Yves Albert Declerck, MD

Title(s)Clinical Professor of Pediatrics (Part-Time)
SchoolKeck School of Medicine of Usc
AddressCHL Mail Stop 54
Off Campus
Los Angeles CA 90027
Phone+1 323 361 2150
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    Collapse Biography 
    Collapse Education and Training
    Notre Dame University , Namur, BelgiumBS06/1969Biology/Pre-Med
    Catholic University of Louvain, Louvain, BelgiumMD07/1973Medicine
    Catholic University of Louvain, Belgium06/1975Pediatric Residency
    University of Montreal, Quebec, Canada06/1977Pediatric Residency
    Children's Hospital Los Angeles, California, USC06/1979Pediatric Hematology-Oncology Fellowship
    Collapse Awards and Honors
    Catholic University of Louvain1973SPECIA prize
    American Cancer Society1982  - 1985Junior Faculty Career Development Award
    Children's Hospital Los Angeles 1987Morris & Mary Press Humanism Award
    Fogarty 1991  - 1992Senior International Fellowship
    Children's Hospital Los Angeles1991H.Russell Smith Award for Innovation in Biomedical Research
    Children's Hospital Los Angeles1994  - presAssociates & Affiliates Endowed Chair in Cancer Biology
    Children's Hospital Los Angeles2010  - presRichard Call Family Endowed Chair in Pediatric Research Innovation
    USC2013Associates Award for Creativity in Research

    Collapse Overview 
    Collapse Overview
    Yves DeClerck MD is a Pediatrician-Scientist at Children’s Hospital Los Angeles and USC. He is leading a cancer biology research program focused on the tumor microenvironment. He is the co-leader of the Tumor Microenvironment Program at the USC-Norris Comprehensive Cancer Center and the Director for Research Education at the Children’s Center for Cancer and Blood Disease.
    Research Focus of the Laboratory: The main focus of investigation in our laboratory is on the Tumor Microenvironment (TME) and its contribution to cancer progression and metastasis (Borriello et al., Cancer Lett. 2016). The main objective of the laboratory is to understand fundamental mechanisms of communication between tumor cells and stromal cells in the TME in order to identify targets for therapeutic intervention that can be tested in relevant pre-clinical models. These data are then used to design early phase clinical trials in children with cancer through collaboration with clinical investigators at the USC-Norris Comprehensive Cancer Center and Children’s Hospital Los Angeles (CHLA). A major focus is on Neuroblastoma (NB), the second most common solid tumor in children and a cancer that is highly metastatic. Our research approach combines cell and molecular biology with pre-clinical animal models in mice. Our research program has 3 major directions:
    1. Contribution of cancer-associated fibroblasts (CAF) to neuroblastoma progression: Our laboratory has recently identified in neuroblastoma tumors, CAFs that share phenotypic and functional properties of bone marrow mesenchymal stromal cells (MSC). These cells are educated by NB cells toward a pro-tumorigenic function that enhance NB cell proliferation, survival and drug-resistance through the production of several pro-tumorigenic cytokines and chemokines such as IL-6, IL-8, VEGF, SDF1 and MCP1 (Borriello et al., Cancer Res. 2017, in press). Downstream of these cytokines is the activation of STAT3 and ERK1/2 in NB cells. Ongoing work investigates the effect of blocking STAT3 and ERK1/2 in combination with chemotherapy and immunotherapy to enhance therapeutic response and prevent resistance.
    2. Contribution of exosomes and extracellular vesicles to the education of CAFs, MSCs and macrophages by tumor cells: Stromal cells in the TME are educated by tumor cells and polarized toward a pro-tumorigenic function (these cells from being foes learn to become friends of the tumor cells). Extracellular vesicles and in particular exosomes released by tumor cells are captured by stromal cells and contribute to their education not only in primary tumors but also in the pre-metastatic niche. Our laboratory has recently shown (Nakata et al., Journal of Extracellular Vesicles 2017, in press) that exosomes released by NB cells are captured by MSCs and macrophages and contribute to the production of pro-tumorigenic cytokines by these cells. Ongoing work is studying the mechanism involved in the capture of tumor-derived exosomes by MSCs and macrophages with a focus on galectin-3 binding protein and integrins in collaboration with Dr. Lyden at Cornell (NYU) and on identifying ways to inhibit the production of exosomes by tumor cells and its effect on tumor progression and metastasis in pre-clinical mouse models.
    3. Role of plasminogen activator inhibitor-1 (PAI-1) in cancer progression: PAI-1 is a serine protease inhibitor which has been shown to have a paradoxically positive effect in cancer progression by promoting angiogenesis and protecting tumor cells from drug-induced apoptosis (Placencio et al., Cancer Res, 2016). More recent work in our laboratory shows that PAI-1 contributes to inflammation in cancer by promoting the recruitment of macrophages into tumors and their polarization (or education) toward a pro-tumorigenic (M2) phenotype.
    Funding of the Laboratory: Our laboratory has been funded by the NIH without interruption since 1986. Current funding incudes 2 R01 grants (work on exosomes described under #2, and work on PAI-1 described under #3), and a project in a larger multi-institutional program project grant on neuroblastoma (work under #1).
    Environment: Our laboratory is located on the 5th floor of the Smith Research Tower at The Saban Research Institute (TSRI) of Children’s Hospital Los Angeles (CHLA). Our research program is part of the Tumor Microenvironment Program of the USC Norris Comprehensive Cancer Center (USC-Norris) and the neuroblastoma research group of the Children’s Center for Cancer and Blood Diseases at CHLA. Both TSRI and USC-Norris provide a rich and interactive environment for the conduct of innovative research in the area of the TME. We have collaborations with faculty at USC, Cornell, City of Hope, Harvard and Children’s Hospital of Philadelphia. The laboratory has trained 10 graduate students and 25 postdoctoral fellows, many presently working at academic institutions and in industry. Career development of highly motivated and dedicated students is an integral part of the research experience in the laboratory.
