Alberto Amadori

University of Padova, Padua, Veneto, Italy

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Publications (143)857.69 Total impact

  • Haematologica 07/2015; DOI:10.3324/haematol.2015.126854 · 5.81 Impact Factor
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    ABSTRACT: The occurrence of a second primary esophageal carcinoma (EC) in long-term cancer survivors may represent a late effect of previous radio-chemotherapeutic treatment. To identify the genetic factors that could increase this risk, we analyzed nine variants within ERCC1, XPD, XRCC1 and XRCC3 DNA repair pathway genes, and GSTP1, TP53 and MDM2 genes in 61 patients who received radio-chemotherapy for a prior lymphoma or breast cancer; 29 of them had a second primary EC. This cohort consists of 22 esophageal squamous cell carcinoma (ESCC) and 7 esophageal adenocarcinoma (EADC) patients. A validation cohort of 154 patients with sporadic EC was also included. The XPD Asp312Asn (rs1799793) was found to be associated with the risk of developing second primary ESCC (P=0.015). The resultant variant was also involved in the onset of sporadic ESCC (P=0.0018). To know in advance who among long-term cancer survivors have an increased risk of EC could lead to a more appropriate follow-up strategy.The Pharmacogenomics Journal advance online publication, 9 June 2015; doi:10.1038/tpj.2015.41.
    The Pharmacogenomics Journal 06/2015; DOI:10.1038/tpj.2015.41 · 4.23 Impact Factor
  • Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 05/2015; DOI:10.1038/leu.2015.117 · 10.43 Impact Factor
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    ABSTRACT: Development of novel therapeutic drugs and regimens for cancer treatment has led to improvements in patient long-term survival. This success has, however, been accompanied by the increased occurrence of second primary cancers. Indeed, patients who received regional radiotherapy for Hodgkin's Lymphoma (HL) or breast cancer may develop, many years later, a solid metachronous tumor in the irradiated field. Despite extensive epidemiological studies, little information is available on the genetic changes involved in the pathogenesis of these solid therapy-related neoplasms. Using microsatellite markers located in 7 chromosomal regions frequently deleted in sporadic esophageal cancer, we investigated loss of heterozygosity (LOH) and microsatellite instability (MSI) in 46 paired (normal and tumor) samples. Twenty samples were of esophageal carcinoma developed in HL or breast cancer long-term survivors: 14 squamous cell carcinomas (ESCC) and 6 adenocarcinomas (EADC), while 26 samples, used as control, were of sporadic esophageal cancer (15 ESCC and 11 EADC). We found that, though the overall LOH frequency at the studied chromosomal regions was similar among metachronous and sporadic tumors, the latter exhibited a statistically different higher LOH frequency at 17q21.31 (p = 0.018). By stratifying for tumor histotype we observed that LOH at 3p24.1, 5q11.2 and 9p21.3 were more frequent in ESCC than in EADC suggesting a different role of the genetic determinants located nearby these regions in the development of the two esophageal cancer histotypes. Altogether, our results strengthen the genetic diversity among ESCC and EADC whether they occurred spontaneously or after therapeutic treatments. The presence of histotype-specific alterations in esophageal carcinoma arisen in HL or breast cancer long-term survivors suggests that their transformation process, though the putative different etiological origin, may retrace sporadic ESCC and EADC carcinogenesis.
    PLoS ONE 01/2015; 10(1):e0117070. DOI:10.1371/journal.pone.0117070 · 3.23 Impact Factor
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    ABSTRACT: Anti-VEGF therapy perturbs tumor metabolism, severely impairing oxygen, glucose and ATP levels. In this study, we investigated the effects of anti-VEGF therapy in multiple experimental tumor models that differ in their glycolytic phenotypes, to gain insights into optimal modulation of the metabolic features of this therapy. Prolonged treatments induced vascular regression and necrosis in tumor xenograft models, with highly glycolytic tumors becoming treatment resistant more rapidly than poorly glycolytic tumors. By PET imaging, prolonged treatments yielded an increase in both hypoxic and proliferative regions of tumors. A selection for highly glycolytic cells was noted and this metabolic shift was stable and associated with increased tumor aggressiveness and resistance to VEGF blockade in serially transplanted mice. Our results support the hypothesis that the highly glycolytic phenotype of tumor cells studied in xenograft models - either primary or secondary - is a cell-autonomous trait conferring resistance to VEGF blockade. The finding that metabolic traits of tumors can be selected by antiangiogenic therapy suggests insights into the evolutionary dynamics of tumor metabolism.
