Carlo M Croce

Ludwig Institute for Cancer Research, La Jolla, California, United States

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Publications (526)4584.94 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: This volume provides an overview of RNA bioinformatics methodologies, including basic strategies to predict secondary and tertiary structures, and novel algorithms based on massive RNA sequencing. Interest in RNA bioinformatics has rapidly increased thanks to the recent high-throughput sequencing technologies allowing scientists to investigate complete transcriptomes at single nucleotide resolution. Adopting advanced computational technics, scientists are now able to conduct more in-depth studies and present them to you in this book. Written in the highly successful Methods of Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and equipment, step-by-step, readily reproducible bioinformatics protocols, and key tips to avoid known pitfalls. Authoritative and practical, RNA Bioinformatics seeks to aid scientists in the further study of bioinformatics and computational biology of RNA.
    RNA Bioinformatics, Methods in Molecular Biology edited by Ernesto Picardi, 02/2015: chapter 25: pages 388; Humana Press, Springer., ISBN: ISBN 978-1-4939-2290-1
  • Michela Garofalo, Carlo M. Croce
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    ABSTRACT: Increasing evidence sustains that the establishment and maintenance of many, if not all, human cancers are due to cancer stem cells (CSCs), tumor cells with stem cell properties, such as the capacity to self-renew or generate progenitor and differentiated cells. CSCs seem to play a major role in tumor metastasis and drug resistance but, albeit the potential clinical importance, their regulation at the molecular level is not clear. Recent studies have highlighted several miRNAs to be differentially expressed in normal and cancer stem cells and established their role in targeting genes and pathways supporting cancer stemness properties. This review focuses on the last advances on the role of microRNAs in the regulation of stem cell properties and cancer stem cells in different tumors.
    Advanced Drug Delivery Reviews. 11/2014;
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    ABSTRACT: Metastasis is the principal cause of cancer death and occurs through multiple, complex processes that involve the concerted action of many genes. A number of studies have indicated that the Fragile Histidine Triad (FHIT) gene product, FHIT, functions as a tumor suppressor in a variety of common human cancers. Although there are suggestions of a role for FHIT loss in progression of various cancers, a role for such loss in metastasis has not been defined. Here, via in vivo and in vitro assays, we reveal that the enforced expression of FHIT significantly suppresses metastasis, accompanied by inhibition of the epithelial-mesenchymal transition (EMT), a process involved in metastasis through coordinate modulation of EMT-related genes. Specifically, miR-30c, a FHIT-upregulated microRNA, contributes to FHIT function in suppression of EMT and metastasis by directly targeting metastasis genes Metadherin (MTDH), High-mobility group AT—hook 2 (HMGA2), and the mesenchymal markers, Vimentin (VIM) and Fibronectin (FN1), in human lung cancer. Finally, we demonstrate that the expression pattern of FHIT and miR-30c is inversely correlated with that of MTDH and HMGA2 in normal tissue, nonmetastatic and metastatic tumors, serving as a potential biomarker for metastasis in lung cancer.