    The Principal Investigator: Dr. DeClerck is a Tenured Professor of Pediatrics and Biochemistry & Molecular Medicine at USC. He started his career as a physician-scientist in the early 1980s and has established an independent research program that has been funded by the NIH without interruption since 1986. He has organized multiple meetings and conferences in the field of metastasis and the tumor microenvironment. He has served and is still serving on multiple study sections at the NIH, was the co-chair of the NCI Tumor Microenvironment Network and is a senior editor for Cancer Research for the Tumor Microenvironment-Immunology section. He has a solid record of accomplishment in education, mentoring and career development, being the PI on a longstanding (1991-present) NCI-funded T32 Program grant, and the chair of multiple mentoring committees of junior faculty members and postdoctoral trainees at USC and CHLA. He is the recipient of the 1991 H. Russell Smith Award for Innovation in Pediatric Biomedical Research, the USC Associates Award for Creativity in Research (2013) and the Richard Call Family Endowed Chair in Pediatric Research Innovation (2010).

    Collapse Research 
    Collapse Research Activities and Funding
    Discovering and Exploiting Mechanisms of Neuroblastoma Therapy Resistance
    NIH/NCI 1P01-CA217959-01Sep 1, 2017 - Aug 30, 2022
    Role: PI on Project 3: Targeting the Pro-Tumorigenic Microenvironment
    Description: The overall objective of Project 3 is to discover and exploit extrinsic mechanisms of therapy resistance by focusing on the contribution of tumor-associated macrophages (TAMs) and tumor-associated fibroblasts (TAFs) in the tumor microenvironment (TME). Our overarching hypothesis is that TAMs and TAFs cooperate in creating a favorable tumorigenic environment that ultimately leads to the emergence of therapeutic resistance and immune escape in NB. We also postulate that as tumors are treated, the TME is altered in its composition and function to become increasingly favorable to therapeutic resistance. This hypothesis is based on published and preliminary data from our group demonstrating that TAMs and TAFs are abundantly present in an inflammatory subtype of NB at diagnosis associated with a high risk of recurrence and extremely poor prognosis. We also have evidence that TAMs and TAFs when exposed to tumor cells stimulate their proliferation, survival and drug-resistance via the paracrine production of pro-tumorigenic cytokines and chemokines that activate in tumor cells signaling pathways such as STAT3 and ERK. Our project has 3 aims. Aim 1, will examine mechanisms of cooperation between TAMs and TAFs, testing the hypothesis that in MYCN amplified tumors that do not produce the TAM chemoattractant CCL-2/MCP-1, TAFs are a source of this chemokine. We will also examine the contribution of cytokines and chemokines generated in co-culture of TAMs, TAFs and NB cells and the signaling pathways they activate in NB cells leading to increased proliferation and survival. Aim 2, will examine changes in the TEM landscape secondary to chemotherapy in syngeneic murine NB models (with Project 2) and validate the data in patients tumor samples obtained via Core B. By examining changes in the transcriptome that occur in NB cells chronically exposed to TAM/TAF and their potential epigenetic origin (with Project 3) aim 2 will also identify vulnerabilities to prevent resistance to chemotherapy or targeted therapy (with Project 1). Aim 3, will then translate these discoveries in pre-clinical tumor models. We will test the therapeutic efficacy of the most promising agents targeting TAFs, TAMs, or pathways they activate in tumor cells in combination with chemotherapy or immunotherapy (with Project 5) using human NB lines and patient-derived xenotransplants in immunodeficient mice as well as murine cell lines in immunocompetent mice (with Project 2), The most effective agent(s) will then be proposed for early phase clinical trial to the NANT (Core B). Thus Project 4 brings a unique contribution to the overall objective of this PPG through its focus on the TME and on non-autonomous mechanisms leading towards therapeutic resistance and immune escape.
