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    Yves Albert Declerck, MD

    TitleProfessor of Pediatrics and Biochemistry and Molecular Medicine
    SchoolKeck School of Medicine of USC
    DepartmentPediatrics
    AddressCHL Mail Stop 54
    Off Campus
    Los Angeles California 90089
    Phone+1 323 361 2150
    vCardDownload vCard

      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 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 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
      Role 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 Cells Interaction
      NIH/NCI R01 CA207983-01A1Jul 1, 2017 - Jun 30, 2022
      Role: Principal Investigator
      Role 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
      Role 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.
      Plasminogen activator inhibitor-1 in tumor progression and metastasis
      NIH R01CA129377Apr 1, 2008 - Apr 30, 2018
      Role: Principal Investigator
      Role 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.
      Training of Physician Scientists in Cancer Research
      NIH T32CA009659Sep 15, 1991 - Jul 31, 2021
      Role: Principal Investigator
      Role 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.

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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.
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      1. Lifshitz V, Priceman SJ, Li W, Cherryholmes G, Lee H, Makovski-Silverstein A, Borriello L, DeClerck YA, Yu H. Sphingosine-1-Phosphate Receptor-1 Promotes Environment-Induced and Acquired Chemoresistance. Mol Cancer Ther. 2017 Jul 17. PMID: 28716816.
        View in: PubMed
      2. Borriello L, Nakata R, Sheard MA, Fernandez GE, Sposto R, Malvar J, Blavier L, Shimada H, Asgharzadeh S, Seeger RC, DeClerck YA. Cancer-Associated Fibroblasts Share Characteristics and Protumorigenic Activity with Mesenchymal Stromal Cells. Cancer Res. 2017 Sep 15; 77(18):5142-5157. PMID: 28687621.
        View in: PubMed
      3. Nakata R, Shimada H, Fernandez GE, Fanter R, Fabbri M, Malvar J, Zimmermann P, DeClerck YA. 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. PMID: 28717423.
        View in: PubMed
      4. 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, Iii WPM, Figueiredo JC. Paternal Risk Factors for Oral Clefts in Northern Africans, Southeast Asians, and Central Americans. Int J Environ Res Public Health. 2017 Jun 19; 14(6). PMID: 28629204.
        View in: PubMed
      5. DeClerck YA, Pienta KJ, Woodhouse EC, Singer DS, Mohla S. The Tumor Microenvironment at a Turning Point Knowledge Gained Over the Last Decade, and Challenges and Opportunities Ahead: A White Paper from the NCI TME Network. Cancer Res. 2017 Mar 01; 77(5):1051-1059. PMID: 28209610.
        View in: PubMed
      6. DeClerck YA. Fat, Calories, and Cancer. Cancer Res. 2016 Feb 01; 76(3):509-10. PMID: 26833663.
        View in: PubMed
      7. Borriello L, Seeger RC, Asgharzadeh S, DeClerck YA. More than the genes, the tumor microenvironment in neuroblastoma. Cancer Lett. 2016 Sep 28; 380(1):304-14. PMID: 26597947.
        View in: PubMed
      8. Placencio VR, Ichimura A, Miyata T, DeClerck YA. Small Molecule Inhibitors of Plasminogen Activator Inhibitor-1 Elicit Anti-Tumorigenic and Anti-Angiogenic Activity. PLoS One. 2015; 10(7):e0133786. PMID: 26207899; PMCID: PMC4514594.
      9. Placencio VR, DeClerck YA. Plasminogen Activator Inhibitor-1 in Cancer: Rationale and Insight for Future Therapeutic Testing. Cancer Res. 2015 Aug 01; 75(15):2969-74. PMID: 26180080; PMCID: PMC4613764.
      10. HaDuong JH, Blavier L, Baniwal SK, Frenkel B, Malvar J, Punj V, Sposto R, DeClerck YA. Interaction between bone marrow stromal cells and neuroblastoma cells leads to a VEGFA-mediated osteoblastogenesis. Int J Cancer. 2015 Aug 15; 137(4):797-809. PMID: 25648303.