    PLoS Genetics 10/2014; 10(10):e1004652. · 8.52 Impact Factor
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    ABSTRACT: Renal cell carcinoma (RCC) accounts for approximately 2% of all adult cancer cases in Europe, by representing the ninth most common malignancy and the most common cancer in the adult kidney (85% of the kidney cancer cases). The clear-cell variant (ccRCC), one of the three major subtypes, occurs in 75% of all RCC cases. Although the advent of new target-oriented therapies, ccRCC responds poorly to chemotherapy and radiotherapy, then radical surgery still represents the best choice for patients diagnosed with ccRCC, but the prognosis remains severe in case of disseminated disease. One of the main challenges in the management of ccRCC is related to stage I patients. Essentially, at present there is no valid biomarker able to differentiate those patients who will benefit from surgical tumor dissection from those who, even after complete surgical resection, will recur and eventually develop a disseminated disease. Such a biomarker would be of great value, since it will select a population to be tested for adjuvant treatments and/or for a more aggressive “follow-up” plan. The transcribed ultraconserved regions (UCRs) are a family of ncRNAs highly conserved (100%) between orthologous regions of the human, rat, and mouse genomes. UCR genes are frequently located at fragile sites and genomic regions involved with cancers, and their expression is dys-regulated in several types of solid and hematological malignancies compared to the adjacent non-tumoral tissue counterpart. While an increasing number of studies supports a role for UCRs in human carcinogenesis, their role as prognostic biomarkers is still unexplored. In this study we collected 136 frozen paired normal and adjacent non-tumoral tissues from stage I ccRCC patients. We assessed the expression of all 482 identified UCRs in primary tumors and in the adjacent non-tumoral tissues from the same patient, by high-throughput microarray profiling using an in house array developed at the Ohio State University. We found a differential expression of 30 UCRs between the two groups, and we validated the most dys-regulated UCRs by quantitative real-time PCR (qRT-PCR). We then correlated the expression of these UCRs, with the overall survival (OS) of our patients by Kaplan-Meier analysis. We observed that the expression of 8 UCRs (namely, uc.115A, uc.466, uc.282, uc.395A, uc.203A, uc.1, uc.332, and uc.243A) significantly correlated with prognosis in stage I ccRCC patients with shorter OS, with respect to patients with better OS. In particular, the expression in "good" prognosis stage I ccRCC was high for uc.115A and uc.466 (p = 0.027 and 0.014, respectively), and low for uc.282, uc.395A, uc.203A, uc.1, uc.332, and uc.243A (p = 0.027, 0.01, 0.002, 0.013, 0.03, and 0.018, respectively). Overall, this study identifies a prognostic signature of UCRs, correlating with survival in stage I ccRCC patients, and could lead to the identification of a new biomarker for a better stratification of ccRCC patients eligible for adjuvant treatments and/or a closer post-surgery clinical follow-up.
    FEBS WORKSHOP "Decoding Non-coding RNAs in Development and Cancer", Capri, Italy; 10/2014
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    ABSTRACT: MicroRNAs (miRNAs) are short non-coding RNAs with a length of ∼22 nucleotides, involved in post-transcriptional regulation of gene expression. Until now, over 2,588 miRNAs have been identified in humans and the list is growing. MicroRNAs have an important role in all biological processes and aberrant miRNA expression is associated with many diseases including cancer. In the year 2002 the first connection between cancer and miRNA deregulation was discovered. Since then, a lot of information about the key role which miRNAs play in cancer development and drug resistance has been gained. However, there is still a long way to go to fully understand the miRNA world. In this review, we briefly describe miRNA biogenesis and discuss the role of miRNAs in cancer development and drug resistance. Finally we explain how miRNAs can be used as biomarkers and as a novel therapeutic approach in cancer.
    Advances in Biological Regulation 09/2014;
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    ABSTRACT: The purpose of this study is to determine whether microRNA for pluripotent stem cells are also expressed in breast cancer and are associated with metastasis and outcome.
    JNCI Journal of the National Cancer Institute 09/2014; · 14.34 Impact Factor
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    ABSTRACT: BackgroundThere are 481 ultra-conserved regions (UCRs) longer than 200 bases in the genomes of human, mouse and rat. These DNA sequences are absolutely conserved and show 100% identity with no insertions or deletions. About half of these UCR are reported as transcribed and many correspond to long non-coding RNAs (lncRNAs).MethodsWe used custom microarrays with 962 probes representing sense and antisense sequences for the 481 UCRs to examine their expression across 374 normal samples from 46 different tissues and 510 samples representing 10 different types of cancer. The expression in embryonic stem cells of selected UCRs was validated by real time PCR.ResultsWe identified tissue selective UCRs and studied UCRs in embryonic and induced pluripotent stem cells. Among the normal tissues, the uc.283 lncRNA was highly specific for pluripotent stem cells. Intriguingly, the uc.283-plus lncRNA was highly expressed in some solid cancers, particularly in one of the most untreatable types, glioma.ConclusionOur results suggest that uc.283-plus lncRNA might have a role in pluripotency of stem cells and in the biology of glioma.
