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CCN Society

ICCNS Award 2024 recipient

Professor Katia Scotlandi

Katia Scotlandi, Chief of the Experimental Oncology Lab, Istituto Ortopedico Rizzoli, Bologna, Italy

Katia Scotlandi graduated in Biomedical Science at the University of Bologna, where she received her training in experimental oncology. thanks to a fellowship from the Italian Association for Cancer Research. In 1990 she moved to the Rizzoli Orthopedic Institute, one of the most important orthopedic Institute in the world with a Dept devoted to the study and the cure of bone and soft tissue sarcomas. In 1996, she received her specialization in Clinical Pathology.

Since 2001 she served as adjunct Professor in molecular biology at the faculty of Pharmacological Science at University of Bologna.

During her training she spent several periods abroad as fellow or visiting Professor either in Europe or US ( Department of Pathology, University of Valencia (Spain), June 14-28, 2009; Hospital University Centre, INSERM, Unit 343, Nice (Prof. A. Bernard), September 17-22, 2001;  The Thomas Jefferson University, Kimmel Cancer Institute (Prof. R. Baserga), June 23-26, 1999;  The University of Illinois at Chicago, College of Medicine, Department of Genetics (Prof. Igor B. Roninson), April-May 1997. Research Project: Multidrug resistance and in situ RT-PCR).

 She has received theTina Anselmi Award, Bologna, March 6, 2019 and the  Oswald Van der Veken 2011 Award, Bruxelles, November 7, 2011 for her studies on bone tumors.

Her research work has been focused on pediatric solid tumors particularly bone sarcomas. The goal of her research activity is to contribute to the definition of biomarkers of risk and response that allow more personalized therapeutic approaches against Ewing sarcoma and osteosarcoma  and to pave the way for accelerating the discovery of the most promising biologically and epigenetically-targeted drug.

Katia Scotlandi has long been committed to advancing research and scientific interest in the field of IGF and insulin system. Her scientific group has demonstrated the importance of the related signalling pathway in sarcomas, particularly in Ewing sarcoma and participated to the development of rationale strategies to inhibit the IGF1R-mediated signalling at preclinical level. She has also highlighted the role of the insulin receptor in the rapid development of resistance to antibodies targeting IGF1R. More recently, she has introduced the concept that the RNA-binding protein IGF2BP3 may regulate the cell sensitivity to anti-IGF1R agents. In addition she has contributed hard to the identification of novel biomarkers of risk and prognosis, including CCN3, as well as of new therapeutic targets for these tumors. More recently, she has developed a platform for sequencing and establishment of complex preclinical models to accelerate our understanding of bone sarcomas.

Starting from 2005, the Scotlandi’s lab has been involved in several European networks and granted projects. At national level, from 2016 to 2019, dr. Scotlandi served as Secretary of the Working Group Sarcoma inside the Italian Alliance against Cancer, the oncologic network of the Italian Ministry of Health, to coordinate preclinical research activities that will ameliorate the diagnosis of sarcomas and facilitate the harmonization of treatments.

Not less important, it is her mentoring activity inside the academia. Over the years, she followed over seventy among graduate students, post-doctoral fellows and junior faculty members, contributing to the career development of young researchers and diffusing knowledge on pediatric oncology.

On the occasion of the ICCNS-Springer Award, Professsor Katia Scotlandi will give a presentation entitled:‪

Ewing’s sarcoma: embracing complexity to identify new therapeutic vulnerabilities


Genome instability and mutations are key elements of cancer initiation and progression. However, non-mutational epigenetic reprogramming can also help the acquisition of the cancer hallmark. This is particularly true for pediatric tumors, which usually derive from incompletely differentiated progenitor cells that are blocked during differentiation by a genetic alteration that freeze transformed cells into a proliferative, stem-like cell state, with unlocked plastic potential. These tumors are suitable models to study critical mediators of gene-regulatory architecture involved in oncogenic and developmental programs responsible of tumor initiation and disease progression. Ewing sarcoma, an aggressive developmental pediatric tumor, is a paradigm of tumors in which malignant progression is based on non-mutational epigenetic reprograming rather than genomic instability. EwS results from a chromosomal translocation that fuses the EWSR1 gene with an ETS family member, most frequently the FLI1 gene , forming the oncogenic driver EWSR1::FLI1. EWSR::FLI1 binds to DNA.  EWSR1::FLI1 reprograms the genetic landscape of EwS, affecting many key cellular processes (i.e. cell cycle, apoptosis, angiogenesis, metabolism, and cell migration) and is the oncogenic driver of this tumor. However, its presence is a necessary but not sufficient condition. Other molecules, such as CD99 and RNA binding proteins, have been demonstrated to have a crucial role in the regulation of Ewing sarcoma malignancy, offering a general vision of how tumors can be dynamically shaped. In fact, although genetically transformed, cancer cells may be actively controlled by the dynamic interactions between the microenvironment elements and nuclear elements that modify chromatin accessibility at transcription factor binding sites and enhancer-promoter interactions. The study of this dynamic interplay will help the development of novel therapeutic strategies.