    Exosomes in tumor cell-mesenchymal stromal cell interaction
    NIH R01CA207983Aug 1, 2017 - May 31, 2022
    Role: Principal Investigator
    Exosomes in Tumor Cell-Mesenchymal Stromal Cells Interaction
    NIH/NCI R01 CA207983-01A1Jul 1, 2017 - Jun 30, 2022
    Role: Principal Investigator
    Description: The bone marrow (BM) is a heterogeneous organ with a central function in cancer progression and metastasis. It constitutes a niche for disseminated tumor cells, protecting them from therapy, promoting their dormancy and allowing them to metastasize to other organs. Cancer cells home to and hijack the BM niche converting it to a malignant niche favorable to tumor cell proliferation and survival. Thus, studying the cross-talk between tumor cells and the BM microenvironment is a subject of high interest. A major effort of our laboratory has been to study the communication between cancer cells and BM-derived mesenchymal stromal cells (BM-MSC) that form the BM-niche and that we have shown to contribute to a protumorigenic tumor microenvironment (TME). We focus on neuroblastoma (NB), a neural crest-derived tumor that is the second most common solid tumor in children, and that frequently and specifically metastasizes to the bone and BM and on tumor exosomes. These extracellular vesicles (EV) have emerged as a new and powerful mechanism of communication between tumor cells and their environment through their ability to convey multi-molecular biological messages of a much higher complexity than single growth factors. Preliminary data in this application demonstrate that NB cells release exosomes enriched in syntenin, ALIX, the tetraspanin CD-63 and Gal-3BP which are captured by BM-MSC and create a pro-tumorigenic inflammatory reaction. Our overarching hypothesis is that as a result of their activity on MSC, NB-derived exosomes prime the BM niche promoting the homing and survival of NB cells in the BM. We specifically hypothesize that syntenin plays a central role in their biogenesis and that Gal-3BP controls their uptake by interacting with a protein at the surface of BM-MSC. In a first aim we will determine the contribution of NB-derived exosomes to the pre-metastatic BM niche and the contribution of syntenin to their biogenesis, combining pharmacological and genetic (knock down and knock out) approaches in vitro in cultures of patient-derived MSC and in vivo in metastatic and non-metastatic NB cells lines. In aim 2, we will identify in BM-MSC the protein(s) interacting with Gal-3BP that contribute(s) to the uptake of exosomes in MSC, and in collaboration with Dr. David Lyden (Cornell University, NY), compare exosomes from NB and breast cancer cell lines that differ in BM tropism for their uptake by BM-MSC and BM hematopoietic stem cells (HSC) focusing on Gal-3BP and integrin in their uptake. These studies will provide novel insight into mechanisms by which exosomes are involved in the communication between tumor cells and the BM niche. It is anticipated that these studies will ultimately identify targets for intervention or prevention of cancer metastasis.
    Children’s Hospital Los Angeles Child Health Research Career Development Award
    NIH/NICHD K12 HD529954-10Dec 1, 2011 - Nov 30, 2017
    Role: Program Director
    Description: The CHLAK12 program, with support from the Department of Pediatrics and the NICHD-Child Health Research Career Development Award, has been successful over the past 10 years in promoting the careers of pediatrician-scientists. The proposed plan will take the CHLAK12 Program to the next level, by bringing together 37 senior and experienced faculty from 16 academic departments located at CHLA and the University of Southern California (USC). These faculty members are drawn from The Saban Research Institute of CHLA, the Norris Comprehensive Cancer Center, the Edythe and Eli Broad Center for Regenerative Medicine and Stem Cell Research, the Department of Preventive Medicine, the Viterbi School of Engineering and the Michelson Center for Convergent Bioscience. These centers will contribute to a scientific environment that will encourage scholars to cross disciplines and will provide them with access to state-of-the art and new emerging technologies. In this context, three scholars each year will be mentored to conduct hypothesis-driven, discovery-based research projects in six areas of scientific priority highly relevant to children’s health: 1) Cancer; 2) Developmental Biology and Regenerative Medicine; 3) Developmental Neuroscience; 4) Metabolism, Immunology, Infection and Inflammation; 5) Human Physiology and Imaging; and 6) Environmental Health Science. The major objective of the CHLAK12 Program is to promote the careers of pediatrician-scientists by assisting them to learn not only to be independent thinkers and innovators, but also to work as members of a team of investigators using a convergent approach to solving important and complex human health problems. While providing one-on-one and team mentoring activities, and a common educational curriculum, the CHLAK12 plan also offers a personalized approach to ensure that scholars acquire the specific skills and knowledge that match their individual needs, in addition to embedding them in teams of senior investigators leading multi-PI and large multi-disciplinary projects. An Infrastructure is in place to continue the mentoring of scholars after completion of the CHLAK12 Program in the planning and submission of NIH-funded grants. The CHLAK12 Leadership will regularly seek the advice of an eight-member Internal Advisory Committee (IAC) and a three-member External Advisory Board (EAB) and will obtain feedback from the scholars in order to constantly improve the Program as successfully done in the past. As our pool of applicants has steadily increased over the years, we are confident that we will be able to recruit individuals for all positions requested. This application reflects the strong commitment of the Department of Pediatrics at CHLA and USC to continue to address the shortage of physician-scientists in Pediatrics, at a time when their contribution to team investigation is critical in resolving complex health problems in children.
