17453, 1989; W. G. Stetler-Stevenson et al., J. Biol. Chem., 264: 17374–17378, 1989). Secretion of functional MI/TIMP-2 protein in stably transfected cells resulted in a marked decrease in metalloproteinase activity. Partial suppression of the formation of lung colonies after i.v. injection in nude mice was observed in a transfected clone expressing high levels of MI/TIMP-2. Production of MI/TIMP-2 in four clones markedly reduced tumor growth rate in vivo after s.c. injection and completely suppressed local tissue invasion. Thus, down-regulation of metalloproteinase activity has a striking effect on local invasion and partially suppresses hematogenous metastasis.

462 citations

Journal ArticleDOI
TL;DR: The tumor microenvironment (TME) consists of cells, soluble factors, signaling molecules, extracellular matrix, and mechanical cues that can promote neoplastic transformation, support tumor growth and invasion, protect the tumor from host immunity, foster therapeutic resistance, and provide niches for dormant metastases to thrive.
Abstract: The tumor microenvironment (TME) consists of cells, soluble factors, signaling molecules, extracellular matrix, and mechanical cues that can promote neoplastic transformation, support tumor growth and invasion, protect the tumor from host immunity, foster therapeutic resistance, and provide niches for dormant metastases to thrive. An American Association for Cancer Research (AACR) special conference held on November 3-6, 2011, addressed five emerging concepts in our understanding of the TME: its dynamic evolution, how it is educated by tumor cells, pathways of communication between stromal and tumor cells, immunomodulatory roles of the lymphatic system, and contribution of the intestinal microbiota. These discussions raised critical questions on how to include the analysis of the TME in personalized cancer diagnosis and treatment.

447 citations

Journal ArticleDOI
TL;DR: The contribution of interleukin-6 (IL-6) produced in the bone marrow microenvironment to bone metastasis is reviewed, which has a strong pro-tumorigenic activity due to its multiple effects on bone metabolism, tumor cell proliferation and survival, angiogenesis, and inflammation.

342 citations

Journal ArticleDOI
TL;DR: The biology and role of MSC in cancer is reviewed with a primary focus on bone marrow-derived MSC, which contributes to a microenvironment that promotes osteolysis, tumor growth, survival, and drug resistance.
Abstract: Over the last decade, there has been a growing interest in the role of mesenchymal stem cells (MSC) in cancer progression. These cells have the potential to give rise to a variety of mesenchymal cells like osteoblasts, chondrocytes, adipocytes, fibroblasts, and muscle cells. In contrast to their hematopoetic counterparts, MSC are not as clearly defined, which makes the interpretation of their role in cancer progression more complex. However, the nature of the relationship between MSC and tumor cells appears dual. Primary and metastatic tumors attract MSC in their microenvironment where they become tumor-associated fibroblasts, affect tumor cell survival and angiogenesis, and have an immunomodulatory function, and vice versa in the bone marrow MSC attract tumor cells and contribute to a microenvironment that promotes osteolysis, tumor growth, survival, and drug resistance. Whether MSC are pro- or anti-tumorigenic is a subject of controversial reports that is in part explained by the complexity of their interaction with tumor cells and the large range of cytokines and growth factors they produce. The study of these interactions is a fertile ground of investigation that—as already demonstrated in the case of myeloma—should lead to novel therapeutic approaches in cancer. In this article, the biology and role of MSC in cancer is reviewed with a primary focus on bone marrow-derived MSC.

319 citations


Cited by
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04 Mar 2011-Cell
TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.

51,099 citations

Journal ArticleDOI
TL;DR: The paradoxical roles of the tumor microenvironment during specific stages of cancer progression and metastasis are discussed, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects.
Abstract: Cancers develop in complex tissue environments, which they depend on for sustained growth, invasion and metastasis. Unlike tumor cells, stromal cell types within the tumor microenvironment (TME) are genetically stable and thus represent an attractive therapeutic target with reduced risk of resistance and tumor recurrence. However, specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and adverse consequences for tumorigenesis. Furthermore, many studies have shown that the microenvironment is capable of normalizing tumor cells, suggesting that re-education of stromal cells, rather than targeted ablation per se, may be an effective strategy for treating cancer. Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and metastasis, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects.

5,396 citations

Journal ArticleDOI
18 Apr 1997-Cell
TL;DR: Data show that OPG can act as a soluble factor in the regulation of bone mass and imply a utility for OPG in the treatment of osteoporosis associated with increased osteoclast activity.

5,050 citations

Journal ArticleDOI
TL;DR: The four stages of orderly inflammation mediated by macrophages are discussed: recruitment to tissues; differentiation and activation in situ; conversion to suppressive cells; and restoration of tissue homeostasis.
Abstract: Macrophages are strategically located throughout the body tissues, where they ingest and process foreign materials, dead cells and debris and recruit additional macrophages in response to inflammatory signals They are highly heterogeneous cells that can rapidly change their function in response to local microenvironmental signals In this Review, we discuss the four stages of orderly inflammation mediated by macrophages: recruitment to tissues; differentiation and activation in situ; conversion to suppressive cells; and restoration of tissue homeostasis We also discuss the protective and pathogenic functions of the various macrophage subsets in antimicrobial defence, antitumour immune responses, metabolism and obesity, allergy and asthma, tumorigenesis, autoimmunity, atherosclerosis, fibrosis and wound healing Finally, we briefly discuss the characterization of macrophage heterogeneity in humans

4,182 citations

Journal ArticleDOI
TL;DR: Recent advances shed light on how the structure and function of the MMPs are related and on how their transcription, secretion, activation, inhibition, localization, and clearance are controlled.
Abstract: ▪ Abstract The matrix metalloproteinases (MMPs) constitute a multigene family of over 25 secreted and cell surface enzymes that process or degrade numerous pericellular substrates. Their targets include other proteinases, proteinase inhibitors, clotting factors, chemotactic molecules, latent growth factors, growth factor–binding proteins, cell surface receptors, cell-cell adhesion molecules, and virtually all structural extracellular matrix proteins. Thus MMPs are able to regulate many biologic processes and are closely regulated themselves. We review recent advances that help to explain how MMPs work, how they are controlled, and how they influence biologic behavior. These advances shed light on how the structure and function of the MMPs are related and on how their transcription, secretion, activation, inhibition, localization, and clearance are controlled. MMPs participate in numerous normal and abnormal processes, and there are new insights into the key substrates and mechanisms responsible for regula...

3,839 citations