CCN Society

ICCNS Award 2022 Recipient

ICCNS Award 2022 Recipient

Professor Lester Lau

Pr. Lester Lau

Department of Biochemistry and Molecular Genetics, University of Illinois Chicago (UIC)

Lester Lau received his Ph.D. in Biochemistry from Cornell University and was a Helen Hay Whitney Fellow at the Johns Hopkins University School of Medicine. He served as a faculty member at Northwestern University Medical School before moving to the University of Illinois at Chicago College of Medicine, where he is a Professor of Biochemistry and Molecular Genetics. He has received the Pew Scholars Award, the American Heart Association Established Investigator Award, the American Cancer Society Junior Faculty Award, and the University Scholar Award at the University of Illinois.

His laboratory has characterized various genes involved in growth control, including the nuclear receptor NUR77, the MAP kinase phosphatase MKP-1, the ribosome biogenesis protein BOP-1, and CCN1, the first member of the CCN family identified. He has established the matricellular nature of CCN proteins and their mechanisms of action through direct binding to integrin receptors. His laboratory has uncovered various CCN functions including cell adhesion and migration, angiogenesis, apoptosis, phagocytosis, and senescence, and demonstrated the biological significance of these functions in vivo using knockin and knockout mice. His recent research has dissected the role of CCN1 in integrating the functions of diverse cell types in inflammation, wound healing, and tissue regeneration in the skin, liver, and intestinal epithelium.

Lester Lau has long been committed to advancing research and scientific interest in the CCN field. He has been actively involved in the ICCNS since its inception and has previously served as the Head of the ICCNS Council and President of the Scientific Advisory Board. 

CCN Society




  • Bank Employee
    Banque Populaire Val de France
  • Institutrice Titulaire (Certificat d’Aptitude Professionnelle)
    Education Nationale
  • Maitresse d’Application (Certificat d’Aptitude Ecole d’Application)
    Education Nationale
  • Professeur des Ecoles
    Education Nationale
  • Financial Manager
    Laboratoire d’Oncologie Virale et Moléculaire
    Université Paris 7 – D. Diderot
  • Secretary of the International CCN Society
  • Treasurer of the International CCN Society
  • Administrative Manager and Coordinator JCCS-ICCNS

Foreign Postings

  • Glasgow Preschool, Scotland
  • Los Angeles, USA
    French Primary School – Mission Laique
  • Lecturer Holmes Junior High School
  • Istituto Rizzoli
    Bologna, Italy

Professional training

  • Desktop Publishing
    Université de Sceaux, France
  • Advanced English Training
    British Council, Paris, France
  • Computer skills : Word, Excel, Power Point, Photoshop, Filemaker


  • Perbal B, Perbal M, Perbal A. Cooperation is the key: the CCN biological system as a gate to high complex protein superfamilies’ signaling. J Cell Commun Signal. 2023
  • Perbal A. The 11th international workshop on the CCN family of genes in pictures. J Cell Commun Signal. 2023 Mar;17(1):13-23.
  • Perbal A. Correction to: 10th international workshop on the CCN family of genes, Niagara Falls, Canada, October 21-24, 2019. J Cell Commun Signal. 2021 Mar;15(1):153
  • Perbal A.
    The disastrous boomerang effects of “citation mania”. J Cell Commun Signal. 2017 Sep;11(3):291-295.
  • Perbal A, Perbal B.
    The CCN family of proteins: a 25th anniversary picture. J Cell Commun Signal. 2016 Sep;10(3):177-190. Epub 2016 Aug 31.
  • Perbal A. 8th international workshop on the CCN family of genes-Nice November 3-8, 2015. J Cell Commun Signal. 2016 Mar;10(1):87-101
  • Perbal B, Perbal A.
    Liberté, liberté chérie. J Cell Commun Signal. 2015 Mar;9(1):1-4.
  • Perbal A, Perbal B.
    CCN proteins, microenvironment, communication and signaling: why did we need a new journal? J Cell Commun Signal. 2007 Jun;1(1):1-3. doi: 10.1007/s12079-007-0007-x. Epub 2007 May 25. No abstract available.