    Cancer Research 11/2014; 75(1). DOI:10.1158/0008-5472.CAN-13-2037 · 9.33 Impact Factor
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    ABSTRACT: Activation of the NOTCH pathway occurs commonly in T acute lymphoblastic leukemia (T-ALL) mainly due to mutations in NOTCH1 or alterations in FBW7 and is involved in the regulation of cell proliferation and survival. Since mutations hit different domains of the receptor, they are predicted to heterogeneously perturb ligand-induced NOTCH1 activity. Moreover, T-ALL cells also co-express NOTCH3 receptors which could be triggered by different ligands. In this study, we aimed to investigate the role of DLL4 in the regulation of NOTCH signaling in T-ALL cells in the context of different types of NOTCH1 mutation or wild-type NOTCH receptor, as well as the effects of DLL4 neutralization on T-ALL engraftment in mice. We found that NOTCH signaling can be stimulated in T-ALL cells in vitro by either human or murine DLL4 with heterogeneous effects, according to NOTCH1/FBW7 mutation status, and that these effects can be blocked by antibodies neutralizing DLL4, NOTCH1 or NOTCH2/3. In vivo, DLL4 is expressed in the spleen and the bone marrow (BM) of NOD/SCID mice bearing T-ALL xenografts as well as the BM of T-ALL patients. Importantly, DLL4 blockade impaired growth of T-ALL cells in NOD/SCID mice and increased leukemia cell apoptosis. These results show that DLL4 is an important component of the tumor microenvironment which contributes to the early steps of T-ALL cell growth.
    Carcinogenesis 10/2014; 36(1). DOI:10.1093/carcin/bgu223 · 5.33 Impact Factor
  • Journal of Clinical Investigation 06/2014; 124(6):2807-2807. DOI:10.1172/JCI76855 · 13.22 Impact Factor
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    ABSTRACT: We investigated the metabolic profile of cancer stem cells (CSC) isolated from patients with epithelial ovarian cancer. CSC overexpressed genes associated with glucose uptake, oxidative phosphorylation (OXPHOS), and fatty acid β-oxidation, indicating higher ability to direct pyruvate towards the Krebs cycle. Consistent with a metabolic profile dominated by OXPHOS, the CSC showed higher mitochondrial reactive oxygen species (ROS) production and elevated membrane potential, and underwent apoptosis upon inhibition of the mitochondrial respiratory chain. The CSC also had a high rate of pentose phosphate pathway (PPP) activity, which is not typical of cells privileging OXPHOS over glycolysis, and may rather reflect the PPP role in recharging scavenging enzymes. Furthermore, CSC resisted in vitro and in vivo glucose deprivation, while maintaining their CSC phenotype and OXPHOS profile. These observations may explain the CSC resistance to anti-angiogenic therapies, and indicate this peculiar metabolic profile as a possible target of novel treatment strategies.
    Oncotarget 05/2014; DOI:10.18632/oncotarget.2010 · 6.36 Impact Factor
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    ABSTRACT: Notch signaling deregulation is linked to the onset of several tumors including T cell acute lymphoblastic leukemia (T-ALL). Deregulated microRNA (miRNA) expression is also associated to several cancers, including leukemias. However, the transcriptional regulators of miRNAs as well as the relationships between Notch signaling and miRNA deregulation are poorly understood. In order to identify miRNAs regulated by Notch pathway, we performed microarray-based miRNA profiling of several Notch-expressing T-ALL models. Among 7 miRNAs, consistently regulated by overexpressing or silencing Notch3, we focused our attention on miR-223, whose putative promoter analysis revealed a conserved RBPjk binding site, which was nested to a NF-kB consensus. Luciferase and ChIP-assays on the promoter region of miR-223 show that both Notch and NF-kB are novel co-regulatory signals of miR-223 expression, being able to cooperatively activate the transcriptional activity of miR-223 promoter. Notably, the Notch-mediated activation of miR-223 represses the tumor suppressor FBXW7 in T-ALL cell lines. Moreover, we observed the inverse correlation of miR-223 and FBXW7 expression in a panel of T-ALL patient-derived xenografts. Finally, we show that miR-223 inhibition prevents T-ALL resistance to GSI-treatment, suggesting that miR-223 could be involved in GSI-sensitivity and its inhibition may be exploited in target therapy protocols.Leukemia accepted article peview online, 14 April 2014. doi:10.1038/leu.2014.133.
    Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 04/2014; 28(12). DOI:10.1038/leu.2014.133 · 10.43 Impact Factor
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    ABSTRACT: Musashi-1 (Msi-1) is a well-established stem cell marker in both normal and malignant colon cells and it acts by positively regulating the Notch pathway through inactivation of Numb, a Notch signalling repressor. To date, the mechanisms of regulation of Msi-1 levels remain largely unknown. Here we investigated the regulation of Msi-1 by Notch signalling in the colorectal cancer cell lines MICOL-14tum and LoVo and in primary cultures of colorectal cancer (CRC) metastases. Stimulation by the Notch ligand DLL4 was associated with an increase of Msi-1 mRNA and protein levels, and this phenomenon was prevented by the addition of antibody neutralizing Notch2/3 but not Notch1. Moreover, forced expression of activated Notch3 increased Msi-1 levels, whereas silencing of Notch3 by shRNA reduced Msi-1 levels in both CRC cells and tumor xenografts. Consistent with these findings, forced Notch3 expression or stimulation by DLL4 increased levels of activated Notch1 in MICOL-14tum and LoVo cells. Finally, treatment of CRC cells with anti-Notch2/3 antibody increased Numb protein while significantly reducing formation of spheroids in both MICOL-14tum cells and primary tumor cultures. This novel feed-forward circuit involving DLL4, Notch3, Msi-1, Numb and Notch1 may be relevant for regulation of Notch signalling in physiological processes as well as in tumor development. With regard to therapeutic implications, Notch3-specific drugs could represent a valuable strategy to limit Notch signaling in the context of colorectal cancers overexpressing this receptor.
    Cancer Research 02/2014; 74(7). DOI:10.1158/0008-5472.CAN-13-2022 · 9.33 Impact Factor
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    ABSTRACT: We investigated whether Circulating Tumor Cells (CTCs) isolated from epithelial tumors could survive and grow in xenotransplants. To this purpose, EpCAM-positive CTCs were enriched by CellSearch platform the only FDA-cleared automated platform that quantifies tumor burden in peripheral blood and provides clinical evidence of predictive and prognostic value. The CTCs were isolated from metastatic prostate (n=6) and breast (n=2) cancer patients. The xenograft assay was developed in 8-week-old NOD/SCID mice that were subcutaneously injected with increasing amounts of CTCs (ranging from 50 to 3000). Human CTCs were found in 8 out of 8 murine peripheral blood (muPB) and in 6 out of 8 murine bone marrow (muBM) samples, after a median follow-up of 10.3 months. Six out of 8 spleens were positive for human cytokeratin. Our assay showed higher successful rate than those previously reported in breast cancer and hepatocellular carcinoma. The role of EpCAM during carcinogenesis is controversial. The identification of human CTCs in muPB, muBM and spleen demonstrates that the EpCAM-positive fraction of CTCs retains the migratory capacity. This is the first experimental evidence that as few as 50 EpCAM-positive prostate cancer CTCs putatively contain metastasis-initiating-cells (MIC).
