Luigi Tornillo

Universitätsspital Basel, Bâle, Basel-City, Switzerland

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Publications (138)638.11 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Tumor budding in colorectal cancer (CRC) is recognized as a valuable prognostic factor but its translation into daily histopathology practice has been delayed by lack of agreement on the optimal method of assessment. Within the context of the Swiss Association of Gastrointestinal Pathology (SAGIP), we performed a multicenter interobserver study on tumor budding, comparing hematoxylin and eosin (H&E) with pan-cytokeratin staining using a 10 high power field (10HPF) and hotspot (1HPF) method. Two serial sections of 50 TNM stage II-IV surgically treated CRC were stained for H&E and pan-cytokeratin. Tumor buds were scored by independent observers at six participating centers in Switzerland and Austria using the 10HPF and 1HPF method on a digital pathology platform. Pearson correlation (r) and intra-class correlation coefficients (ICC) comparing scores between centers were calculated. Three to four times more tumor buds were detected in pan-cytokeratin compared to H&E slides. Correlation coefficients for tumor budding counts between centers ranged from r = 0.46 to r = 0.91 for H&E and from r = 0.73 to r = 0.95 for pan-cytokeratin slides. Interobserver agreement across all centers was excellent for pan-cytokeratin [10HPF: ICC = 0.83 and 1HPF: ICC = 0.8]. In contrast, assessment of tumor budding on H&E slides reached only moderate agreement [10HPF: ICC = 0.58 and 1HPF: ICC = 0.49]. Based on previous literature and our findings, we recommend (1) pan-cytokeratin staining whenever possible, (2) 10HPF method for resection specimens, and (3) 1HPF method for limited material (preoperative biopsy or pT1). Since tumor budding counts can be used to determine probabilities of relevant outcomes and as such more optimally complement clinical decision making, we advocate the avoidance of cutoff scores.
    Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin 02/2015; DOI:10.1007/s00428-015-1740-9 · 2.56 Impact Factor
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    ABSTRACT: Aims. A trend towards local excision of early rectal cancers has prompted us to investigate if immunoprofiling might help in predicting lymph node involvement in this subgroup. Methods. A tissue microarray of 126 biopsies of early rectal cancer (T1 and T2) was stained for several immunomarkers of the innate and the adaptive immune response. Patients' survival and nodal status were analyzed and correlated with infiltration of the different immune cells. Results. Of all tested markers, only CD8 (P = 0.005) and TIA-1 (P = 0.05) were significantly more frequently detectable in early rectal cancer biopsies of node negative as compared to node positive patients. Although these two immunomarkers did not display prognostic effect "per se," CD8+ and, marginally, TIA-1 T cell infiltration could predict nodal involvement in univariate logistic regression analysis (OR 0.994; 95% CI 0.992-0.996; P = 0.009 and OR 0.988; 95% CI 0.984-0.994; P = 0.05, resp.). An algorithm significantly predicting the nodal status in early rectal cancer based on CD8 together with vascular invasion and tumor border configuration could be calculated (P < 0.00001). Conclusion. Our data indicate that in early rectal cancers absence of CD8+ T-cell infiltration helps in predicting patients' nodal involvement.
    Disease markers 12/2014; 2014:792183. DOI:10.1155/2014/792183 · 2.17 Impact Factor
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    ABSTRACT: Recent evidence suggests that natural killer (NK) cells are typically defective in infiltrating solid tumors, with the exception of gastrointestinal stromal tumors (GIST). Interestingly, however, infrequently infiltrating NK cells do not appear to have a direct effect on tumor progression. Here, prompted by the recent evidence that NK cell and T cell crosstalk may trigger, or enhance, tumor antigen-specific immune responses, we have tested the clinical significance of this reciprocal signaling. To this end, a tissue microarray constructed with 1410 colorectal carcinoma (CRC) patient specimens was stained with NK and T cell antigen-specific monoclonal antibodies, utilizing the immunoperoxidase staining technique. Cut-off scores for positive (>4 NK cells) and negative (�4 NK cells) NK cell CRC patient samples were determined using receiver operating characteristic curve analysis. Using this approach, NK cells were detected in 423 (30%) of the 1410 CRC specimens evaluated. The number of NK cells was >4 in only 132 (9%) of CRC samples. Correlation of the immunohistochemical staining results together with analysis of the clinical course of the disease revealed that the infiltration of colorectal tumors with both NK cells and CD8C T cells is associated with prolonged patient survival. In contrast, infiltration of tumors with NK cells in combination with CD3C and CD4C T lymphocytes had no detectable effect on the clinical course of the disease. These results suggest that NK cell and CD8C T cell crosstalk in the tumor microenvironment may benefit patient outcome and further, that the enumeration of infiltrating NK and CD8C T cells in CRC tumors may provide useful prognostic information.