    Genome Medicine 09/2014; · 4.94 Impact Factor
  • S Nana-Sinkam, Carlo M Croce
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    ABSTRACT: In the past two decades, microRNAs have emerged as crucial mediators of organ development and human disease. Here, we discuss their role as drivers or suppressors of the hallmarks of cancer during tumorigenesis and progression, in defining interpatient heterogeneity and the promise of therapeutic application.
    Genome Biology 08/2014; 15(9):445. · 10.30 Impact Factor
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    ABSTRACT: Barrett's esophagus (BE) involves a metaplastic replacement of native esophageal squamous epithelium (Sq) by columnar-intestinalized mucosa, and it is the main risk factor for Barrett-related adenocarcinoma (BAc). Ultra-conserved regions (UCRs) are a class non-coding sequences that are conserved in humans, mice and rats. More than 90% of UCRs are transcribed (T-UCRs) in normal tissues, and are altered at transcriptional level in tumorigenesis. To identify the T-UCR profiles that are dysregulated in Barrett's mucosa transformation, microarray analysis was performed on a discovery set of 51 macro-dissected samples obtained from 14 long-segment BE patients. Results were validated in an independent series of esophageal biopsy/surgery specimens and in two murine models of Barrett's esophagus (i.e. esophagogastric-duodenal anastomosis). Progression from normal to BE to adenocarcinoma was each associated with specific and mutually exclusive T-UCR signatures that included up-regulation of uc.58-, uc.202-, uc.207-, and uc.223- and down-regulation of uc.214+. A 9 T-UCR signature characterized BE versus Sq (with the down-regulation of uc.161-, uc.165-, and uc.327-, and the up-regulation of uc.153-, uc.158-, uc.206-, uc.274-, uc.472-, and uc.473-). Analogous BE-specific T-UCR profiles were shared by human and murine lesions. This study is the first demonstration of a role for T-UCRs in the transformation of Barrett's mucosa.
    Oncotarget 08/2014; 5(16):7162-7171. · 6.64 Impact Factor
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    ABSTRACT: Glioblastoma (GBM) frequently displays amplification and/or mutation of the epidermal growth factor receptor (EGFR) gene. Highlighting the importance of EGFR in the pathogenesis of GBM, aberrant EGFR (ΔEGFR, also known as EGFRvIII) confers a variety of biological effects upon its expression, including resistance to radiation and chemotherapeutic agents, promotion of tumor cell motility and invasion, enhancement of tumorigenicity in vivo, and maintenance of GBM growth and heterogeneity. We hypothesized that this diverse oncogenic pathophysiology exerted by ΔEGFR is regulated, in part, through the modulation of microRNA (miR) activity, widely shown to be involved in many biological processes including cancer initiation, maintenance and progression.
    Neuro-Oncology 07/2014; 16 Suppl 3:iii14-iii15. · 6.18 Impact Factor
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    ABSTRACT: High-level leukemia-cell expression of miR-155 is associated with more aggressive disease in patients with chronic lymphocytic leukemia (CLL), including those cases with low-level expression of zeta-chain associated protein of 70 kD (ZAP-70). CLL with high-level miR-155 expressed lower levels of Src homology-2 domain-containing inositol 5-phosphatase 1 (SHIP1) and were more responsive to B-cell-receptor (BCR) ligation than CLL with low-level miR-155. Transfection with miR-155 enhanced responsiveness to BCR ligation, whereas transfection with a miR-155 inhibitor had the opposite effects. CLL in lymphoid tissue expressed higher levels of miR155HG than CLL in the blood of the same patient. Also, isolated CD5(bright)CXCR4(dim) cells, representing CLL that had been newly-released from the microenvironment, expressed higher levels of miR-155 and were more responsive to BCR ligation, than isolated CD5(dim)CXCR4(bright) cells of the same patient. Treatment of CLL or normal B-cells with CD40-ligand or B-cell-activating factor (BAFF) upregulated miR-155, and enhanced sensitivity to BCR ligation, effects that could be blocked by inhibitors to miR-155. This study demonstrates that the sensitivity to BCR ligation can be enhanced by high-level expression of miR-155, which in turn can be induced by cross-talk within the tissue microenvironment, potentially contributing to its association with adverse clinical outcome in patients with CLL.
