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302 results on '"Quagliata, Luca"'

1. The TGF-β1 target WISP1 is highly expressed in liver cirrhosis and cirrhotic HCC microenvironment and involved in pro- and anti-tumorigenic effects

Author

Dropmann, Anne, Alex, Sophie, Schorn, Katharina, Tong, Chenhao, Caccamo, Tiziana, Godoy, Patricio, Ilkavets, Iryna, Liebe, Roman, Gonzalez, Daniela, Hengstler, Jan G., Piiper, Albrecht, Quagliata, Luca, Matter, Matthias S., Waidmann, Oliver, Finkelmeier, Fabian, Feng, Teng, Weiss, Thomas S., Rahbari, Nuh, Birgin, Emrullah, Rasbach, Erik, Roessler, Stephanie, Breuhahn, Kai, Tóth, Marcell, Ebert, Matthias P., Dooley, Steven, Hammad, Seddik, and Meindl-Beinker, Nadja M.

Published
2024
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3. Up-regulation of miR-34b/c by JNK and FOXO3 protects from liver fibrosis

Author

Piccolo, Pasquale, Ferriero, Rosa, Barbato, Anna, Attanasio, Sergio, Monti, Marcello, Perna, Claudia, Borel, Florie, Annunziata, Patrizia, Carissimo, Annamaria, De Cegli, Rossella, Quagliata, Luca, Terracciano, Luigi M., Housset, Chantal, Teckman, Jeffrey H., Mueller, Christian, and Brunetti-Pierri, Nicola

Published
2021

4. Non-viral gene delivery of the oncotoxic protein NS1 for treatment of hepatocellular carcinoma

Author

Witzigmann, Dominik, Grossen, Philip, Quintavalle, Cristina, Lanzafame, Manuela, Schenk, Susanne H., Tran, Xue-Ting, Englinger, Bernhard, Hauswirth, Patrick, Grünig, David, van Schoonhoven, Sushilla, Krähenbühl, Stephan, Terracciano, Luigi M., Berger, Walter, Piscuoglio, Salvatore, Quagliata, Luca, Rommelaere, Jean, Nüesch, Jürg P.F., and Huwyler, Jörg

Published
2021
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7. Cetuximab monotherapy and cetuximab plus capecitabine as first-line treatment in older patients with RAS- and BRAF wild-type metastatic colorectal cancer. Results of the multicenter phase II trial SAKK 41/10

Author

Kienle, Dirk L., Dietrich, Daniel, Ribi, Karin, Wicki, Andreas, Quagliata, Luca, Winterhalder, Ralph C., Koeberle, Dieter, Horber, Daniel, Bastian, Sara, Kueng, Marc, Saletti, Piercarlo, Helbling, Daniel, Baertschi, Daniela, Lugli, Alessandro, Bernhard, Juerg, Andrieu, Christiane, and von Moos, Roger

Published
2019
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9. Compromised Outcomes in Stage IV Non–Small-Cell Lung Cancer With Actionable Mutations Initially Treated Without Tyrosine Kinase Inhibitors: A Retrospective Analysis of Real-World Data

Author

Scott, Jeffrey A., primary, Lennerz, Jochen, additional, Johnson, Melissa Lynne, additional, Gordan, Lucio N., additional, Dumanois, Robert H., additional, Quagliata, Luca, additional, Ritterhouse, Lauren L., additional, Cappuzzo, Federico, additional, Wang, Brandon, additional, Xue, Mei, additional, Vasudevan, Anupama, additional, Varughese, Prateesh, additional, Vaidya, Varun, additional, Gart, Mike, additional, Dorrow, Natalie, additional, Gierman, Hinco J., additional, and Choksi, Rushir J., additional

Published
2023
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10. Real-world testing and treatment patterns among patients with stage IV non-small cell lung cancer: A retrospective observational study.