    OncoImmunology 11/2014; 3(August):e952157. DOI:10.4161/21624011.2014.952197 · 6.28 Impact Factor
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    Luigi Tornillo
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    ABSTRACT: Gastrointestinal stromal tumors (GISTs) are the most frequent mesenchymal tumors of the gastrointestinal tract. The discovery that these tumors, formerly thought of smooth muscle origin, are indeed better characterized by specific activating mutation in genes coding for the receptor tyrosine kinases (RTKs) CKIT and PDGFRA and that these mutations are strongly predictive for the response to targeted therapy with RTK inhibitors has made GISTs the typical example of the integration of basic molecular knowledge in the daily clinical activity. The information on the mutational status of these tumors is essential to predict (and subsequently to plan) the therapy. As resistant cases are frequently wild type, other possible oncogenic events, defining other "entities," have been discovered (e.g., succinil dehydrogenase mutation/dysregulation, insuline growth factor expression, and mutations in the RAS-RAF-MAPK pathway). The classification of disease must nowadays rely on the integration of the clinico-morphological characteristics with the molecular data.
    11/2014; 1:43. DOI:10.3389/fmed.2014.00043
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    ABSTRACT: Background:Agents targeting programmed death-1 receptor (PD-1) and its ligand (PD-L1) are showing promising results in non-small-cell lung cancer (NSCLC). It is unknown whether PD-1/PD-L1 are differently expressed in oncogene-addicted NSCLC.Methods:We analysed a cohort of 125 NSCLC patients, including 56 EGFR mutated, 29 KRAS mutated, 10 ALK translocated and 30 EGFR/KRAS/ALK wild type. PD-L1 and PD-1 expression were assessed by immunohistochemistry. All cases with moderate or strong staining (2+/3+) in >5% of tumour cells were considered as positive.Results:PD-1 positive (+) was significantly associated with current smoking status (P=0.02) and with the presence of KRAS mutations (P=0.006), whereas PD-L1+ was significantly associated to adenocarcinoma histology (P=0.005) and with presence of EGFR mutations (P=0.001). In patients treated with EGFR tyrosine kinase inhibitors (N=95), sensitivity to gefitinib or erlotinib was higher in PD-L1+ vs PD-L1 negative in terms of the response rate (RR: P=0.01) time to progression (TTP: P<0.0001) and survival (OS: P=0.09), with no difference in PD1+ vs PD-1 negative. In the subset of 54 EGFR mutated patients, TTP was significantly longer in PD-L1+ than in PD-L1 negative (P=0.01).Conclusions:PD-1 and PD-L1 are differentially expressed in oncogene-addicted NSCLC supporting further investigation of specific checkpoint inhibitors in combination with targeted therapies.British Journal of Cancer advance online publication 28 October 2014; doi:10.1038/bjc.2014.555
    British Journal of Cancer 10/2014; 112(1). DOI:10.1038/bjc.2014.555 · 4.82 Impact Factor
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    ABSTRACT: Tumour budding (TBU) is recognized by the WHO classification as an additional prognostic factor in colorectal cancer (CRC). Lack of a standardized scoring system inhibits implementation of TBU in daily diagnostic practice. This multicentre study aims to determine the inter-observer reproducibility of a simple 10HPF method using H&E and immunohistochemistry for assessment of TBU. Patients and Methods: Representative sections from 50 CRC patients were stained for H&E and pan-cytokeratin, and then uploaded to a digital pathology platform. Expert gastrointestinal pathologists from five independent academic/non-academic centres scored TBU in 10HPFs. Inter-observer reproducibility was assessed using the intra-class correlation coefficient (ICC). Results: Three times more buds were identified with pan-cytokeratin in comparison to H&E (total number of buds across 10HPFs: 93.0 vs. 30.3; p<0.0001). ICC between centres ranged from 0.46-0.91 for H&E and 0.73-0.95 for pan-cytokeratin. Across all 5 centres ICC values were 0.61 for H&E and 0.844 for pan-cytokeratin indicating excellent agreement with the latter. Similar results for agreement were obtained for node-negative (ICC: 0.78) and node-positive (ICC: 0.85) patients. Interpretation: The 10HPF method is a simple and reproducible scoring system for TBU and therefore a solid proposal for use in daily diagnostic practice.