        View in: PubMed
      11. Solari V, Borriello L, Turcatel G, Shimada H, Sposto R, Fernandez GE, Asgharzadeh S, Yates EA, Turnbull JE, DeClerck YA. MYCN-dependent expression of sulfatase-2 regulates neuroblastoma cell survival. Cancer Res. 2014 Nov 01; 74(21):5999-6009. PMID: 25164011; PMCID: PMC4216758.
      12. Borriello L, DeClerck YA. [Tumor microenvironment and therapeutic resistance process]. Med Sci (Paris). 2014 Apr; 30(4):445-51. PMID: 24801042.
        View in: PubMed
      13. Bergfeld SA, Blavier L, DeClerck YA. Bone marrow-derived mesenchymal stromal cells promote survival and drug resistance in tumor cells. Mol Cancer Ther. 2014 Apr; 13(4):962-75. PMID: 24502925; PMCID: PMC4000239.
      14. Fang H, Declerck Y. Targeting the tumor microenvironment: from understanding pathways to effective clinical trials. Cancer Res. 2013 Aug 15; 73(16):4965-77. PMID: 23913938; PMCID: PMC3815577.
      15. Ara T, Nakata R, Sheard MA, Shimada H, Buettner R, Groshen SG, Ji L, Yu H, Jove R, Seeger RC, DeClerck YA. Critical role of STAT3 in IL-6-mediated drug resistance in human neuroblastoma. Cancer Res. 2013 Jul 01; 73(13):3852-64. PMID: 23633489; PMCID: PMC3740971.
      16. Fang H, Placencio VR, DeClerck YA. Protumorigenic activity of plasminogen activator inhibitor-1 through an antiapoptotic function. J Natl Cancer Inst. 2012 Oct 03; 104(19):1470-84. PMID: 22984202; PMCID: PMC3529616.
      17. DeClerck YA. Desmoplasia: a response or a niche? Cancer Discov. 2012 Sep; 2(9):772-4. PMID: 22969116.
        View in: PubMed
      18. Yang F, Jove V, Buettner R, Xin H, Wu J, Wang Y, Nam S, Xu Y, Ara T, DeClerck YA, Seeger R, Yu H, Jove R. Sorafenib inhibits endogenous and IL-6/S1P induced JAK2-STAT3 signaling in human neuroblastoma, associated with growth suppression and apoptosis. Cancer Biol Ther. 2012 May; 13(7):534-41. PMID: 22406995.
        View in: PubMed
      19. Swartz MA, Iida N, Roberts EW, Sangaletti S, Wong MH, Yull FE, Coussens LM, DeClerck YA. Tumor microenvironment complexity: emerging roles in cancer therapy. Cancer Res. 2012 May 15; 72(10):2473-80. PMID: 22414581; PMCID: PMC3653596.
      20. Silverman AM, Nakata R, Shimada H, Sposto R, DeClerck YA. A galectin-3-dependent pathway upregulates interleukin-6 in the microenvironment of human neuroblastoma. Cancer Res. 2012 May 01; 72(9):2228-38. PMID: 22389450; PMCID: PMC3815584.
      21. Fang H, Harned TM, Kalous O, Maldonado V, DeClerck YA, Reynolds CP. Synergistic activity of fenretinide and the Bcl-2 family protein inhibitor ABT-737 against human neuroblastoma. Clin Cancer Res. 2011 Nov 15; 17(22):7093-104. PMID: 21933888; PMCID: PMC4193939.
      22. Baniwal SK, Shah PK, Shi Y, Haduong JH, Declerck Y, Gabet Y, Frenkel B. Runx2 promotes both osteoblastogenesis and novel osteoclastogenic signals in ST2 mesenchymal progenitor cells. Osteoporos Int. 2012 Apr; 23(4):1399-413. PMID: 21881969.
        View in: PubMed
      23. Isono M, Suzuki T, Hosono K, Hayashi I, Sakagami H, Uematsu S, Akira S, DeClerck YA, Okamoto H, Majima M. Microsomal prostaglandin E synthase-1 enhances bone cancer growth and bone cancer-related pain behaviors in mice. Life Sci. 2011 Apr 11; 88(15-16):693-700. PMID: 21324324.