Organization of International Conferences

  • International Workshop on Retroviral Pathogenesis
    1996, 2005, Saint-Malo, France
  • International Workshop on the CCN family of Genes
    Organizer,2000, 2002, 2004, Saint-Malo, France
    Co-Organiser, 2006, Okayama, Japan
    Co-Organiser, 2008, Toronto, Canada
    Co-Organiser, 2010, Newcastle, Ireland
    Organiser, 2013, Nice, France
    Organiser, 2015, Nice, France
    Organiser, 2017, Saint-Malo, France
    Co-Organiser, 2019, Niagara Falls, Canada Organiser, 2022, Nice, France
About The Iccns


Bernard Perbal, D.Sc., LL.D

Degrees and Positions

  • Diploma of Advanced Studies (DEA), “Enzymology” (1968)
  • Doctorate of Sciences (D. Sc.) Biochemistry and Genetics. University of Paris (1974).
  • Post-doctoral fellow Western Infirmary- Intitute of Virology, Glagow Scotland UK (1974-1975)
  • Invited Professor, UCLA, Dpt of Molecualr Biology and Immunology Los Angeles CA USA (1980-1982)
  • Founder and Director of the Viral and Molecular Oncology Laboratory at the Curie Institute CNRS
  • Research Director (1982-1988)
  • Full Professor of Biotechnologies, Molecular Genetics and Biochemistry, Molecular Pathology
  • (1988-2007) University of Paris VI P.M. Curie, and Paris 7, D. Diderot.
  • Associate Principal Scientist – Open Research Dpt. L’Oréal USA Clark NJ (2008-2010)
  • Senior Research Associate Scientific Direction, L’Oréal Clichy France (2010-2011)
  • Professional Master’s Degree: Economy, Law and Finance. Option Law of Intellectual Property and New technologies. University of Nice, (2011-2012)
  • Law Doctorate (LL.D.): Genetic Personal data and Self ownership. University of Nice, (2018)
  • Attorney at Law. Oath-taking (2021) – Court of Appeal Aix en Provence – Bar of Marseille France.
  • Couple and Sexology therapist (2023)


  • American Association for Cancer Research
  • American Association for the Advancement of Science
  • American Society for Microbiology, Molecular Biology Society
  • American Society for Virology
  • Founder of the International CCN Society


  • 1965 Laureate of the Concours Général de Sciences Naturelles (France)
  • 1990 Laureate of the French Académie des Sciences (Prix G. Rousseau)
  • 1992 Laureate of the Académie des Sciences (Grand Prix INSERM et Académie des Sciences )
  • 1992 Laureate of the French Ligue Nationale Contre le Cancer (Prix S. Dumonteil)
  • 2012 International CCN Society Award

Books and Reports

  • A Practical Guide to Molecular Cloning (Wiley, 1988, 1992)
  • Molecular Biology of Polyomaviruses and Herpes viruses (Wiley, 1982)
  • Clonage Moléculaire : Un Guide Pratique (Vigot, 1989)
  • CCN Proteins: A New Family of Cell Growth and Differentiation Regulators (Editor, Imperial College Press, 2005)
  • CCN Proteins in Health and Disease (Editor, Springer, 2010)
  • Focus on the patentability of computer programs (2014) J Cell Commun Signal.8(1):67-70

Editorial Board

  • Founder and former Editor in Chief of Methods in Molecular and Cellular Biology (Wiley, New York, 1989)
  • Founder and Editor in Chief of “Cell Communication and signaling” (2003) a former publication of BMC
  • Founder and Editor in Chief of “Journal of Cell Communication and signaling” published by Springer (2007-2023) and by Wiley from Januaray 2024