    AACR Special Conference on Tumor Microenvironment Complexity: Emerging Roles in C
    NIH R13CA165612Nov 1, 2011 - Oct 31, 2012
    Role: Principal Investigator
    Center for Environment-Mediated Drug Resistance in Pediatric Cancer
    NIH U54CA163117Sep 20, 2011 - Jul 31, 2017
    Role: Principal Investigator
    Fifth International Conference on Tumor Microenvironment: Progression, Therapy a
    NIH R13CA144431Sep 1, 2009 - Feb 28, 2010
    Role: Principal Investigator
    Plasminogen activator inhibitor-1 in tumor progression and metastasis
    NIH R01CA129377Apr 1, 2008 - Apr 30, 2019
    Role: Principal Investigator
    Description: Plasminogen activator inhibitor-1 (PAI-1) is a member of the family of endogenous serine protease inhibitors (serpins) that controls the activation of plasminogen into plasmin by tissue and urokinase type plasminogen activators (tPA and uPA, respectively). In the late 1990’s multiple clinical studies revealed that cancer patients whose tumors have a high content of uPA have worse clinical outcomes and are less responsive to chemotherapy. It was, however, unanticipated when these same studies and others reported that high levels of PAI-1 in tumors were also an indicator of a poor rather than a favorable clinical outcome. One explanation for the paradoxical role attributed to PAI-1 in cancer has been its pro-angiogenic function. During the past funding period of the grant, we have published two fundamental observations that further elucidate the pro-tumorigenic function of PAI-1. We first reported that PAI-1 exerts its pro-angiogenic activity in part through a novel mechanism whereby PAI-1 protects endothelial cells from Fas-mediated apoptosis through inhibition of the shedding by plasmin of a soluble mFasL proteolytic fragment that is pro-apoptotic. Secondly, we demonstrated that PAI-1 also protects tumor cells from apoptosis, but that the mechanism is only partially dependent on plasmin and Fas. Emphasizing the role of the tumor microenvironment, we also demonstrated that stromal-derived PAI-1 compensates for a lack of tumor-derived PAI-1, and that PAI-1 contributes to the recruitment of macrophages by tumor cells. The overarching hypothesis of this application is that PAI-1 exerts its pro-tumorigenic activity through a combination of effects on endothelial cells (pro-angiogenic activity), macrophages (promotion of migration) and tumor cells (promotion of survival) that involves specific protein-protein interactions. We will test this hypothesis in vitro in several human cancer cell lines of different origins and producing variable amounts of PAI-1, and in vivo by combining genetic approaches with a pharmacologic approach with newly developed small molecule inhibitors of PAI-1. In Aim 1, we will investigate the mechanism by which the interaction between PAI-1 and one of its cell surface receptors, the low density protein receptor-like protein 1 (LRP1) signals and protects tumor cells from spontaneous and drug-induced apoptosis. In Aim 2, we will determine whether PAI-1 is necessary to allow tumors to promote angiogenesis, recruit macrophages and exit dormancy in immunodeficient PAI-1 null mice implanted with human tumor cells in which the suppression of PAI-1 expression is controlled by doxycycline. We will also investigate the effect of PAI-1 suppression on tumor initiation in PAI-1 null mice crossed with transgenic NB-Tag mice that have a 100% penetrance in neuroblastoma tumor formation. In Aim 3, we will test the effect of pharmacological inhibition of PAI-1 in pre-clinical mouse models of tumorigenesis and tumor initiation. These studies will provide not only a better fundamental understanding of the mechanisms responsible for the pro-tumorigenic activity of PAI-1, but also a more definitive answer on the potential therapeutic value of targeting PAI-1 as part of cancer treatment strategies.
    Developing And Improving Institutional Animal Resources
    NIH G20RR024015May 15, 2007 - May 14, 2009
    Role: Principal Investigator
    Tumor Microenvironment: Progression, Therapy and Prevention
    NIH R13CA128588Mar 1, 2007 - Feb 29, 2008
    Role: Principal Investigator
    Cancer, Proteases and the Microenvironment
    NIH R13CA119825Sep 15, 2005 - Sep 14, 2006
    Role: Principal Investigator
    MOLECULAR MECHANISMS AND IMAGING OF BONE INVASION
    NIH R21AR051247Sep 17, 2003 - Jun 30, 2007
    Role: Principal Investigator
    DEVELOPING AND IMPROVING ANIMAL RESOURCES
    NIH G20RR017067Jun 1, 2003 - May 31, 2004
    Role: Principal Investigator
    ECM MATRIX, PROTEASE AND MELANOMA PROLIFERATION
    NIH R01CA098469Jan 10, 2003 - Dec 31, 2009
    Role: Principal Investigator
    Conference on Proteases, Extracellular Matrix, &Cancer
    NIH R13CA099296Aug 1, 2002 - Jul 31, 2003
    Role: Principal Investigator
    EXTRAMURAL RESEARCH FACILITIES CONSTRUCTION
    NIH C06RR011246Sep 30, 1995 - Sep 29, 1998
    Role: Principal Investigator
    FUNC. AND REG. STUDIES OF METALLOPROTEINASE INHIBITOR
    NIH F06TW001736Jul 11, 1992
    Role: Principal Investigator
    Training Physician Scientists in Pediatric Oncology
    NIH T32CA009659Sep 15, 1991 - Jul 31, 2021
    Role: Principal Investigator
    Description: Our T32 training grant (T32 Program) that has been funded by the NCI since 1991. The Program is located within the Children’s Center for Cancer and Blood Diseases (CCCBD), which is among the largest and top-ranked pediatric oncology programs in the US. This T32 Program entitled “Training Physician-Scientists in Pediatric Oncology” is composed of two well integrated training units, the CCCBD located on the Children’s Hospital Los Angeles (CHLA) campus and the NCI funded Norris Comprehensive Cancer Center of the University of Southern California (USC-Norris) located on the Health Sciences Campus (HSC) of USC and of which the CCCBD is an integral part. The Program will provide vital support for three years of intensive interdisciplinary laboratory research training for one MD trainee each year selected among 4-5 subspecialty oncology fellows who have been accepted from a pool of 20-30 applicants into the Pediatric Hematology-Oncology Fellowship program of the CCCBD. The final goal is to prepare them for full-time academic careers in pediatric cancer research. Trainees conduct research relevant to the biology of childhood cancer in the laboratories of 16 T32 Program Research Mentors at CHLA and USC-Norris, who have a solid track record of NIH funding (88% currently NIH funded) and mentoring accomplishments. By performing these research projects within the larger interactive environment of an NCI-funded Comprehensive Cancer Center and participating in formal and customized curricula that include career development and strong oversight by mentoring committees, trainees develop the knowledge base, critical abilities and technical skills necessary to develop into successful independent investigators. A key focus of this T32 Program is to instill the philosophy of bridging interactions between physician-scientist trainees and integrated translational research teams. In support of this aim, trainees actively participate in one of four Team Science Programs of the CCCBD (Neuroblastoma, Leukemia, Neural Tumors and Bone Marrow Transplant/Cellular Therapies). The institutional environment provides abundant resources and a rich intellectual milieu for training in research relevant to human disease and pediatric oncology. This includes core training resources, the strong faculties and programs of the CCCBD, The Saban Research Institute of CHLA and USC-Norris, and access to state of the art core facilities and equipment. This revised application requests a progressive increase in the number of positions each year from one the first year to three the third year and thereafter.