    Blood 06/2014; · 9.78 Impact Factor
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    ABSTRACT: Autophagy is crucial for cellular homeostasis and plays important roles in tumorigenesis. FIP200 (FAK family-interacting protein of 200 kDa) is an essential autophagy gene required for autophagy induction, functioning in the ULK1-ATG13-FIP200 complex. Our previous studies showed that conditional knockout of FIP200 significantly suppressed mammary tumorigenesis, which was accompanied by accumulation of p62 in tumor cells. However, it is not clear whether FIP200 is also required for maintaining tumor growth and how the increased p62 level affects the growth in autophagy-deficient FIP200-null tumors in vivo. Here, we describe a new system to delete FIP200 in transformed mouse embryonic fibroblasts as well as mammary tumor cells following their transplantation and show that ablation of FIP200 significantly reduced growth of established tumors in vivo. Using similar strategies, we further showed that either p62 knockdown or p62 deficiency in established FIP200-null tumors dramatically impaired tumor growth. The stimulation of tumor growth by p62 accumulation in FIP200-null tumors is associated with the up-regulated activation of the NF-κB pathway by p62. Last, we showed that overexpression of the autophagy master regulator TFEB(S142A) increased the growth of established tumors, which correlated with the increased autophagy of the tumor cells. Together, our studies demonstrate that p62 and autophagy synergize to promote tumor growth, suggesting that inhibition of both pathways could be more effective than targeting either alone for cancer therapy.
    Genes & development. 06/2014; 28(11):1204-16.
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    ABSTRACT: -Low high-density lipoprotein-cholesterol (HDL-C) constitutes a major risk factor for atherosclerosis. Recent studies from our group reported a genetic association between the WW domain-containing oxidoreductase (WWOX) gene and HDL-C levels. Here, through next-generation resequencing, in vivo functional studies and gene microarray analyses, we investigated the role of WWOX in HDL and lipid metabolism.
    Circulation Cardiovascular Genetics 05/2014; · 6.73 Impact Factor
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    ABSTRACT: Recent investigations of chromosomal aberrations in CLL led to a better understanding of the molecular causes of chronic lymphocytic leukemia. Here we report a rearrangement between MAML2 (mastermind like protein 2) and CXCR4 (specific receptor for CXC chemokine stromal cell-derived factor-1) in CLL cells of a patient with a t(2;11)(q22.1;q21) chromosomal translocation. The rearrangement between MAML2 and CXCR4, created by a t(2;11)(q22.1;q21) translocation, results in a new fusion gene in which a portion of CXCR4 is linked to the MAML2 gene. This fusion gene encodes for CXCR4/MAML2 protein chimera in which the N-terminal basic domain of MAML2 is replaced by the N-terminal domain of CXCR4.