Author

Scott, Jeffrey A., primary, Katzen, Harvey I., additional, Lennerz, Jochen K, additional, Johnson, Melissa Lynne, additional, Gordan, Lucio N., additional, Dumanois, Robert H, additional, Quagliata, Luca, additional, Ritterhouse, Lauren, additional, Cappuzzo, Federico, additional, Vasudevan, Anupama, additional, Sura, Teena, additional, English, Sandy, additional, Wang, Brandon, additional, Varughese, Prateesh, additional, and Choksi, Rushir J., additional

Published
2023
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11. Compromised Outcomes in Stage IV Non–Small-Cell Lung Cancer With Actionable Mutations Initially Treated Without Tyrosine Kinase Inhibitors: A Retrospective Analysis of Real-World Data.

Author

Scott, Jeffrey A., Lennerz, Jochen, Johnson, Melissa Lynne, Gordan, Lucio N., Dumanois, Robert H., Quagliata, Luca, Ritterhouse, Lauren L., Cappuzzo, Federico, Wang, Brandon, Mei Xue, Vasudevan, Anupama, Varughese, Prateesh, Vaidya, Varun, Gart, Mike, Dorrow, Natalie, Gierman, Hinco J., and Choksi, Rushir J.

Subjects
PROTEIN analysis, LUNG cancer, GENETIC mutation, SCIENTIFIC observation, CONFIDENCE intervals, RETROSPECTIVE studies, REGRESSION analysis, TUMOR classification, PROTEIN-tyrosine kinase inhibitors, TREATMENT effectiveness, COMPARATIVE studies, GENOMICS, KAPLAN-Meier estimator, DESCRIPTIVE statistics, DATA analysis software, OVERALL survival
Abstract

Purpose Identification and targeting of actionable oncogenic drivers (AODs) in advanced non–small-cell lung cancer (NSCLC) has dramatically improved outcomes. However, genomic testing uptake is variable and hampered by factors including slow turnaround time, frequently resulting in initial non–tyrosine kinase inhibitor (TKI) treatment. We investigate how this behavior affects outcomes. Methods This retrospective analysis of real-world, deidentified data from the Integra Connect Database included adults with stage IV NSCLC newly diagnosed from January 1, 2018, to December 31, 2020, with mutations of EGFR, ALK, ROS1, BRAF, MET, RET, ERBB2, or NTRK. Outcomes were reported as time to next treatment or death (TTNT) and overall survival (OS). Results Five hundred ten patients harboring AODs were identified and grouped as follows: group A (n = 379) were treated after the AOD was reported and served as the comparator. One hundred thirty-one patients treated before their AOD report were divided into group B (n = 47) who were initially started on chemotherapy and/or checkpoint inhibitor but switched to appropriate TKI within 35 days and group C (n = 84) who were also started empirically on non-TKI and did not switch within 35 days. Survival (OS) was significantly superior in group A compared with group C; TTNT was significantly superior in group A compared with groups B and C. Conclusion For patients harboring AODs in advanced NSCLC, initial treatment before receipt of genomic test results yields significantly inferior outcomes and should be avoided. Molecular profiling panels with rapid turnaround times are essential to optimize patient outcomes and should be standard of care. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Supplementary Figures 1-10 from Human and Mouse VEGFA-Amplified Hepatocellular Carcinomas Are Highly Sensitive to Sorafenib Treatment

Author

Horwitz, Elad, primary, Stein, Ilan, primary, Andreozzi, Mariacarla, primary, Nemeth, Julia, primary, Shoham, Avivit, primary, Pappo, Orit, primary, Schweitzer, Nora, primary, Tornillo, Luigi, primary, Kanarek, Naama, primary, Quagliata, Luca, primary, Zreik, Farid, primary, Porat, Rinnat M., primary, Finkelstein, Rutie, primary, Reuter, Hendrik, primary, Koschny, Ronald, primary, Ganten, Tom, primary, Mogler, Carolin, primary, Shibolet, Oren, primary, Hess, Jochen, primary, Breuhahn, Kai, primary, Grunewald, Myriam, primary, Schirmacher, Peter, primary, Vogel, Arndt, primary, Terracciano, Luigi, primary, Angel, Peter, primary, Ben-Neriah, Yinon, primary, and Pikarsky, Eli, primary