    TWO STEP INHIBITION OF INVASION AND METASTASIS
    NIH R03CA054861Aug 1, 1991 - Jul 31, 1994
    Role: Principal Investigator
    METALLOPROTEINASE INHIBITORS IN TUMOR PROGRESSION
    NIH R01CA042919May 1, 1987 - Feb 28, 2010
    Role: Principal Investigator

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    Collapse Publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Researchers can login to make corrections and additions, or contact us for help. to make corrections and additions.
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    Altmetrics Details PMC Citations indicate the number of times the publication was cited by articles in PubMed Central, and the Altmetric score represents citations in news articles and social media. (Note that publications are often cited in additional ways that are not shown here.) Fields are based on how the National Library of Medicine (NLM) classifies the publication's journal and might not represent the specific topic of the publication. Translation tags are based on the publication type and the MeSH terms NLM assigns to the publication. Some publications (especially newer ones and publications not in PubMed) might not yet be assigned Field or Translation tags.) Click a Field or Translation tag to filter the publications.
    1. Envision the future of precision medicine in pediatric cancer. Cancer Cell. 2024 Feb 12; 42(2):177-179. DeClerck YA. PMID: 38350420.
      View in: PubMed   Mentions:    Fields:    Translation:Humans
    2. The capture of extracellular vesicles endogenously released by xenotransplanted tumours induces an inflammatory reaction in the premetastatic niche. J Extracell Vesicles. 2023 05; 12(5):e12326. Blavier L, Nakata R, Neviani P, Sharma K, Shimada H, Benedicto A, Matei I, Lyden D, DeClerck YA. PMID: 37194998; PMCID: PMC10190125.
      View in: PubMed   Mentions: 5     Fields:    Translation:HumansAnimalsCells
    3. Fibroblasts and macrophages cooperate to create a pro-tumorigenic and immune resistant environment via activation of TGF-β/IL-6 pathway in neuroblastoma. Oncoimmunology. 2022; 11(1):2146860. Louault K, Porras T, Lee MH, Muthugounder S, Kennedy RJ, Blavier L, Sarte E, Fernandez GE, Yang F, Pawel BR, Shimada H, Asgharzadeh S, DeClerck YA. PMID: 36479153; PMCID: PMC9721439.
      View in: PubMed   Mentions: 5     Fields:    Translation:HumansAnimalsCells
    4. Cancer-Associated Fibroblasts: Understanding Their Heterogeneity. Cancers (Basel). 2020 Oct 24; 12(11). Louault K, Li RR, DeClerck YA. PMID: 33114328; PMCID: PMC7690906.
      View in: PubMed   Mentions: 56  
    5. The Tumor Microenvironment in Neuroblastoma: New Players, New Mechanisms of Interaction and New Perspectives. Cancers (Basel). 2020 Oct 10; 12(10). Blavier L, Yang RM, DeClerck YA. PMID: 33050533; PMCID: PMC7599920.
      View in: PubMed   Mentions: 29  
    6. Extracellular Vesicle and Particle Biomarkers Define Multiple Human Cancers. Cell. 2020 08 20; 182(4):1044-1061.e18. Hoshino A, Kim HS, Bojmar L, Gyan KE, Cioffi M, Hernandez J, Zambirinis CP, Rodrigues G, Molina H, Heissel S, Mark MT, Steiner L, Benito-Martin A, Lucotti S, Di Giannatale A, Offer K, Nakajima M, Williams C, Nogués L, Pelissier Vatter FA, Hashimoto A, Davies AE, Freitas D, Kenific CM, Ararso Y, Buehring W, Lauritzen P, Ogitani Y, Sugiura K, Takahashi N, Aleckovic M, Bailey KA, Jolissant JS, Wang H, Harris A, Schaeffer LM, García-Santos G, Posner Z, Balachandran VP, Khakoo Y, Raju GP, Scherz A, Sagi I, Scherz-Shouval R, Yarden Y, Oren M, Malladi M, Petriccione M, De Braganca KC, Donzelli M, Fischer C, Vitolano S, Wright GP, Ganshaw L, Marrano M, Ahmed A, DeStefano J, Danzer E, Roehrl MHA, Lacayo NJ, Vincent TC, Weiser MR, Brady MS, Meyers PA, Wexler LH, Ambati SR, Chou AJ, Slotkin EK, Modak S, Roberts SS, Basu EM, Diolaiti D, Krantz BA, Cardoso F, Simpson AL, Berger M, Rudin CM, Simeone DM, Jain M, Ghajar CM, Batra SK, Stanger BZ, Bui J, Brown KA, Rajasekhar VK, Healey JH, de Sousa M, Kramer K, Sheth S, Baisch J, Pascual V, Heaton TE, La Quaglia MP, Pisapia DJ, Schwartz R, Zhang H, Liu Y, Shukla A, Blavier L, DeClerck YA, LaBarge M, Bissell MJ, Caffrey TC, Grandgenett PM, Hollingsworth MA, Bromberg J, Costa-Silva B, Peinado H, Kang Y, Garcia BA, O'Reilly EM, Kelsen D, Trippett TM, Jones DR, Matei IR, Jarnagin WR, Lyden D. PMID: 32795414; PMCID: PMC7522766.