    Blood 05/2014; · 9.78 Impact Factor
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    ABSTRACT: The leukocyte adhesion cascade is important in chronic lymphocytic leukemia (CLL) as it controls migration of malignant cells into the pro-survival lymph node microenvironment. Circulating trisomy 12 CLL cells have increased expression of the integrins CD11a and CD49d as well as CD38, but the tissue expression of these and other molecules as well as the functional and clinical sequelae of these changes have not been described. Here we demonstrate that circulating trisomy 12 CLL cells also have increased expression of the integrins CD11b, CD18, CD29, and ITGB7, and the adhesion molecule CD323. Notably, there was reduced expression of CD11a, CD11b and CD18 in trisomy 12 cases with NOTCH1 mutations compared to wild type. Trisomy 12 cells also exhibit up-regulation of intra-cellular integrin signaling molecules CALDAG-GEFI, RAP1B and RAPL resulting in enhanced VLA-4 directed adhesion and motility. CD38 expression in CLL has prognostic significance, but the increased CD38 expression in trisomy 12 CLL cells must be taken into account in this subgroup and the threshold of CD38 positivity raised to 40% for this marker to retain its prognostic value. In conclusion, trisomy 12 CLL cells exhibit functional up-regulation of integrin signaling, with β2-integrin expression being modulated by NOTCH1 mutation status.
    Blood 05/2014; · 9.78 Impact Factor
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    ABSTRACT: Understanding the mechanisms that sustain pluripotency in human embryonic stem cells (hESCs) is an active area of research that may prove useful in regenerative medicine and will provide fundamental information relevant to development and cancer. hESCs and cancer cells share the unique ability to proliferate indefinitely and rapidly. Because the protein survivin is uniquely overexpressed in virtually all human cancers and in hESCs, we sought to investigate its role in supporting the distinctive capabilities of these cell types. Results presented here suggest that survivin contributes to the maintenance of pluripotency and that post-transcriptional control of survivin isoform expression is selectively regulated by microRNAs. miR-203 has been extensively studied in human tumors, but has not been characterized in hESCs. We show that miR-203 expression and activity is consistent with the expression and subcellular localization of survivin isoforms that in turn modulate expression of the Oct4 and Nanog transcription factors to sustain pluripotency. This study contributes to understanding of the complex regulatory mechanisms that govern whether hESCs proliferate or commit to lineages. © 2014 Wiley Periodicals, Inc.
    Journal of Cellular Physiology 05/2014; · 4.22 Impact Factor
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    ABSTRACT: MicroRNA deregulation is frequent in human colorectal cancers (CRCs), but little is known as to whether it represents a bystander event or actually drives tumor progression in vivo. We show that miR-135b overexpression is triggered in mice and humans by APC loss, PTEN/PI3K pathway deregulation, and SRC overexpression and promotes tumor transformation and progression. We show that miR-135b upregulation is common in sporadic and inflammatory bowel disease-associated human CRCs and correlates with tumor stage and poor clinical outcome. Inhibition of miR-135b in CRC mouse models reduces tumor growth by controlling genes involved in proliferation, invasion, and apoptosis. We identify miR-135b as a key downsteam effector of oncogenic pathways and a potential target for CRC treatment.
    Cancer cell 04/2014; 25(4):469-83. · 25.29 Impact Factor
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    ABSTRACT: RNAi is a powerful tool for the regulation of gene expression. It is widely and successfully employed in functional studies and is now emerging as a promising therapeutic approach. Several RNAi-based clinical trials suggest encouraging results in the treatment of a variety of diseases, including cancer. Here we present miR-Synth, a computational resource for the design of synthetic microRNAs able to target multiple genes in multiple sites. The proposed strategy constitutes a valid alternative to the use of siRNA, allowing the employment of a fewer number of molecules for the inhibition of multiple targets. This may represent a great advantage in designing therapies for diseases caused by crucial cellular pathways altered by multiple dysregulated genes. The system has been successfully validated on two of the most prominent genes associated to lung cancer, c-MET and Epidermal Growth Factor Receptor (EGFR). (See http://microrna.osumc.edu/mir-synth).