Published
2023
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14. Supplementary Tables from Human and Mouse VEGFA-Amplified Hepatocellular Carcinomas Are Highly Sensitive to Sorafenib Treatment

Author

Horwitz, Elad, primary, Stein, Ilan, primary, Andreozzi, Mariacarla, primary, Nemeth, Julia, primary, Shoham, Avivit, primary, Pappo, Orit, primary, Schweitzer, Nora, primary, Tornillo, Luigi, primary, Kanarek, Naama, primary, Quagliata, Luca, primary, Zreik, Farid, primary, Porat, Rinnat M., primary, Finkelstein, Rutie, primary, Reuter, Hendrik, primary, Koschny, Ronald, primary, Ganten, Tom, primary, Mogler, Carolin, primary, Shibolet, Oren, primary, Hess, Jochen, primary, Breuhahn, Kai, primary, Grunewald, Myriam, primary, Schirmacher, Peter, primary, Vogel, Arndt, primary, Terracciano, Luigi, primary, Angel, Peter, primary, Ben-Neriah, Yinon, primary, and Pikarsky, Eli, primary

Published
2023
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15. Data from Human and Mouse VEGFA-Amplified Hepatocellular Carcinomas Are Highly Sensitive to Sorafenib Treatment

Author

Horwitz, Elad, primary, Stein, Ilan, primary, Andreozzi, Mariacarla, primary, Nemeth, Julia, primary, Shoham, Avivit, primary, Pappo, Orit, primary, Schweitzer, Nora, primary, Tornillo, Luigi, primary, Kanarek, Naama, primary, Quagliata, Luca, primary, Zreik, Farid, primary, Porat, Rinnat M., primary, Finkelstein, Rutie, primary, Reuter, Hendrik, primary, Koschny, Ronald, primary, Ganten, Tom, primary, Mogler, Carolin, primary, Shibolet, Oren, primary, Hess, Jochen, primary, Breuhahn, Kai, primary, Grunewald, Myriam, primary, Schirmacher, Peter, primary, Vogel, Arndt, primary, Terracciano, Luigi, primary, Angel, Peter, primary, Ben-Neriah, Yinon, primary, and Pikarsky, Eli, primary

Published
2023
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35. Integrated analysis of the prostate cancer small-nucleolar transcriptome reveals SNORA55 as a driver of prostate cancer progression

Author

Crea, Francesco, Quagliata, Luca, Michael, Agnieszka, Liu, Hui Hsuan, Frumento, Paolo, Azad, Arun A., Xue, Hui, Pikor, Larissa, Watahiki, Akira, Morant, Rudolf, Eppenberger-Castori, Serenella, Wang, Yuwei, Parolia, Abhijit, Lennox, Kim A., Lam, Wan L., Gleave, Martin, Chi, Kim N., Pandha, Hardev, Wang, Yuzhuo, and Helgason, Cheryl D.

Published
2016
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37. The protein histidine phosphatase LHPP is a tumour suppressor

Author

Hindupur, Sravanth K., Colombi, Marco, Fuhs, Stephen R., Matter, Matthias S., Guri, Yakir, Adam, Kevin, Cornu, Marion, Piscuoglio, Salvatore, Ng, Charlotte K. Y., Betz, Charles, Liko, Dritan, Quagliata, Luca, Moes, Suzette, Jenoe, Paul, Terracciano, Luigi M., Heim, Markus H., Hunter, Tony, and Hall, Michael N.

Subjects
Histidine -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Sravanth K. Hindupur [1]; Marco Colombi [1]; Stephen R. Fuhs [2]; Matthias S. Matter [3]; Yakir Guri [1]; Kevin Adam [2]; Marion Cornu [1]; Salvatore Piscuoglio [3]; Charlotte K. [...]