    01/2014; 1(1). DOI:10.18632/oncoscience.8
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    ABSTRACT: Temozolomide (TMZ) administered daily with radiation therapy (RT) for 6 weeks, followed by adjuvant TMZ for 6 cycles, is the standard therapy for newly diagnosed glioblastoma (GBM) patients. Although TMZ is considered to be a safe drug, it has been demonstrated to cause severe myelotoxicity; in particular, some case reports and small series studies have reported severe myelotoxicity developing during TMZ and concomitant RT. We performed a prospective study to analyze the incidence of early severe myelotoxicity and its possible clinical and genetic factors. From November 2010 to July 2012, newly diagnosed GBM patients were enrolled. They were eligible for the study if they met the following criteria: pathologically proven GBM, age 18 years and older, an Eastern Cooperative Oncology Group performance status of 0 to 2, adequate renal and hepatic function, and adequate blood cell counts before starting TMZ plus RT. Grading of hematologic toxicity developing during radiation and TMZ was based on the National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0. Clinical factors from all patients were recorded. The methylation status and polymorphic variants of O-methylguanine-DNAmethyl-transferase gene in peripheral blood mononuclear cells, and polymorphic genetic variants of genes involved in the pharmacokinetics and pharmacodynamics of TMZ, were analyzed. For genetic analyses, patients with toxicity were matched (1:2) for age, performance status, anticonvulsants, and proton pump inhibitors with patients without myelotoxicity. We enrolled 87 consecutive GBM patients: 32 women and 55 men; the average age was 60 years. During TMZ and RT, 4 patients (5%) showed grade 3-4 myelotoxicity, and its median duration was 255 days. Predictor factors of severe myelotoxicity were female sex, pretreatment platelet count of ≤3,00,000/mm, methylated O-methylguanine-DNA methyltransferase promoter in the hematopoietic cell system, and specific polymorphic variants of the cytochrome P450 oxidoreductase and methionine adenosyltransferase 1A genes. Although we studied a small population, we suggest that both clinical and genetic factors might simultaneously be associated with severe myelosuppression developed during TMZ plus RT. However, our results deserve validation in larger prospective studies and, if the factors associated with severe myelotoxicity are validated, dose adjustments of TMZ for those patients may reduce the risk of severe myelotoxicity during the concomitant treatment.
    American journal of clinical oncology 09/2013; 38(5). DOI:10.1097/COC.0b013e3182a790ea · 3.06 Impact Factor
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    ABSTRACT: At present, no consensus exists on the beneficial effect of preoperative cisplatin/5-fluorouracil (5-FU)-based chemotherapy versus primary surgery in the management of patients with esophageal cancer. The aim of this study was to evaluate the impact of some relevant genetic polymorphisms, within drug-related and DNA repair genes, on the clinical outcome of esophageal cancer patients subjected to cisplatin/5-FU-based neoadjuvant treatment. DNA from 143 esophageal cancer patients, 63 receiving neoadjuvant therapy and 80 receiving primary surgery, was analyzed for the following polymorphisms: the GSTM1 null, GSTT1 null, and GSTP1 Ile105Val (rs16953) in glutathione S-transferase (GST) family, 2 in thymidylate synthase (TS) gene, and the ERCC1 Asn118Asn (rs11615), ERCC1 C8092A (rs3212986), XPD/ERCC2 Asp312Asn (rs1799793), and XPD/ERCC2 Lys751Gln (rs13181) of the nucleotide excision repair pathway. We found that the ERCC1 rs3212986, although not associated with therapeutic response, is an independent predictive marker of better outcome in a cisplatin/5-FU-based neoadjuvant setting (hazard ratio: 0.38, 95% confidence interval: 0.2-0.73, P=0.008). In contrast, no association with clinical outcome was observed for this polymorphism in the primary surgery group. Our study indicates the ERCC1 rs3212986 as a predictive marker in the cisplatin/5-FU-based neoadjuvant setting, and also suggests its use as a marker to select the appropriate therapeutic approach in esophageal cancer patients.
    Pharmacogenetics and Genomics 08/2013; 23(11). DOI:10.1097/FPC.0b013e3283653afc · 3.48 Impact Factor
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    ABSTRACT: T acute lymphoblastic leukemia (T-ALL) is characterized by several genetic alterations and poor prognosis in about 20-25% of patients. Notably, about 60% of T-ALL shows increased Notch1 activity, due to activating NOTCH1 mutations, or alterations in the FBW7 gene, which confer to the cell a strong growth advantage. Therapeutic targeting of Notch signaling could be clinically relevant, especially for chemotherapy refractory patients. This study investigated the therapeutic efficacy of a novel anti-Notch1 monoclonal antibody by taking advantage of a collection of pediatric T-ALL engrafted systemically in NOD/SCID mice and genetically characterized with respect to NOTCH1/FBW7 mutations. Anti-Notch1 treatment greatly delayed engraftment of T-ALL cells bearing Notch1 mutations, including samples derived from poor responders or relapsed patients. Notably, the therapeutic efficacy of anti-Notch1 therapy was significantly enhanced in combination with dexamethasone. Anti-Notch1 treatment increased T-ALL cell apoptosis, decreased proliferation and caused strong inhibitory effects on Notch target genes expression along with complex modulations of gene expression profiles involving cell metabolism. Serial transplantation experiments suggested that anti-Notch1 therapy could compromise leukemia initiating cell functions. These results show therapeutic efficacy of Notch1 blockade for T-ALL, highlight the potential of combination with dexamethasone and identify surrogate biomarkers of the therapeutic response.Leukemia accepted article preview online, 18 June 2013; doi:10.1038/leu.2013.183.
    Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 06/2013; 28(2). DOI:10.1038/leu.2013.183 · 10.43 Impact Factor
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    Enrica Rumiato · Elisa Boldrin · Alberto Amadori · Daniela Saggioro
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    ABSTRACT: Purpose: 5-fluorouracil (5-FU) has been widely used since the 1980s, and it remains the backbone of many chemotherapeutic combination regimens. However, its use is often limited by the occurrence of severe toxicity. Although several reports have shown the detrimental effect of some dihydropyrimidine dehydrogenase (DPYD) and thymidylate synthase (TYMS) gene polymorphisms in patients undergoing 5-FU-based treatment, they account for only a minority of toxicities. Methods: Looking for new candidate genetic variants associated with 5-FU-induced toxicity, we used the innovative genotyping microarray Affymetrix Drug-Metabolizing Enzymes and Transporters (DMET)™ Plus GeneChip that interrogates 1,936 genetic variants distributed in 231 genes involved in drug metabolism, excretion, and transport. To reduce variability, we analyzed samples from colorectal cancer patients who underwent fairly homogenous treatments (i.e., Machover or Folfox) and experienced G3 or G4 toxicity; control patients were matched for therapy and selected from those who did not disclose toxicity (G0-G1). Results: Pharmacogenetic genotyping showed no significant difference in DPYD and TYMS genetic variants distribution between cases and controls. However, other polymorphisms could account for 5-FU-induced toxicity, with the CHST1 rs9787901 and GSTM3 rs1799735 having the strongest association. Conclusions: Although exploratory, this study suggests that genetic polymorphisms not directly related to 5-FU pharmacokinetics and pharmacodynamics are involved in 5-FU-induced toxicity. Our data also indicates DMET™ microarray as a valid approach to discover new genetic determinants influencing chemotherapy-induced toxicity.
    Cancer Chemotherapy and Pharmacology 06/2013; 72(2). DOI:10.1007/s00280-013-2210-1 · 2.77 Impact Factor
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    ABSTRACT: We report the case of a 68-year-old woman who underwent heart transplantation for hypertrophic cardiomyopathy. Two months after the transplant she developed mild fever and dyspnea with a marked drop in left ventricle ejection fraction of 31%. Coronary angiography was negative for cardiac allograft vasculopathy. Endomyocardial biopsy revealed ischemic damage with no evidence of acute cellular rejection, antibody-mediated rejection or viral myocarditis. A neoplastic process was suspected even though full-body computerized tomography was negative for malignancy. The patient died 4 months after transplantation. The autopsy showed acute antero-septal myocardial infarction due to a nodular epicardial EBV-related posttransplant lymphoproliferative disorder (PTLD) infiltrating the left anterior descending coronary artery with occlusive neoplastic thrombosis. We highlight two major aspects of this case: (1) the unusual occurrence of early PTLD involving the cardiac allograft and causing a fatal outcome, (2) the application of an immunological technique for HLA-DRB1 typing to posttransplant paraffin-embedded autopsy material to identify the recipient origin of this early malignancy, thus excluding a possible donor-transmitted neoplasm.
    American Journal of Transplantation 01/2013; 13(3). DOI:10.1111/ajt.12063 · 5.68 Impact Factor
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    ABSTRACT: Background: Recently, we developed an apoptotic assay for expanding the monitoring capabilities of the circulating tumour cells (CTC) test during therapy. An automated platform for computing CTCs was integrated with a mAb (M30) targeting a neoepitope disclosed by caspase cleavage at cytokeratin 18 in early apoptosis; we showed that live CTCs were associated with progression, consistent with enhanced cell migration and invasion. The test was first applied here to mRCC. Methods: Live/apoptotic CTCs changes were measured in mRCC patients receiving first-line Sunitinib and compared with circulating endothelial cell (CEC) levels. Results: The presence of EpCAM-positive, live CTCs predicts progression in individual mRCC patient, being associated with distant metastasis under first-line Sunitinib. Synchronous detection of CTCs and CEC levels discloses for the first time an association between their dynamic changes and outcome: a rapid increase of the CEC number as early as the first cycle of therapy is associated with CTC decrease in non-progressed patients, whereas a delayed response of CECs is related to higher CTC values in the progressed group indicating treatment failure. Conclusion: We demonstrated that a delayed response to antiangiogenic treatment indicated by persistent detection of CECs correlates with persistent live CTCs and more aggressive disease.