    26th European Congress of Pathology, London, United Kingdom; 09/2014
  • 06/2014; 3(2):91-102. DOI:10.3390/microarrays3020091
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    ABSTRACT: Colorectal cancer (CRC) infiltration by CD16+ myeloid cells correlates with improved prognosis. We addressed mechanistic clues, and gene and protein expression of cytokines potentially associated with macrophage polarization. GM-CSF or M-CSF stimulated peripheral blood CD14+ cells from healthy donors were co-cultured with CRC cells. Tumor cell proliferation was assessed by 3H-Thymidine incorporation. Expression of cytokine (CK) genes in CRC and autologous healthy mucosa (HM) was tested by quantitative, real-time PCR. A tumor microarray (TMA) including >1200 CRC specimens was stained with GM-CSF and M-CSF specific antibodies. Clinic-pathological features and overall survival were analyzed. GM-CSF induced CD16 expression in 66±8% of monocytes, as compared to 28±1% in cells stimulated by M-CSF (P=0.011). GM-CSF but not M-CSF stimulated macrophages significantly (P<0.02) inhibited CRC cell proliferation. GM-CSF gene was expressed to significantly (n=45, P<0.0001) higher extents in CRC than in HM whereas M-CSF gene expression was similar in HM and CRC. Accordingly, IL-1β and IL-23 genes, typically expressed by M1 macrophages, were expressed to significantly (P<0.001) higher extents in CRC than in HM. TMA staining revealed that GM-CSF production by tumor cells is associated with lower T stage (p=0.02), "pushing" growth pattern (P=0.004) and significantly (P=0.0002) longer survival in mismatch-repair proficient (MMRp) CRC. Favorable prognostic effect of GM-CSF production by CRC cells was confirmed by multivariate analysis and was independent from CD16+ and CD8+ cell CRC infiltration. M-CSF expression had no significant prognostic relevance. GM-CSF production by tumor cells is an independent favorable prognostic factor in CRC.
    Clinical Cancer Research 04/2014; 20(12). DOI:10.1158/1078-0432.CCR-13-2774 · 8.19 Impact Factor
  • Journal of Hepatology 04/2014; 60(1):S98-S99. DOI:10.1016/S0168-8278(14)60260-9 · 10.40 Impact Factor
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    ABSTRACT: Death rates from hepatocellular carcinoma (HCC) are steadily increasing yet therapeutic options for advanced HCC are limited. We identify a subset of mouse and human HCCs harboring VEGFA genomic amplification, displaying distinct biological characteristics. Unlike common tumor amplifications, this one appears to work via heterotypic paracrine interactions: stromal VEGF receptors (VEGFRs), responding to tumor VEGF-A, produce hepatoycte growth factor (HGF) that reciprocally affects tumor cells. VEGF-A inhibition results in HGF downregulation and reduced proliferation, specifically in amplicon-positive mouse HCCs. Sorafenib - the first-line drug in advanced HCC - targets multiple kinases including VEGFRs, but has only an overall mild beneficial effect. We found that VEGFA amplification specifies mouse and human HCCs that are distinctly sensitive to sorafenib. FISH analysis of a retrospective patient cohort showed markedly improved survival of sorafenib-treated patients withVEGFA amplified HCCs, suggesting that VEGFA amplification is a potential biomarker for HCC response to VEGF-A blocking drugs.