      View in: PubMed   Mentions: 383     Fields:    Translation:HumansAnimalsCells
    7. The plasminogen activator inhibitor-1 paradox in cancer: a mechanistic understanding. Cancer Metastasis Rev. 2019 09; 38(3):483-492. Kubala MH, DeClerck YA. PMID: 31734763; PMCID: PMC7001780.
      View in: PubMed   Mentions: 61     Fields:    Translation:HumansAnimals
    8. Anti-CD105 Antibody Eliminates Tumor Microenvironment Cells and Enhances Anti-GD2 Antibody Immunotherapy of Neuroblastoma with Activated Natural Killer Cells. Clin Cancer Res. 2019 08 01; 25(15):4761-4774. Wu HW, Sheard MA, Malvar J, Fernandez GE, DeClerck YA, Blavier L, Shimada H, Theuer CP, Sposto R, Seeger RC. PMID: 31068371; PMCID: PMC6738573.
      View in: PubMed   Mentions: 41     Fields:    Translation:HumansAnimalsCells
    9. Plasminogen Activator Inhibitor-1 Promotes the Recruitment and Polarization of Macrophages in Cancer. Cell Rep. 2018 11 20; 25(8):2177-2191.e7. Kubala MH, Punj V, Placencio-Hickok VR, Fang H, Fernandez GE, Sposto R, DeClerck YA. PMID: 30463014; PMCID: PMC6876299.
      View in: PubMed   Mentions: 52     Fields:    Translation:HumansAnimalsCells
    10. Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment. J Vis Exp. 2017 11 23; (129). Kubala MH, DeClerck YA. PMID: 29286360; PMCID: PMC5755478.
      View in: PubMed   Mentions: 3     Fields:    Translation:HumansAnimalsCells
    11. Tumor-associated macrophages promote neuroblastoma via STAT3 phosphorylation and up-regulation of c-MYC. Oncotarget. 2017 Oct 31; 8(53):91516-91529. Hadjidaniel MD, Muthugounder S, Hung LT, Sheard MA, Shirinbak S, Chan RY, Nakata R, Borriello L, Malvar J, Kennedy RJ, Iwakura H, Akamizu T, Sposto R, Shimada H, DeClerck YA, Asgharzadeh S. PMID: 29207662; PMCID: PMC5710942.
      View in: PubMed   Mentions: 36     Fields:    
    12. Sphingosine-1-Phosphate Receptor-1 Promotes Environment-Mediated and Acquired Chemoresistance. Mol Cancer Ther. 2017 11; 16(11):2516-2527. Lifshitz V, Priceman SJ, Li W, Cherryholmes G, Lee H, Makovski-Silverstein A, Borriello L, DeClerck YA, Yu H. PMID: 28716816; PMCID: PMC5669816.
      View in: PubMed   Mentions: 13     Fields:    Translation:HumansAnimalsCells
    13. Cancer-Associated Fibroblasts Share Characteristics and Protumorigenic Activity with Mesenchymal Stromal Cells. Cancer Res. 2017 09 15; 77(18):5142-5157. Borriello L, Nakata R, Sheard MA, Fernandez GE, Sposto R, Malvar J, Blavier L, Shimada H, Asgharzadeh S, Seeger RC, DeClerck YA. PMID: 28687621; PMCID: PMC5600847.
      View in: PubMed   Mentions: 95     Fields:    Translation:HumansAnimalsCells
    14. Contribution of neuroblastoma-derived exosomes to the production of pro-tumorigenic signals by bone marrow mesenchymal stromal cells. J Extracell Vesicles. 2017; 6(1):1332941. Nakata R, Shimada H, Fernandez GE, Fanter R, Fabbri M, Malvar J, Zimmermann P, DeClerck YA. PMID: 28717423; PMCID: PMC5505006.
      View in: PubMed   Mentions: 33     Fields:    
    15. Paternal Risk Factors for Oral Clefts in Northern Africans, Southeast Asians, and Central Americans. Int J Environ Res Public Health. 2017 06 19; 14(6). Ly S, Burg ML, Ihenacho U, Brindopke F, Auslander A, Magee KS, Sanchez-Lara PA, Nguyen TH, Nguyen V, Tangco MI, Hernandez AR, Giron M, Mahmoudi FJ, DeClerck YA, Magee WP, Figueiredo JC. PMID: 28629204; PMCID: PMC5486343.
      View in: PubMed   Mentions: 3     Fields:    Translation:HumansPHPublic Health
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    88. Structure and characterization of the human tissue inhibitor of metalloproteinases-2 gene. J Biol Chem. 1996 Oct 11; 271(41):25498-505. Hammani K, Blakis A, Morsette D, Bowcock AM, Schmutte C, Henriet P, DeClerck YA. PMID: 8810321.
      View in: PubMed   Mentions: 23     Fields:    Translation:HumansCells
    89. Overexpression of tissue inhibitor of metalloproteinases-2 retroviral-mediated gene transfer in vivo inhibits tumor growth and invasion. Cancer Res. 1996 Jul 01; 56(13):2891-5. Imren S, Kohn DB, Shimada H, Blavier L, DeClerck YA. PMID: 8674034.
      View in: PubMed   Mentions: 37     Fields:    Translation:HumansAnimalsCells
    90. Cloning and partial structure of the gene encoding human tissue inhibitor of metalloproteinases-3. Gene. 1996 May 08; 170(2):287-8. Hammani K, Henriet P, Silbiger SM, DeClerck YA. PMID: 8666262.