Published
2018
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39. The evolutionarily conserved long non-coding RNA LINC00261 drives neuroendocrine prostate cancer proliferation and metastasis via distinct nuclear and cytoplasmic mechanisms

Author

Mather, Rebecca L., Parolia, Abhijit, Carson, Sandra E., Venalainen, Erik, Roig-Carles, David, Jaber, Mustapha, Chu, Shih Chun, Alborelli, Ilaria, Wu, Rebecca, Lin, Dong, Nabavi, Noushin, Jachetti, Elena, Colombo, Mario P., Xue, Hui, Pucci, Perla, Ci, Xinpei, Hawkes, Cheryl, Li, Yinglei, Pandha, Hardev, Ulitsky, Igor, Marconett, Crystal, Quagliata, Luca, Jiang, Wei, Romero, Ignacio, Wang, Yuzhuo, Crea, Francesco, Mather, Rebecca L., Parolia, Abhijit, Carson, Sandra E., Venalainen, Erik, Roig-Carles, David, Jaber, Mustapha, Chu, Shih Chun, Alborelli, Ilaria, Wu, Rebecca, Lin, Dong, Nabavi, Noushin, Jachetti, Elena, Colombo, Mario P., Xue, Hui, Pucci, Perla, Ci, Xinpei, Hawkes, Cheryl, Li, Yinglei, Pandha, Hardev, Ulitsky, Igor, Marconett, Crystal, Quagliata, Luca, Jiang, Wei, Romero, Ignacio, Wang, Yuzhuo, and Crea, Francesco

Abstract

Metastatic neuroendocrine prostate cancer (NEPC) is a highly aggressive disease, whose incidence is rising. Long noncoding RNAs (lncRNAs) represent a large family of disease- and tissue-specific transcripts, most of which are still functionally uncharacterized. Thus, we set out to identify the highly conserved lncRNAs that play a central role in NEPC pathogenesis. To this end, we performed transcriptomic analyses of donor-matched patient-derived xenograft models (PDXs) with immunohistologic features of prostate adenocarcinoma (AR+/PSA+) or NEPC (AR−/SYN+/CHGA+) and through differential expression analyses identified lncRNAs that were upregulated upon neuroendocrine transdifferentiation. These genes were prioritized for functional assessment based on the level of conservation in vertebrates. Here, LINC00261 emerged as the top gene with over 3229-fold upregulation in NEPC. Consistently, LINC00261 expression was significantly upregulated in NEPC specimens in multiple patient cohorts. Knockdown of LINC00261 in PC-3 cells dramatically attenuated its proliferative and metastatic abilities, which are explained by parallel downregulation of CBX2 and FOXA2 through distinct molecular mechanisms. In the cell cytoplasm, LINC00261 binds to and sequesters miR-8485 from targeting the CBX2 mRNA, while inside the nucleus, LINC00261 functions as a transcriptional scaffold to induce SMAD-driven expression of the FOXA2 gene. For the first time, these results demonstrate hyperactivation of the LINC00261-CBX2-FOXA2 axes in NEPC to drive proliferation and metastasis, and that LINC00261 may be utilized as a therapeutic target and a biomarker for this incurable disease.

Published
2021

40. Long noncoding RNA HOTTIP/HOXA13 expression is associated with disease progression and predicts outcome in hepatocellular carcinoma patients

Author

Quagliata, Luca, Matter, Matthias S., Piscuoglio, Salvatore, Arabi, Leila, Ruiz, Christian, Procino, Alfredo, Kovac, Michal, Moretti, Francesca, Makowska, Zuzanna, Boldanova, Tujana, Andersen, Jesper B., Hämmerle, Monika, Tornillo, Luigi, Heim, Markus H., Diederichs, Sven, Cillo, Clemente, and Terracciano, Luigi M.

Published
2014
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41. The evolutionarily conserved long non‐coding RNA LINC00261 drives neuroendocrine prostate cancer proliferation and metastasis via distinct nuclear and cytoplasmic mechanisms