    Cancer Discovery 03/2014; 4(6). DOI:10.1158/2159-8290.CD-13-0782 · 15.93 Impact Factor
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    ABSTRACT: Hepatocellular carcinoma (HCC) is among the leading causes of cancer-related death. Despite the advances in diagnosis and management of HCC, the biology of this tumor remains poorly understood. Recent evidence highlighted long non-coding RNAs (lncRNAs) as crucial determinants of HCC development. In this study, we report the lncRNA HOTTIP as significantly up-regulated in HCC specimens. HOTTIP gene is located in physical contiguity with HOXA13 and directly controls the HOXA locus gene expression via interaction with the WDR5 / MLL complex. HOX genes encode transcription factors regulating embryonic development and cell fate. We previously described HOX genes deregulation to be involved in hepatocarcinogenesis. Indeed, we observed the marked up-regulation of HOXA13 in HCC. Here, by correlating clinico-pathological and expression data, we demonstrate that the levels of HOTTIP and HOXA13 are associated with HCC patients' clinical progression and predict disease outcome. In contrast to the majority of similar studies, our data are obtained from snap-frozen needle HCC biopsies (n=52) matched with their non-neoplastic counterparts collected from patients that had not yet received any HCC-tailored therapeutic treatments at the time of biopsy. In addition, taking advantage of gain and loss of function experiments in liver cancer-derived cell lines (HuH-6 and HuH-7), we uncover a novel bidirectional regulatory loop between HOTTIP / HOXA13. Conclusion: our study highlights the key role of HOTTIP and HOXA13 in HCC development by associating their expression to metastasis and survival in HCC patients, provides novel insights on the function of lncRNA-driven hepatocarcinogenesis and paves the way for further investigation about the possible role of HOTTIP as predictive biomarker of HCC. (Hepatology 2013;).
    Hepatology 03/2014; 59(3). DOI:10.1002/hep.26740 · 11.19 Impact Factor
  • Molecular Cancer Therapeutics 01/2014; 12(11_Supplement):C25-C25. DOI:10.1158/1535-7163.TARG-13-C25 · 6.11 Impact Factor
  • Journal of Clinical Oncology 01/2014; 32(5). DOI:10.1200/JCO.2012.45.3092 · 17.88 Impact Factor
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    ABSTRACT: The goal of this study was to determine the frequency of HLA class II antigen expression in colorectal carcinoma (CRC) tumors, its association with the clinical course of the disease, and the underlying mechanism(s). Two tissue microarrays constructed with 220 and 778 CRC tumors were stained with HLA-DR, DQ, and DP antigen-specific monoclonal antibody LGII-612.14, using the immunoperoxidase staining technique. The immunohistochemical staining results were correlated with the clinical course of the disease. The functional role of HLA class II antigens expressed on CRC cells was analyzed by investigating their in vitro interactions with immune cells. HLA class II antigens were expressed in about 25% of the 220 and 21% of the 778 tumors analyzed with an overall frequency of 23%. HLA class II antigens were detected in 19% of colorectal adenomas. Importantly, the percentage of stained cells and the staining intensity were significantly lower than those detected in CRC tumors. However, HLA class II antigen staining was weakly detected only in 5.4% of 37 normal mucosa tissues. HLA class II antigen expression was associated with a favorable clinical course of the disease. In vitro stimulation with interferon gamma (IFNγ) induced HLA class II antigen expression on two of the four CRC cell lines tested. HLA class II antigen expression on CRC cells triggered interleukin-1β (IL-1β) production by resting monocytes. HLA class II antigen expression in CRC tumors is a favorable prognostic marker. This association may reflect stimulation of IL-1β production by monocytes.