Research Themes

The studies performed in the laboratory of Viral Oncology that I created in 1982 were aimed at understanding :
• the molecular basis for the Myeloblastosis Associated Virus (MAV) tumorigenic potential.
• the biochemical properties, mode of action and biological role of the CCN3 (NOV) protein in normal and pathological conditions with a particular emphasis to the potential use of the CCN3 protein as a new tool for molecular medicine
The MAV strains usually induce osteopetrosis, lymphomas, and nephroblastomas in chicken (Perbal, 1995). MAV is the natural helper virus of Avian Myelobalstosis virus (AMV). Molecular cloning of a MAV strain inducing specifically nephroblastoma when injected in day-old chicken (Perbal 1985, Soret et al. 1985) allowed to establish that MAV-induced nephroblastoma represent a unique animal model for the Wilms’ tumor (Perbal 1994). The molecular cloning of MAV integration sites in the host genome, identified several genes whose viral induced alteration is associated to cancer development (Li et al. 2006). One of them, CCN3 was one of the three founding members of the CCN family of 6 proteins involved in the regulation of cell proliferation and differentiation in several normal and tumoral contexts (Joliot et al., 1992, Perbal , 2001).
Functionally bipartite, with members acting negatively or positively on cell communication and signaling, the CCN proteins are subject to complex fine tuning regulation from which stemmed the concept of their biological properties being based on a spatio-temporal combinatorial events model (Perbal . 2013, 2018, 2023)
Disregulation of the ccn3 gene expression and abnormal production, processing or localization of the CCN3 protein is associated to malignancy in several tumor cases. CCN3 detection in tumor samples is associated to a favorable outcome in several types of tumors and in some documented cases its expression is associated to metastatic potentiality of the tumor cells (Planque and Perbal 2003, Perbal 2003). The value of CCN3 as a prognostic marker has been established in the case of osteosarcomas (Perbal et al. 2008) and melanomas (Vallacchi et al. 2008). CCN3 is reducing the tumorigenic potential of glioblastomas, choriocarcinomas, Ewing’s tumors and melanomas. These observations set the stage for developing protocols for genetic therapy of these tumors.
Proteins and ligands interacting with CCN3 allow it to play its regulatory role in the control of cell attachement, spreading, proliferation and differentiation. After biologically active truncated CCN3 proteins with different sub cellular localization (Perbal 2004, Planque et al. 2006), were identified in our laboratory, several groups reported the existence of truncated and rearranged forms of other CCN proteins (Perbal et al. 2023). Since the nuclear CCN3 proteins detected in cancer cells have been shown to regulate transcription, we have proposed that a balanced production of secreted CCN3 protein with anti-proliferative activity and nuclear CCN3 protein with pro-proliferative and oncogenic activities is required for the spatio temporal combinatorial events control of its biological activities (Perbal et al 2023).
Recent Orientations
My interest in the molecular basis of genetic diseases which stemmed from my early retrovirology studies, led me to undertake investigations in the legal aspects related to genetic information protection of human. Further to the COVID pandemic and interrogations expressed by the public, I became interested in social approches of medical diseases and the combination power of my scientific and legal activities culminated in my certification as a couple therapist and sexologist.

Selected Publications in the field of cell communication and signaling

Full list available on

Perbal B, Perbal M, Perbal A. Cooperation is
the key: the CCN biological system as a gate to high complex protein
superfamilies’ signaling.J Cell Commun Signal. 2023 Jun;17(2):233-253. doi:
10.1007/s12079-023-00749-8.PMID: 37166690Free PMC article. 2

Perbal B.J Time has come to address the
spatiotemporal combinatorial model for CCN proteins biological activitites by
spatial transcriptomics and genome wide association studies
. Cell Commun Signal. 2023 Mar;17(1):1-3.

Kubota S, Kawaki H, Perbal
, Takigawa M, Kawata K, Hattori T, Nishida T. Do not overwork:
cellular communication network factor 3 for life in cartilage
.J Cell Commun Signal. 2023 Jun;17(2):353-359.

Perbal B. The power of combined spatial
transcriptomics and genome wide association studies (GWAS) approaches to heritable prostate cancer. J Cell Commun Signal. 2023 Mar;17(1):5-6. doi:10.1007/s12079-023-00724-3.6

Yeger H, Perbal B. The CCN axis in cancer development and progression. J Cell Commun Signal. 2021Dec;15(4):491-517.

Perbal B.J Cell Commun Signal. 2019 Dec;13(4):437-439. doi: 10.1007/s12079-019-00543-5. CCN proteins are part of a
multilayer complex system: a working model.