Author

Mather, Rebecca L., primary, Parolia, Abhijit, additional, Carson, Sandra E., additional, Venalainen, Erik, additional, Roig‐Carles, David, additional, Jaber, Mustapha, additional, Chu, Shih‐Chun, additional, Alborelli, Ilaria, additional, Wu, Rebecca, additional, Lin, Dong, additional, Nabavi, Noushin, additional, Jachetti, Elena, additional, Colombo, Mario P., additional, Xue, Hui, additional, Pucci, Perla, additional, Ci, Xinpei, additional, Hawkes, Cheryl, additional, Li, Yinglei, additional, Pandha, Hardev, additional, Ulitsky, Igor, additional, Marconett, Crystal, additional, Quagliata, Luca, additional, Jiang, Wei, additional, Romero, Ignacio, additional, Wang, Yuzhuo, additional, and Crea, Francesco, additional

Published
2021
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43. Long non-coding RNAs are key players in Prostate cancer tumorigenesis and drug resistance

Author

Pucci, Perla, Crea, Francesco, Alborelli, Ilaria, Quagliata, Luca, Bootman, Martin, Rigas, Sushilaben, Romero, Ignacio, and Wang, Yuzhuo

Abstract

"Long non-coding RNAs (lncRNAs) have been characterized as key players in several cancer-associated processes such as tumorigenesis and drug resistance. Emerging evidence indicates that lncRNAs affect initiation and progression of several cancers, including prostate cancer (PCa) and its advanced forms, such as metastatic castration resistant prostate cancer (mCRPC).\ud Among others, H19 is one of the most studied oncogenic lncRNAs in cancer and has been associated with cancer tumorigenesis and progression, via mediating several pathways an acting in different mechanisms of action, including epigenetic and miRNA regulation.\ud We have investigated lncRNA roles in PCa tumorigenesis by analysing the E006AA cell model. Emerging evidence has shown that parental E006AA are not tumorigenic in nude mice, while its derived E006AA-ht, is highly tumorigenic. Via high-throughput RNA sequencing we have shown that E006AA-ht overexpress different lncRNAs compared to E006AA. Interestingly, we found a high upregulation of H19 in E006AA-ht vs the parental cell line. Our in vitro validation has confirmed the sequencing data and further research could unravel a crucial role of H19 in PCa tumorigenesis, opening a new challenging chapter of lncRNAs research. We hypothesize that H19 could be involved in in vivo immunity suppression and our further studies aim at investigating H19 in this molecular and clinical context.\ud Furthermore, we have studied lncRNAs as key players in cancer aggressiveness by using cellular models of mCRPC. From our studies, HORAS5 (i.e. linc00161) emerged as the most consistently upregulated lncRNA in CRPC patient-derived xenografts. This lncRNAs was previously associated with cancer drug-response in osteosarcoma, ovarian cancer and hepatocellular carcinoma. Our study has shown for the first time that HORAS5 promotes drug resistance in CRPC. After a preliminary drug screen, we have selected the chemotherapeutics cabazitaxel for further investigation. Via lentiviral-mediated overexpression and siRNA-based silencing we have regulated HORAS5 expression and analysed cell count and apoptosis of CRPC cells exposed to clinically achievable concentrations of cabazitaxel.\ud The overexpression of HORAS5 increases cabazitaxel resistance, while HORAS5 silencing has an opposite effect, via inhibition of apoptosis. RNA sequencing and RT-qPCR revealed that BCL2A1 is the most upregulated transcript in HORAS5 overexpressing cells exposed to cabazitaxel, and that BCL2A1 silencing decreases cell count and increases caspase activity. Our data suggest that BCL2A1 expression is induced by HORAS5, thereby enhancing CRPC cells resistance to cabazitaxel. Transfection of CRPC cells with HORAS5-targeting ASOs can effectively silence this lncRNA and determine a decrease of cabazitaxel resistance. We have also shown that both HORAS5 and BCL2A1 upregulation results in decreased survival in PCa patients and samples from mCRPC patients treated with taxanes have upregulation of HORAS5.\ud Overall, our studies bring novel insights into crucial roles of lncRNAs in PCa progression and aggressiveness making them emerging targets for cancer treatment at different stages."