    Neoplasia (New York, N.Y.) 01/2014; 16(1):31-42. · 5.40 Impact Factor
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    ABSTRACT: Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. The lack of effective therapeutic options for advanced stage HCCs combined with an increasing incidence rate calls for the identification of early stage HCC molecular markers. SH2 Domain Containing 4A (SH2D4A) gene maps to human chromosome 8p21.3 and encodes for SH(2)A. The chromosomal region containing SH2D4A is frequently lost in colorectal, lung and HCC cancers. Our study aimed to investigate SH2D4A involvement in HCC pathogenesis combining mRNA expression, protein and clinical data. Transcriptome analysis performed on 37 HCC needle biopsies (matched with their corresponding non-neoplastic parenchyma) and five normal liver donor samples revealed that SH2D4A is downregulated in HCC. Results were confirmed by quantitative real-time-polymerase chain reaction (qRT-PCR), 25 out of 37 (67.6%) fresh frozen samples showed SH2D4A downregulation (p=0.026). Furthermore, combining qRT-PCR and immunohistochemistry data we demonstrated a direct correlation between SH2D4A mRNA and SH(2)A protein levels. The analysis of a tissue microarray (TMA) containing 336 specimens confirmed that SH(2)A is frequently reduced in HCC (56.8%) as well as in cirrhotic nodules (50.5%) compared to normal liver samples (31.1%). To conclude, our study revealed that SH2D4A is frequently downregulated in HCC samples thus corroborating its putative role as a tumour suppressor gene. In addition, we provide new evidence for SH2D4A involvement in HCC pathogenesis demonstrating for the first time its deregulation in cirrhotic nodules.
    European journal of cancer (Oxford, England: 1990) 12/2013; 50(4). DOI:10.1016/j.ejca.2013.11.018 · 4.82 Impact Factor
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    ABSTRACT: Angiogenesis plays a pivotal role in neoplastic growth and metastasis formation. Vascular endothelial growth factor A (VEGFA) is a major player in physiological and tumour-induced angiogenesis and numerous human tumours have been show to overexpress VEGFA. Moreover increased VEGFA gene expression has been found frequently to correlate with tumour progression, recurrences and survival. Interestingly, several studies have demonstrated that gene amplification may result in protein overexpression and that amplification of the therapeutics' target gene can serve as an excellent predictive marker (i.e. HER2 and trastuzumab). However the impact of VEGFA gene amplification has been only recently assessed for some cancer types such as osteosarcoma, colorectal, breast and liver cancer. This study aimed to assess VEGFA gene amplification status using fluorescent in situ hybridization (FISH) in a large cohort of different tumour entities. Thus, we investigated the incidence of VEGFA amplification using a multi-tumour tissue microarray (TMA) containing 2,837 evaluable specimens from 80 different tumour entities and 31 normal tissue types. Moreover, we validated FISH analysis as reference method to evaluate VEGFA gene status by comparing it to comparative genomic hybridization (CGH). We observed that VEGFA locus amplification and/or polysomy represented a small but regularly detected population in several tumour entities while was not present in normal tissues. VEGFA gene alterations were predominantly observed in hepatocarcinomas, adenocarcinomas of the pancreas and intestine, large cell carcinoma of the lung and in endometrium serous carcinoma. Furthermore our data demonstrated that VEGFA detection by FISH provided highly comparable results to those generated by CGH. Albeit with low percentage, VEGFA amplification is commonly observed across several tumour entities. Furthermore, our results demonstrated that FISH test could be used as a reliable diagnostic tool to evaluate VEGFA gene status in human specimens.
    Angiogenesis 10/2013; DOI:10.1007/s10456-013-9396-z · 4.41 Impact Factor
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    ABSTRACT: The prognostic relevance of innate immune cells infiltrating colorectal carcinoma lesions is highly debated. By evaluating the expression of myeloperoxidase (MPO) as a marker of neutrophil granulocytes in a large cohort of colorectal carcinoma specimens, we have observed that robust tumor-infiltration by MPO(+) cells correlates with improved patient survival independently of other histopathological parameters, including disease stage.