Perbal B, Tweedie S, Bruford E.J The official unified nomenclature adopted by the HGNC calls for the use of the acronyms, CCN1-6, and discontinuation in the use of CYR61, CTGF, NOV and WISP 1-3 respectively.Cell Commun Signal. 2018 Dec;12(4):625-629. doi: 10.1007/s12079-018-0491-1. Epub 2018 Nov5.

Perbal B. The concept of the CCN protein family revisited: a
centralized coordination network. J Cell Commun Signal. 2018
Mar;12(1):3-12. doi: 10.1007/s12079-018-0455-5. Epub 2018 Feb 22.

Dombrowski Y, O’Hagan T, Dittmer M, Penalva R, Mayoral SR, Bankhead P, Fleville S,Eleftheriadis G, Zhao C, Naughton M, Hassan R, Moffat J, Falconer J, Boyd A,Hamilton P, Allen IV, Kissenpfennig A, Moynagh PN, Evergren E, Perbal B, Williams AC, Ingram RJ, Chan JR, Franklin RJM, Fitzgerald DC.Regulatory T cells promote myelin regeneration in the central nervous system Nat Neurosci. 2017
May;20(5):674-680. doi: 10.1038/nn.4528. Epub 2017 Mar 13.

Perbal B, Tweedie S, Bruford E The official unified nomenclature adopted by the HGNC calls for the use of the acronyms, CCN1-6, and discontinuation in the use of CYR61, CTGF, NOV and WISP 1-3 respectively. J Cell Commun Signal. 2018 Dec;12(4):625-629

Perbal B. The concept of the CCN protein family revisited: a centralized coordination network. J Cell Commun Signal. 2018 Mar;12(1):3-12.

Yeger H, Perbal B. CCN family of proteins: critical modulators of the tumor cell microenvironment. J Cell Commun Signal. 2016

Zhang C, van der Voort D, Shi H, Zhang R, Qing Y, Hiraoka S, Takemoto M, Yokote K, Moxon JV, Norman P, Rittié L, Kuivaniemi H, Atkins GB, Gerson SL, Shi GP, Golledge J,
Dong N, Perbal B, Prosdocimo DA, Lin Z.
Matricellular protein CCN3 mitigates abdominal aortic aneurysm. J Clin Invest. 2016 May 2;126(5):2012.

Perbal B CCN Proteins : A Centralized Communication System.
J Cell Commun Signal. 2013 Aug;7(3):169-77..May;180(5):1979-90.

Ouellet V, Tiedemann K, Mourskaia A, Fong JE, Tran-Thanh D, Amir E, Clemons M, Perbal B, Komarova SV, Siegel P. CCN3 impairs osteoblast and stimulates osteoclast differentiation to favor breast cancer metastasis to boneAm J Pathol 2011 May;178(5):2377-88

Rittié L,Perbal B,Castellot JJ, Orringer JS, Voorhees JJ, Fisher GJ Spatial-temporal modulation of CCN
proteins during wound healing in human skin in vivo J Cell Commun Signal. 2011 Mar;5(1):69-80

Lin Z, Natesan V, Shi H, Hamik A, Kawanami D, Hao C, Mahabaleshwar GH, Wang W, Jin ZG, Atkins GB, Firth SM, Rittié L, Perbal B, Jain MK A novel role of CCN3 in regulating endothelial inflammation. J Cell Commun Signal. 2010 Oct;4(3):141-53.

Perbal B, Lazar N, Zambelli D, Lopez-Guerrero JA, Llombart-Bosch A, Scotlandi K, Picci P. ‪Prognostic relevance of CCN3 in Ewing sarcoma. ‪Hum Pathol. 2009 Oct;40(10):1479-86. Epub 2009 Aug 19. ‪

Perbal B. ‪Alternative splicing of CCN mRNAs…. it has been upon us. ‪J Cell Commun Signal. 2009 Jun;3(2):153-7. Epub 2009
Apr 28.