Published
2020

44. LncRNA HORAS5 promotes taxane resistance in castration-resistant prostate cancer via a BCL2A1-dependent mechanism

Author

Pucci, Perla, Venalainen, Erik, Alborelli, Ilaria, Quagliata, Luca, Hawkes, Cheryl, Mather, Rebecca, Romero, Ignacio, Rigas, Sushilaben H, Wang, Yuzhuo, Crea, Francesco, Mather, Rebecca [0000-0002-9813-7587], and Apollo - University of Cambridge Repository

Subjects
Male, drug resistance, Antineoplastic Agents, Apoptosis, BCL2A1, Oligonucleotides, Antisense, urologic and male genital diseases, Gene Expression Regulation, Neoplastic, Minor Histocompatibility Antigens, Prostatic Neoplasms, Castration-Resistant, HORAS5, lncRNA, Proto-Oncogene Proteins c-bcl-2, Drug Resistance, Neoplasm, Cell Line, Tumor, Humans, castration-resistant prostate cancer, RNA, Long Noncoding, Taxoids, Cell Proliferation, Research Article
Abstract

Background: Castration-resistant prostate cancer (CRPC) is an incurable malignancy. Long noncoding RNAs (lncRNAs) play key roles in drug resistance. Materials & methods: LncRNA HORAS5 role in cabazitaxel resistance (i.e., cell-count, IC50 and caspase activity) was studied via lentiviral-mediated overexpression and siRNA-based knockdown. Genes expression was analyzed with RNA-sequencing, reverse transcription quantitative PCR (RT-qPCR) and western blot. HORAS5 expression was queried in clinical database. Results: Cabazitaxel increased HORAS5 expression that upregulated BCL2A1, thereby protecting CRPC cells from cabazitaxel-induced apoptosis. BCL2A1 knockdown decreased cell-count and increased apoptosis in CRPC cells. HORAS5-targeting antisense oligonucleotide decreased cabazitaxel IC50. In CRPC clinical samples, HORAS5 expression increased upon taxane treatment. Conclusion: HORAS5 stimulates the expression of BCL2A1 thereby decreasing apoptosis and enhancing cabazitaxel resistance in CRPC cells.

Published
2020

45. Phosphoprotein enriched in diabetes (PED/PEA15) promotes migration in hepatocellular carcinoma and confers resistance to sorafenib

Author

Quintavalle, Cristina, Hindupur, Sravanth Kumar, Quagliata, Luca, Pallante, Pierlorenzo, Nigro, Cecilia, Condorelli, Gerolama, Andersen, Jesper Bøje, Tagscherer, Katrin Elisabeth, Roth, Wilfried, Beguinot, Francesco, Heim, Markus Hermann, Ng, Charlotte Kiu Yan, Piscuoglio, Salvatore, and Matter, Matthias Sebastian

Published
2017
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48. Corrigendum to “HMGA1 expression in human hepatocellular carcinoma correlates with poor prognosis and promotes tumor growth and migration in in vitro models” [Neoplasia 18 (2016) 724–731]

Author

Andreozzi, Mariacarla, primary, Quintavalle, Cristina, additional, Benz, David, additional, Quagliata, Luca, additional, Matter, Matthias, additional, Calabrese, Diego, additional, Tosti, Nadia, additional, Ruiz, Christian, additional, Trapani, Francesca, additional, Tornillo, Luigi, additional, Fusco, Alfredo, additional, Heim, Markus H., additional, Ng, Charlotte K.Y., additional, Pallante, Pierlorenzo, additional, Terracciano, Luigi M., additional, and Piscuoglio, Salvatore, additional

Published
2020
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50. VEGFA gene locus analysis across 80 human tumour types reveals gene amplification in several neoplastic entities

Author

Andreozzi, Mariacarla, Quagliata, Luca, Gsponer, Joel, Ruiz, Christian, Vuaroqueaux, Vincent, Eppenberger-Castori, Serenella, Tornillo, Luigi, Terracciano, Luigi, Andreozzi, Mariacarla, Quagliata, Luca, Gsponer, Joel, Ruiz, Christian, Vuaroqueaux, Vincent, Eppenberger-Castori, Serenella, Tornillo, Luigi, and Terracciano, Luigi

Abstract

Background: 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. Aims: 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). Results: 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. Conclusion: 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 re

Published
2019

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