    OncoImmunology 10/2013; 2(10):e25990. DOI:10.4161/onci.25990 · 6.28 Impact Factor
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    ABSTRACT: Nodular regenerative hyperplasia (NRH) is a rare liver disease characterized by small regenerative nodules without fibrosis and can cause portal hypertension. Aetiology and pathogenesis of NRH remain unclear. We have recently shown that Notch1 knockout induces NRH with portal hypertension through vascular remodelling in mice. The aim of this study was to analyse histological and clinical data of NRH patients and to explore if the endothelial pathways identified in our NRH mouse model are also regulated in human NRH. Patients were identified retrospectively from the pathology database. Clinical and laboratory patient data were retrieved. mRNA expression was measured in liver biopsies from a subset of NRH patients. Diagnosis of NRH was confirmed in needle biopsies of 51 patients, including 31 patients with grade 1, 12 patients with grade 2 and 8 patients with grade 3 NRH. Grade 3 nodularity significantly correlated with the presence of portal hypertension: 50% of the patients with grade 3 NRH vs. 6.5% with grade 1 (P = 0.0105). mRNA expression analysis in liver biopsies from 14 NRH patients and in primary human sinusoidal endothelial cells revealed downregulation of identical genes as in the murine NRH model, which are implicated in vascular differentiation: Notch1, delta-like 4 (Dll4) and ephrinB2. In this large NRH needle biopsy cohort, we demonstrated that advanced nodularity correlates with presence of portal hypertension. Downregulation of the endothelial signalling pathways Dll4/Notch1 and ephrinB2/EphB4 supports the hypothesis that human NRH is caused by a sinusoidal injury providing first insights into the molecular pathogenesis of this liver condition.
    Liver international: official journal of the International Association for the Study of the Liver 06/2013; 34(4). DOI:10.1111/liv.12261 · 4.41 Impact Factor
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    ABSTRACT: Colorectal cancer (CRC) infiltration by adaptive immune system cells correlates with favorable prognosis. The role of the innate immune system is still debated. Here we addressed the prognostic impact of CRC infiltration by neutrophil granulocytes (NG). A TMA including healthy mucosa and clinically annotated CRC specimens (n = 1491) was stained with MPO and CD15 specific antibodies. MPO+ and CD15+ positive immune cells were counted by three independent observers. Phenotypic profiles of CRC infiltrating MPO+ and CD15+ cells were validated by flow cytometry on cell suspensions derived from enzymatically digested surgical specimens. Survival analysis was performed by splitting randomized data in training and validation subsets. MPO+ and CD15+ cell infiltration were significantly correlated (p<0.0001; r = 0.76). However, only high density of MPO+ cell infiltration was associated with significantly improved survival in training (P = 0.038) and validation (P = 0.002) sets. In multivariate analysis including T and N stage, vascular invasion, tumor border configuration and microsatellite instability status, MPO+ cell infiltration proved an independent prognostic marker overall (P = 0.004; HR = 0.65; CI:±0.15) and in both training (P = 0.048) and validation (P = 0.036) sets. Flow-cytometry analysis of CRC cell suspensions derived from clinical specimens showed that while MPO+ cells were largely CD15+/CD66b+, sizeable percentages of CD15+ and CD66b+ cells were MPO-. High density MPO+ cell infiltration is a novel independent favorable prognostic factor in CRC.
    PLoS ONE 05/2013; 8(5):e64814. DOI:10.1371/journal.pone.0064814 · 3.53 Impact Factor
  • Journal of Hepatology 04/2013; 58:S39-S40. DOI:10.1016/S0168-8278(13)60092-6 · 10.40 Impact Factor

Publication Stats

3k Citations
638.11 Total Impact Points


  • 2004–2014
    • Universitätsspital Basel
      • Institut für Pathologie
      Bâle, Basel-City, Switzerland
  • 1999–2014
    • Universität Basel
      • Institute of Geology and Paleontology
      Bâle, Basel-City, Switzerland
    • Cardarelli Hospital
      Napoli, Campania, Italy
  • 2012
    • University of Strasbourg
      Strasburg, Alsace, France
  • 2010
    • Attikon University Hospital
      Athínai, Attica, Greece
  • 2008
    • Klinikum Nürnberg
      Nuremberg, Bavaria, Germany
  • 2007
    • King Faisal Specialist Hospital and Research Centre
      • Department of Surgery
      Ar Riyāḑ, Ar Riyāḑ, Saudi Arabia
    • McGill University
      • Department of Pathology
      Montréal, Quebec, Canada
  • 2006
    • University of Zurich
      • Internal Medicine Unit
      Zürich, ZH, Switzerland
  • 2005
    • University of Turku
      Turku, Varsinais-Suomi, Finland
    • Otto-von-Guericke-Universität Magdeburg
      Magdeburg, Saxony-Anhalt, Germany
  • 1999–2003
    • University of Naples Federico II
      • Section of Psychology
      Napoli, Campania, Italy