 Holbourn KP, Acharya KR, Perbal B. ‪The CCN family of proteins: structure-function relationships. ‪Trends Biochem Sci. 2008
Oct;33(10):461-73. Epub 2008 Sep 11. ‪

 Kawaki H, Kubota S, Suzuki A, Lazar N, Yamada T, Matsumura T, Ohgawara T, Maeda T, Perbal B, Lyons KM,
Takigawa M. ‪
Cooperative regulation of chondrocyte differentiation by CCN2 and CCN3 shown by a comprehensive analysis of the CCN family proteins in cartilage. ‪J Bone Miner Res. 2008
Nov;23(11):1751-64. ‪

Yeger H, Perbal B. The CCN family of genes: a perspective on CCN biology and therapeutic potential. J Cell Commun Signal.
2008 Jun 21. [Epub ahead of print]

Perbal B, Zuntini M, Zambelli D, Serra M, Sciandra M, Cantiani L, Lucarelli E, Picci P, Scotlandi K. Prognostic
value of CCN3 in osteosarcoma. Clin Cancer Res. 2008 Feb 1;14(3):701-9.

Vallacchi V, Daniotti M, Ratti F, Di Stasi D, Deho P, De Filippo A, Tragni G, Balsari A, Carbone A, Rivoltini L, Parmiani G, Lazar N, Perbal B, Rodolfo M. CCN3/nephroblastoma overexpressed matricellular protein regulates integrin expression, adhesion, and dissemination in melanoma. Cancer Res. 2008 Feb 1;68(3):715-23. Erratum in: Cancer Res. 2008 Mar 15;68(6):2051.

Lazar N, Manara C, Navarro S, Bleau A-M, Llombart-Bosch A, Scotlandi K, Planque N, Perbal B. Domain-specific CCN3 antibodies asunique tools for structural and functional studies
J. Cell Commun Signal. 2007 Sep;1(2):91-102. Epub 2007 Sep 8.

Fukunaga-Kalabis M, Martinez G, Telson SM, Liu ZJ, Balint K, Juhasz I, Elder DE, Perbal B, Herlyn M.
Downregulation of CCN3 expression as a potential mechanism for melanoma progression. Oncogene. 2008 Apr 17;27(18):2552-60. Epub 2007 Oct 29.

van Roeyen CR, Eitner F, Scholl T, Boor P, Kunter U, Planque N, Grone HJ, Bleau AM, Perbal B, Ostendorf T, Floege J. CCN3 is a novel endogenous PDGF-regulated inhibitor of glomerular cell proliferation. Kidney Int. 2007 Oct 3; [Epub ahead of print]

Bleau AM, Planque N, Lazar N, Zambelli D, Ori A, Quan T, Fisher G, Scotlandi K, Perbal B. Antiproliferative activity of CCN3: Involvement of the C-terminal module and post-translational regulation. J Cell Biochem. 2007 Mar 5; [Epub ahead of print]

Perbal B. The CCN3 protein and cancer. Adv Exp Med Biol. 2006;587:23-40. Review.

Fukunaga-Kalabis M, Martinez G, Liu ZJ, Kalabis J, Mrass P, Weninger W, Firth SM, Planque N, Perbal B, Herlyn M. CCN3 controls 3D spatial localization of melanocytes in the human skin through DDR1. J Cell Biol. 2006 Nov 20;175(4):563-9. Epub 2006 Nov 13..

Perbal B. New insight into CCN3 interactions – Nuclear CCN3
: fact or fantasy? Cell Commun Signal. 2006 Aug 8;4:6.

McCallum L, Price S, Planque N, Perbal B, Pierce A, Whetton AD, Irvine AE. A novel mechanism for BCR-ABL action: stimulated secretion of CCN3 is involved in growth and differentiation regulation. Blood. 2006 Sep 1;108(5):1716-23. Epub 2006 May 2.

Planque N, Long Li C, Saule S, Bleau AM, Perbal B. Nuclear
addressing provides a clue for the transforming activity of amino-truncated CCN3 proteins. J Cell Biochem. 2006 Sep 1;99(1):105-16.

Perbal B. NOV story: the way to CCN3. Cell Commun Signal.
2006 Feb 20;4:3.

Benini S, Perbal B, Zambelli D, Colombo MP, Manara MC, Serra M, Parenza M, Martinez V, Picci P, Scotlandi K. In Ewing’s sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type. Oncogene. 2005 Jun 23;24(27):4349-61.

Bleau AM, Planque N, Perbal B. CCN proteins and cancer: two
to tango. Front Biosci. 2005 May 1;10:998-1009.

Kyurkchiev S, Yeger H, Bleau AM, Perbal B. Potential
cellular conformations of the CCN3(NOV) protein. Cell Commun Signal. 2004 Sep 10;2(1):9.