      View in: PubMed   Mentions:    Fields:    Translation:HumansCells
    91. Independent regulation of matrix metalloproteinases and plasminogen activators in human fibrosarcoma cells. J Cell Physiol. 1996 May; 167(2):333-40. Lim YT, Sugiura Y, Laug WE, Sun B, Garcia A, DeClerck YA. PMID: 8613475.
      View in: PubMed   Mentions: 5     Fields:    Translation:HumansCells
    92. Cooperation between matrix metalloproteinases and the plasminogen activator-plasmin system in tumor progression. Enzyme Protein. 1996; 49(1-3):72-84. DeClerck YA, Laug WE. PMID: 8796998.
      View in: PubMed   Mentions: 19     Fields:    Translation:HumansAnimalsCells
    93. Effect of tissue inhibitor of the matrix metalloproteinases-2 expression on the growth and spontaneous metastasis of a human melanoma cell line. Cancer Res. 1994 Oct 15; 54(20):5467-73. Montgomery AM, Mueller BM, Reisfeld RA, Taylor SM, DeClerck YA. PMID: 7923181.
      View in: PubMed   Mentions: 35     Fields:    Translation:AnimalsCells
    94. Protease inhibitors: role and potential therapeutic use in human cancer. Eur J Cancer. 1994; 30A(14):2170-80. DeClerck YA, Imren S. PMID: 7857719.
      View in: PubMed   Mentions: 29     Fields:    Translation:HumansAnimalsCells
    95. Direct activation of human neutrophil procollagenase by recombinant stromelysin. Biochem J. 1993 Oct 15; 295 ( Pt 2):581-6. Knäuper V, Wilhelm SM, Seperack PK, DeClerck YA, Langley KE, Osthues A, Tschesche H. PMID: 8240261; PMCID: PMC1134920.
      View in: PubMed   Mentions: 23     Fields:    Translation:HumansCells
    96. Fragmentation of human polymorphonuclear-leucocyte collagenase. Biochem J. 1993 May 01; 291 ( Pt 3):847-54. Knäuper V, Osthues A, DeClerck YA, Langley KE, Bläser J, Tschesche H. PMID: 8489511; PMCID: PMC1132446.
      View in: PubMed   Mentions: 25     Fields:    Translation:HumansCells
    97. Characterization of the functional domain of tissue inhibitor of metalloproteinases-2 (TIMP-2). Biochem J. 1993 Jan 01; 289 ( Pt 1):65-9. DeClerck YA, Yean TD, Lee Y, Tomich JM, Langley KE. PMID: 8424773; PMCID: PMC1132131.
      View in: PubMed   Mentions: 7     Fields:    Translation:AnimalsCells
    98. Prolonged clinical response to vincristine treatment in two patients with idiopathic hypereosinophilic syndrome. Am J Pediatr Hematol Oncol. 1992 Nov; 14(4):348-51. Sakamoto K, Erdreich-Epstein A, deClerck Y, Coates T. PMID: 1456402.
      View in: PubMed   Mentions: 4     Fields:    Translation:Humans
    99. Inhibition of invasion and metastasis in cells transfected with an inhibitor of metalloproteinases. Cancer Res. 1992 Feb 01; 52(3):701-8. DeClerck YA, Perez N, Shimada H, Boone TC, Langley KE, Taylor SM. PMID: 1732058.
      View in: PubMed   Mentions: 106     Fields:    Translation:HumansAnimals
    100. Inhibition of tumor invasion of smooth muscle cell layers by recombinant human metalloproteinase inhibitor. Cancer Res. 1991 Apr 15; 51(8):2151-7. DeClerck YA, Yean TD, Chan D, Shimada H, Langley KE. PMID: 2009533.
      View in: PubMed   Mentions: 33     Fields:    Translation:HumansCells
    101. Inhibition of autoproteolytic activation of interstitial procollagenase by recombinant metalloproteinase inhibitor MI/TIMP-2. J Biol Chem. 1991 Feb 25; 266(6):3893-9. DeClerck YA, Yean TD, Lu HS, Ting J, Langley KE. PMID: 1847392.
      View in: PubMed   Mentions: 22     Fields:    Translation:AnimalsCells
    102. Inhibition of collagenolytic activity and metastasis of tumor cells by a recombinant human tissue inhibitor of metalloproteinases. J Natl Cancer Inst. 1990 Apr 04; 82(7):589-95. Alvarez OA, Carmichael DF, DeClerck YA. PMID: 2156082.
      View in: PubMed   Mentions: 53     Fields:    Translation:AnimalsCells
    103. Purification and characterization of a collagenase inhibitor produced by bovine vascular smooth muscle cells. Arch Biochem Biophys. 1988 Aug 15; 265(1):28-37. DeClerck YA. PMID: 2843102.
      View in: PubMed   Mentions: 9     Fields:    Translation:HumansAnimalsCells
    104. Differential collagen biosynthesis by human neuroblastoma cell variants. Cancer Res. 1987 Dec 15; 47(24 Pt 1):6505-10. DeClerck YA, Bomann ET, Spengler BA, Biedler JL. PMID: 2445473.
      View in: PubMed   Mentions: 11     Fields:    Translation:HumansCells
    105. Cellular interactions in graft-v-host disease. Transplant Proc. 1987 Dec; 19(6 Suppl 7):52-4. Parkman R, Champagne J, DeClerck Y, Cooper M, Draper V, Walker S. PMID: 2962354.
      View in: PubMed   Mentions: 2     Fields:    Translation:AnimalsCells
    106. c-myc amplification and expression in newly established human osteosarcoma cell lines. Cancer Res. 1987 Jul 15; 47(14):3808-14. Bogenmann E, Moghadam H, DeClerck YA, Mock A. PMID: 3297309.