    Nucleic Acids Research 03/2014; · 8.81 Impact Factor
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    ABSTRACT: MicroRNAs (miRNAs) are small, noncoding RNAs that regulate gene expression and, in cancers, are often packaged within secreted microvesicles. The cachexia syndrome is a debilitating state of cancer that predominantly results from the loss of skeletal muscle mass, which is in part associated with apoptosis. How tumors promote apoptosis in distally located skeletal muscles has not been explored. Using both tumor cell lines and patient samples, we show that tumor-derived microvesicles induce apoptosis of skeletal muscle cells. This proapoptotic activity is mediated by a microRNA cargo, miR-21, which signals through the Toll-like 7 receptor (TLR7) on murine myoblasts to promote cell death. Furthermore, tumor microvesicles and miR-21 require c-Jun N-terminal kinase activity to regulate this apoptotic response. Together, these results describe a unique pathway by which tumor cells promote muscle loss, which might provide a great insight into elucidating the causes and treatment options of cancer cachexia.
    Proceedings of the National Academy of Sciences 03/2014; · 9.81 Impact Factor
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    ABSTRACT: Cell survival after DNA damage relies on DNA repair, the abrogation of which causes genomic instability and development of cancer. However, defective DNA repair in cancer cells can be exploited for cancer therapy using DNA-damaging agents. DNA double-strand breaks are the major lethal lesions induced by ionizing radiation (IR) and can be efficiently repaired by DNA homologous recombination, a system that requires numerous factors including the recombinase RAD51 (RAD51). Therapies combined with adjuvant radiotherapy have been demonstrated to improve the survival of triple-negative breast cancer patients; however, such therapy is challenged by the emergence of resistance in tumor cells. It is, therefore, essential to develop novel therapeutic strategies to overcome radioresistance and improve radiosensitivity. In this study we show that overexpression of microRNA 155 (miR-155) in human breast cancer cells reduces the levels of RAD51 and affects the cellular response to IR. miR-155 directly targets the 3'-untranslated region of RAD51. Overexpression of miR-155 decreased the efficiency of homologous recombination repair and enhanced sensitivity to IR in vitro and in vivo. High miR-155 levels were associated with lower RAD51 expression and with better overall survival of patients in a large series of triple-negative breast cancers. Taken together, our findings indicate that miR-155 regulates DNA repair activity and sensitivity to IR by repressing RAD51 in breast cancer. Testing for expression levels of miR-155 may be useful in the identification of breast cancer patients who will benefit from an IR-based therapeutic approach.
    Proceedings of the National Academy of Sciences 03/2014; · 9.81 Impact Factor

Publication Stats

50k Citations
4,584.94 Total Impact Points

Institutions

  • 2014
    • Ludwig Institute for Cancer Research
      La Jolla, California, United States
    • University of California, Los Angeles
      • Department of Medicine
      Los Angeles, California, United States
  • 2005–2014
    • The Ohio State University
      • • Department of Molecular Virology, Immunology and Medical Genetics
      • • Division of Hematology
      Columbus, Ohio, United States
    • Istituto Nazionale Tumori "Fondazione Pascale"
      Napoli, Campania, Italy
  • 2013
    • University of Southern California
      • Department of Molecular Microbiology and Immunology
      Los Angeles, CA, United States
    • Sapienza University of Rome
      • Department of Clinical and Molecular Medicine
      Roma, Latium, Italy
    • IOR Institute of Oncology Research
      Bellinzona, Ticino, Switzerland
    • University of Catania
      • Department of Clinical and Molecular Biomedicine (MEDBIO)
      Catania, Sicily, Italy
  • 2008–2013