        View in: PubMed
      24. Russell HV, Groshen SG, Ara T, DeClerck YA, Hawkins R, Jackson HA, Daldrup-Link HE, Marachelian A, Skerjanec A, Park JR, Katzenstein H, Matthay KK, Blaney SM, Villablanca JG. A phase I study of zoledronic acid and low-dose cyclophosphamide in recurrent/refractory neuroblastoma: a new approaches to neuroblastoma therapy (NANT) study. Pediatr Blood Cancer. 2011 Aug; 57(2):275-82. PMID: 21671363; PMCID: PMC3117015.
      25. Blavier L, Lazaryev A, Shi XH, Dorey FJ, Shackleford GM, DeClerck YA. Stromelysin-1 (MMP-3) is a target and a regulator of Wnt1-induced epithelial-mesenchymal transition (EMT). Cancer Biol Ther. 2010 Jul 15; 10(2):198-208. PMID: 20534975; PMCID: PMC3040898.
      26. Bergfeld SA, DeClerck YA. Bone marrow-derived mesenchymal stem cells and the tumor microenvironment. Cancer Metastasis Rev. 2010 Jun; 29(2):249-61. PMID: 20411303.
        View in: PubMed
      27. Ara T, Declerck Y. Interleukin-6 in bone metastasis and cancer progression. Eur J Cancer. 2010 May; 46(7):1223-31. PMID: 20335016; PMCID: PMC2917917.
      28. Song L, Asgharzadeh S, Salo J, Engell K, Wu HW, Sposto R, Ara T, Silverman AM, DeClerck YA, Seeger RC, Metelitsa LS. Valpha24-invariant NKT cells mediate antitumor activity via killing of tumor-associated macrophages. J Clin Invest. 2009 Jun; 119(6):1524-36. PMID: 19411762; PMCID: PMC2689106.
      29. Ara T, Song L, Shimada H, Keshelava N, Russell HV, Metelitsa LS, Groshen SG, Seeger RC, DeClerck YA. Interleukin-6 in the bone marrow microenvironment promotes the growth and survival of neuroblastoma cells. Cancer Res. 2009 Jan 01; 69(1):329-37. PMID: 19118018; PMCID: PMC2761219.
      30. Bajou K, Peng H, Laug WE, Maillard C, Noel A, Foidart JM, Martial JA, DeClerck YA. Plasminogen activator inhibitor-1 protects endothelial cells from FasL-mediated apoptosis. Cancer Cell. 2008 Oct 07; 14(4):324-34. PMID: 18835034; PMCID: PMC2630529.
      31. Chantrain CF, Feron O, Marbaix E, DeClerck YA. Bone marrow microenvironment and tumor progression. Cancer Microenviron. 2008 Dec; 1(1):23-35. PMID: 19308682; PMCID: PMC2654350.
      32. Fukaya Y, Shimada H, Wang LC, Zandi E, DeClerck YA. Identification of galectin-3-binding protein as a factor secreted by tumor cells that stimulates interleukin-6 expression in the bone marrow stroma. J Biol Chem. 2008 Jul 04; 283(27):18573-81. PMID: 18450743.
        View in: PubMed
      33. Peng H, Sohara Y, Moats RA, Nelson MD, Groshen SG, Ye W, Reynolds CP, DeClerck YA. The activity of zoledronic Acid on neuroblastoma bone metastasis involves inhibition of osteoclasts and tumor cell survival and proliferation. Cancer Res. 2007 Oct 01; 67(19):9346-55. PMID: 17909043.
        View in: PubMed
      34. Song L, Ara T, Wu HW, Woo CW, Reynolds CP, Seeger RC, DeClerck YA, Thiele CJ, Sposto R, Metelitsa LS. Oncogene MYCN regulates localization of NKT cells to the site of disease in neuroblastoma. J Clin Invest. 2007 Sep; 117(9):2702-12. PMID: 17710228; PMCID: PMC1940236.
      35. Wall SJ, Zhong ZD, DeClerck YA. The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest. J Biol Chem. 2007 Aug 17; 282(33):24471-6. PMID: 17553787.
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