      View in: PubMed   Mentions: 11     Fields:    Translation:HumansAnimalsCells
    107. The contribution of tissue culture to the study of solid tumors of childhood. Perspect Pediatr Pathol. 1987; 9:214-43. DeClerck YA, Neustein HB. PMID: 3029663.
      View in: PubMed   Mentions:    Fields:    Translation:HumansCells
    108. Inhibition of tumor cell collagenolytic activity by bovine endothelial cells. Cancer Res. 1986 Jul; 46(7):3580-6. DeClerck YA, Laug WE. PMID: 3708589.
      View in: PubMed   Mentions: 5     Fields:    Translation:HumansAnimalsCells
    109. Patterns of DNA methylation and gene expression in human tumor cell lines. Cancer Res. 1986 Jun; 46(6):2944-9. Chandler LA, DeClerck YA, Bogenmann E, Jones PA. PMID: 3698018.
      View in: PubMed   Mentions: 9     Fields:    Translation:HumansCells
    110. Clonal analysis of murine graft-vs-host disease. II. Leukokines that stimulate fibroblast proliferation and collagen synthesis in graft-vs. host disease. J Immunol. 1986 May 15; 136(10):3549-52. DeClerck Y, Draper V, Parkman R. PMID: 3486213.
      View in: PubMed   Mentions: 14     Fields:    Translation:AnimalsCells
    111. Primary central nervous system lymphoma without intracranial mass in a child. Diagnosis by documentation of monoclonality. Cancer. 1985 Dec 15; 56(12):2804-8. Jones GR, Mason WH, Fishman LS, DeClerck YA. PMID: 3876878.
      View in: PubMed   Mentions: 5     Fields:    Translation:HumansCells
    112. Collagen biosynthesis in human neuroblastoma cell lines: evidence for expression of glial cell properties. J Natl Cancer Inst. 1985 Sep; 75(3):431-9. DeClerck YA, Lee C. PMID: 3928957.
      View in: PubMed   Mentions: 3     Fields:    Translation:HumansAnimalsCells
    113. Collagen synthesis by short-term explants of pediatric tumors. Cancer Res. 1985 Mar; 45(3):1229-38. DeClerck YA, Bogenmann E, Jones PA. PMID: 2982485.
      View in: PubMed   Mentions: 7     Fields:    Translation:HumansCells
    114. Collagen synthesis by human neuroblastoma cells. Prog Clin Biol Res. 1985; 175:239-47. DeClerck YA, Lee C. PMID: 3857637.
      View in: PubMed   Mentions:    Fields:    Translation:HumansCells
    115. Degradation of the subendothelial matrix by tumor cells. Cancer Res. 1983 Apr; 43(4):1827-34. Laug WE, DeClerck YA, Jones PA. PMID: 6572556.
      View in: PubMed   Mentions: 18     Fields:    Translation:HumansCells
    116. Degradation of artificial tissue substrates. Symp Fundam Cancer Res. 1983; 36:177-85. Jones PA, Bogenmann E, DeClerck YA, Laug WE, Heisel M, Neustein HB, Isaacs H. PMID: 6089292.
      View in: PubMed   Mentions: Translation:HumansAnimalsCells
    117. Destruction of extracellular matrices containing glycoproteins, elastin, and collagen by metastatic human tumor cells. Cancer Res. 1980 Sep; 40(9):3222-7. Jones PA, DeClerck YA. PMID: 7000340.
      View in: PubMed   Mentions: 57     Fields:    Translation:HumansCells
    118. Effect of ascorbic acid on the resistance of the extracellular matrix to hydrolysis by tumor cells. Cancer Res. 1980 Sep; 40(9):3228-31. DeClerck YA, Jones PA. PMID: 7000341.
      View in: PubMed   Mentions: 2     Fields:    Translation:HumansCells
    119. Macrocytosis and pure RBC anemia caused by azathioprine. Am J Dis Child. 1980 Apr; 134(4):377-9. DeClerck YA, Ettenger RB, Ortega JA, Pennisi AJ. PMID: 6989234.
      View in: PubMed   Mentions: 5     Fields:    Translation:Humans
    120. A fatal case of inappropriate ADH secretion induced by cyclophosphamide therapy. Cancer. 1979 Sep; 44(3):896-8. Harlow PJ, DeClerck YA, Shore NA, Ortega JA, Carranza A, Heuser E. PMID: 476599.
      View in: PubMed   Mentions: 14     Fields:    Translation:Humans
    121. Septicemia in children with leukemia. Can Med Assoc J. 1978 Jun 24; 118(12):1523-6. DeClerck Y, DeClerck D, Rivard GE, Benoit P. PMID: 657049; PMCID: PMC1818088.
      View in: PubMed   Mentions: 1     Fields:    Translation:Humans
    122. Hyaline membrane disease: prognostic factors and medium-term follow-up. Eur J Pediatr. 1978 Mar 13; 127(3):181-9. Goenen M, Ninane J, Ducoffre B, Declerck Y, Claus D, Ferriere G, Thomas-van Moerbeke RM, Moulin D, De Meyer R, Tremouroux J. PMID: 648540.
      View in: PubMed   Mentions:    Fields:    Translation:Humans
    123. Hemophilus influenzae type b infections: recurrent disease due to ampicillin-resistant strains. J Pediatr. 1977 Feb; 90(2):319-20. Delage G, DeClerck Y, Lescop J, Bery P, Shareck F. PMID: 299773.
      View in: PubMed   Mentions: 4     Fields:    Translation:HumansCells
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