Fu CT, Bechberger JF, Ozog MA, Perbal B, Naus CC.
CCN3 (NOV) interacts with connexin43 in C6 glioma cells: possible mechanism of connexin-mediated growth suppression. J Biol Chem. 2004 Aug 27;279(35):36943-50. Epub 2004 Jun 21.

Gellhaus A, Dong X, Propson S, Maass K, Klein-Hitpass L, Kibschull M, Traub O, Willecke K, Perbal B, Lye SJ, Winterhager E. Connexin43 interacts with NOV: a possible mechanism for negative regulation of cell growth in choriocarcinoma cells. J Biol Chem. 2004 Aug 27;279(35):36931-42. Epub 2004
Jun 4.

Katsube K, Chuai ML, Liu YC, Kabasawa Y, Takagi M, Perbal B, Sakamoto K. The expression of chicken NOV, a member of the CCN gene family, in early stage development. Brain Res Gene Expr Patterns. 2001 Aug;1(1):61-5.

Perbal B. CCN proteins : multifunctional signalling regulators. Lancet 2004 Jan;363(9) :62-64

Perbal B. Communication is the key. Cell Commun Signal.
2003 Oct 27;1(1):3.

Perbal B. The CCN3 (NOV) cell growth regulator: a new tool
for molecular medicine. Expert Rev Mol Diagn. 2003 Sep;3(5):597-604.

Planque N, Perbal B. A structural approach to the role of
CCN (CYR61/CTGF/NOV) proteins in tumourigenesis. Cancer Cell Int. 2003 Aug 22;3(1):15.

Li CL, Martinez V, He B, Lombet A, Perbal B. A role for
CCN3 (NOV) in calcium signalling. Mol Pathol. 2002 Aug;55(4):250-61.

Sakamoto K, Yamaguchi S, Ando R, Miyawaki A, Kabasawa Y, Takagi M, Li CL, Perbal B, Katsube K. The nephroblastoma overexpressed gene (NOV/ccn3) protein associates with Notch1 extracellular domain and inhibits myoblast differentiation via Notch signaling pathway. J Biol Chem. 2002 Aug 16;277(33):29399-405. Epub 2002 Jun 05.

Manara MC, Perbal B, Benini S, Strammiello R, Cerisano V,
Perdichizzi S, Serra M, Astolfi A, Bertoni F, Alami J, Yeger H, Picci P, Scotlandi K.
The expression of ccn3(nov) gene in musculoskeletal tumors. Am J Pathol. 2002 Mar;160(3):849-59.

Perbal B. Les protéines CCN : quand multimodulaire rime
avec multifonctionnel. Médecine-Sciences. 2002 Jun;18 :745-56

Thomopoulos GN, Kyurkchiev S, Perbal B. Immunocytochemical localization of NOVH protein and ultrastructural characteristics of NCI-H295R cells. J Submicrosc Cytol Pathol. 2001 Jul;33(3):251-60.

Gupta N, Wang H, McLeod TL, Naus CC, Kyurkchiev S, Advani S, Yu J, Perbal B, Weichselbaum RR. Inhibition of glioma cell growth and tumorigenic potential by CCN3 (NOV).
Mol Pathol. 2001 Oct;54(5):293-9.

Maillard M, Cadot B, Ball RY, Sethia K, Edwards DR, Perbal B, Tatoud R. Differential expression of the ccn3 (nov) proto-oncogene in human prostate cell lines and tissues Mol Pathol. 2001 Aug;54(4):275-80

Su BY, Cai WQ, Zhang CG, Martinez V, Lombet A, Perbal B.
The expression of ccn3 (nov) RNA and protein in the rat central nervous system is developmentally regulated Mol Pathol 2001 Jun;54(3):184-91.

Perbal B. NOV (nephroblastoma overexpressed) and the CCN
family of genes: structural and functional issues. Mol Pathol. 2001
Apr;54(2):57-79. doi: 10.1136/mp.54.2.57

Joliot V, Martinerie C, Dambrine G, Plassiart G, Brisac M, Crochet J, Perbal B . Proviral rearrangements and overexpression of a newcellular gene (nov) in myeloblastosis-associated virus type 1-induced nephroblastomas. Mol Cell Biol. 1992 Jan;12(1):10-21.