    • Fondazione IRCCS Istituto Nazionale dei Tumori di Milano
      • Dipartimento di Oncologia Sperimentale e Medicina Molecolare
      Milano, Lombardy, Italy
  • 2006–2013
    • The Feinstein Institute for Medical Research
      • • Center for Oncology and Cell Biology
      • • Laboratory of Experimental Rheumatology
      New York City, New York, United States
  • 2002–2013
    • University of Naples Federico II
      • Department of Molecular Medicine and Health Biotechnology
      Portici, Campania, Italy
    • The University of Tokyo
      Tōkyō, Japan
  • 1995–2013
    • Universita degli studi di Ferrara
      • • Department of Morphology, Surgery and Experimental Medicine
      • • Sezione di Microbiologia
      Ferrara, Emilia-Romagna, Italy
  • 2012
    • SDN Istituto di Ricerca Diagnostica e Nucleare
      Napoli, Campania, Italy
    • Università degli Studi di Napoli L'Orientale
      Napoli, Campania, Italy
    • Università degli Studi G. d'Annunzio Chieti e Pescara
      Chieta, Abruzzo, Italy
  • 2006–2012
    • Universita' degli Studi "Magna Græcia" di Catanzaro
      • Department of Health Sciences
      Catanzaro, Calabria, Italy
  • 2000–2012
    • University of Massachusetts Medical School
      • Department of Cancer Biology
      Worcester, Massachusetts, United States
  • 2011
    • Catholic University of Louvain
      Walloon Region, Belgium
  • 2010–2011
    • University of Padova
      Padua, Veneto, Italy
    • IDIBELL Bellvitge Biomedical Research Institute
      • Programa de Epigenética y Biología del Cáncer - PEBC
      Barcelona, Catalonia, Spain
  • 1998–2011
    • Weizmann Institute of Science
      • Department of Molecular Cell Biology
      Israel
  • 1995–2011
    • Thomas Jefferson University
      • • Department of Pharmacology & Experimental Therapeutics
      • • Department of Urology
      • • Department of Pathology, Anatomy & Cell Biology
      • • Kimmel Cancer Center
      • • Division of Clinical Pharmacology
      Philadelphia, PA, United States
  • 2008–2010
    • University of Texas MD Anderson Cancer Center
      • Department of Experimental Therapeutics
      Houston, TX, United States
  • 2006–2010
    • Istituto Superiore di Sanità
      • Department of Haematology, Oncology and Molecular Medicine
      Roma, Latium, Italy
    • Università degli Studi di Genova
      • Dipartimento di Scienze della salute (DISSAL)
      Genova, Liguria, Italy
  • 2009
    • University of California, San Diego
      • Moores Cancer Center/Oncology
      San Diego, CA, United States
    • Comprehensive Cancer Centers of Nevada
      Las Vegas, Nevada, United States
  • 2007–2009
    • University of Bologna
      • Department of Experimental, Diagnostic and Specialty Medicine DIMES
      Bolonia, Emilia-Romagna, Italy
    • Istituto di Cura e Cura a Carattere Scientifico Basilicata
      Rionero in Vulture, Basilicate, Italy
    • CRO Centro di Riferimento Oncologico di Aviano
      • Division of Experimental Oncology 2
      Aviano, Friuli Venezia Giulia, Italy
  • 2006–2009
    • National Institutes of Health
      • Laboratory of Human Carcinogenesis
      Bethesda, MD, United States
  • 1981–2009
    • National Cancer Institute (USA)
      • • Laboratory of Human Carcinogenesis
      • • Laboratory of Cell Biology
      Maryland, United States
  • 2004–2007
    • Jichi Medical University
      • Center for Molecular Medicine
      Totigi, Tochigi, Japan
  • 1993–2002
    • Thomas Jefferson University Hospitals
      Philadelphia, Pennsylvania, United States
  • 2001
    • Second University of Naples
      • Faculty of Medicine and Surgery
      Napoli, Campania, Italy
  • 1999
    • The Philadelphia Center
      Philadelphia, Pennsylvania, United States
  • 1996
    • Wills Eye Institute
      Philadelphia, Pennsylvania, United States
    • University of Texas Health Science Center at San Antonio
      • Department of Biochemistry
      San Antonio, TX, United States
  • 1985–1989
    • Wistar Institute
      Philadelphia, Pennsylvania, United States