    British Journal of Cancer 09/2012; 107(8):1286-94. DOI:10.1038/bjc.2012.388 · 4.84 Impact Factor
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    ABSTRACT: Background and Aim Colon crypts are characterized by a hierarchy of cells distributed along the crypt axis. Aim of this paper was to develop an in vitro system for separation of epithelial cell subsets in different maturation stages from normal human colon. Methodology and Major Findings Dissociated colonic epithelial cells were stained with PKH26, which allows identification of distinct populations based on their proliferation rate, and cultured in vitro in the absence of serum. The cytofluorimetric expression of CK20, Msi-1 and Lgr5 was studied. The mRNA levels of several stemness-associated genes were also compared in cultured cell populations and in three colon crypt populations isolated by microdissection. A PKHpos population survived in culture and formed spheroids; this population included subsets with slow (PKHhigh) and rapid (PKHlow) replicative rates. Molecular analysis revealed higher mRNA levels of both Msi-1 and Lgr-5 in PKHhigh cells; by cytofluorimetric analysis, Msi-1+/Lgr5+ cells were only found within PKHhigh cells, whereas Msi-1+/Lgr5− cells were also observed in the PKHlow population. As judged by qRT-PCR analysis, the expression of several stemness-associated markers (Bmi-1, EphB2, EpCAM, ALDH1) was highly enriched in Msi-1+/Lgr5+ cells. While CK20 expression was mainly found in PKHlow and PKHneg cells, a small PKHhigh subset co-expressed both CK20 and Msi-1, but not Lgr5; cells with these properties also expressed Mucin, and could be identified in vivo in colon crypts. These results mirrored those found in cells isolated from different crypt portions by microdissection, and based on proliferation rates and marker expression they allowed to define several subsets at different maturation stages: PKHhigh/Lgr5+/Msi-1+/CK20−, PKHhigh/Lgr5−/Msi-1+/CK20+, PKHlow/Lgr5−/Msi-1+/Ck20−, and PKHlow/Lgr5−/Msi-1−/CK20+ cells. Conclusions Our data show the possibility of deriving in vitro, without any selection strategy, several distinct cell subsets of human colon epithelial cells, which recapitulate the phenotypic and molecular profile of cells in a discrete crypt location.
    PLoS ONE 08/2012; 7(8):e43379. DOI:10.1371/journal.pone.0043379 · 3.23 Impact Factor
  • European Journal of Cancer 07/2012; 48:S226. DOI:10.1016/S0959-8049(12)71562-9 · 5.42 Impact Factor
  • European Journal of Cancer 07/2012; 48:S184. DOI:10.1016/S0959-8049(12)71410-7 · 5.42 Impact Factor

Publication Stats

3k Citations
857.69 Total Impact Points


  • 1987–2015
    • University of Padova
      • • Department of Surgery, Oncology and Gastroenterology DISCOG
      • • Department of Pediatrics
      • • Department of Biomedical Sciences - DSB
      Padua, Veneto, Italy
  • 2006–2014
    • Istituto Oncologico Veneto
      • Immunology and Diagnostic Molecular Oncology
      Padua, Veneto, Italy
  • 2010
    • Istituto di Cura e Cura a Carattere Scientifico Basilicata
      Rionero in Vulture, Basilicate, Italy
  • 2004
    • IRCCS Istituto G. Gaslini
      • Department of Experimental and Laboratory Medicine
      Genova, Liguria, Italy
  • 1995–1999
    • Interuniversity Research Centre on Bioactive Peptides
      Napoli, Campania, Italy
  • 1996
    • Istituto Superiore di Sanità
      • Laboratory of Virology
      Roma, Latium, Italy
  • 1989–1996
    • It-Robotics
      Vicenza, Veneto, Italy