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1. DNA methylation-based classification of sinonasal tumors

Author

Jurmeister, Philipp, Glöß, Stefanie, Roller, Renée, Leitheiser, Maximilian, Schmid, Simone, Mochmann, Liliana H., Payá Capilla, Emma, Fritz, Rebecca, Dittmayer, Carsten, Friedrich, Corinna, Thieme, Anne, Keyl, Philipp, Jarosch, Armin, Schallenberg, Simon, Bläker, Hendrik, Hoffmann, Inga, Vollbrecht, Claudia, Lehmann, Annika, Hummel, Michael, Heim, Daniel, Haji, Mohamed, Harter, Patrick, Englert, Benjamin, Frank, Stephan, Hench, Jürgen, Paulus, Werner, Hasselblatt, Martin, Hartmann, Wolfgang, Dohmen, Hildegard, Keber, Ursula, Jank, Paul, Denkert, Carsten, Stadelmann, Christine, Bremmer, Felix, Richter, Annika, Wefers, Annika, Ribbat-Idel, Julika, Perner, Sven, Idel, Christian, Chiariotti, Lorenzo, Della Monica, Rosa, Marinelli, Alfredo, Schüller, Ulrich, Bockmayr, Michael, Liu, Jacklyn, Lund, Valerie J., Forster, Martin, Lechner, Matt, Lorenzo-Guerra, Sara L., Hermsen, Mario, Johann, Pascal D., Agaimy, Abbas, Seegerer, Philipp, Koch, Arend, Heppner, Frank, Pfister, Stefan M., Jones, David T. W., Sill, Martin, von Deimling, Andreas, Snuderl, Matija, Müller, Klaus-Robert, Forgó, Erna, Howitt, Brooke E., Mertins, Philipp, Klauschen, Frederick, and Capper, David

Published
2022
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2. Whole exome sequencing of human papillomavirus-related multiphenotypic sinonasal carcinoma: a case report.

Author

Cubides-Córdoba, María Camila, Sánchez-Fernández, Paula, Mendoza-Pacas, Guillermo E., Cabal, Virginia N., García-Marín, Rocío, Lucila Lorenzo-Guerra, Sara, García-Velasco, Fabián, Hermsen, Mario A., and Luis Llorente, José

Subjects
SOMATIC mutation, GENE expression, NUCLEIC acid hybridization, HUMAN papillomavirus, DRUG target, ADENOID cystic carcinoma
Abstract

Human Papillomavirus (HPV) related Multiphenotypic Sinonasal Carcinoma (HMSC) is a rare tumor with features of both atypical squamous cell and adenoid cystic carcinoma, making diagnosis challenging. Approximately 80% of HMSC cases carries HPV type 33 followed by type 35. We present a patient with HMSC. Pathological classification was aided by immunohistochemistry (IHC). The presence of HPV-DNA was tested using PCR and HPV E6/E7 expression by RNA in situ hybridization (RNA ISH). Whole exome sequencing (WES) was used to identify somatic gene mutations and copy number alterations. A 55-year-old male presented with an HMSC in the right nostril. Histological examination showed a solid basaloid subtype with mucinous spaces and ductal structures. IHC showed positive staining for SOX-10, SMA, p40, p63, PanCK, CK8 and MYB. Diffuse positive staining for p16 was observed and PCR and RNA ISH indicated the presence of HPV type 35. The patient was treated with endoscopic surgery and radiotherapy and is currently alive and recurrence-free after 16 months of followup. WES revealed 38 somatic sequence variants and several chromosomal regions with copy number alterations, including a copy number gain at 6q23 where MYB is located. EP300, ZNF22, ZNF609 and LRIG3 are some of the genes whose mutations were indicated as probably pathogenic. We did not find mutations predictive for drug response according to the ESMO Scale for Clinical Actionability of Molecular Targets database. This is the first report of WES analysis of an HMSC, in this case associated with HPV type 35. The detected mutation in EP300 and the overexpression of MYB may serve as molecular targets for personalized therapy. [ABSTRACT FROM AUTHOR]

Published
2024
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4. O180 / #616 - RADGESS: PRELIMINARY RESULTS OF THE IN SILICO STUDY FOR RADIORESISTANCE GENOMIC SIGNATURES IN SINONASAL CANCERS EXPERIMENTAL MODELS AFTER PARTICLE THERAPY

Author

Giorgia, Fulgini, Charalampopoulou, Alexandra, Molinelli, Silvia, Pullia, Marco, Codina-Martinez, Helena, Lenoci, Deborah, Lucchetta, Marta, Takahashi, Yoko, Hanna, Hehab, Locati, Laura Deborah, Ivaldi, Giovanni B, De Cecco, Loris, Hermsen, Mario, Facoetti, Angelica, and Orlandi, Ester

Published
2024
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5. Sox2 and βIII-Tubulin as Biomarkers of Drug Resistance in Poorly Differentiated Sinonasal Carcinomas

Author

López, Luis, primary, Fernández-Vañes, Laura, additional, Cabal, Virginia N., additional, García-Marín, Rocío, additional, Suárez-Fernández, Laura, additional, Codina-Martínez, Helena, additional, Lorenzo-Guerra, Sara L., additional, Vivanco, Blanca, additional, Blanco-Lorenzo, Verónica, additional, Llorente, José L., additional, López, Fernando, additional, and Hermsen, Mario A., additional

Published
2023
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6. Signaling Pathways mTOR and ERK as Therapeutic Targets in Sinonasal Intestinal-Type Adenocarcinoma

Author

Codina-Martínez, Helena, primary, Lorenzo-Guerra, Sara Lucila, additional, Cabal, Virginia N., additional, García-Marín, Rocío, additional, Suárez-Fernández, Laura, additional, Vivanco, Blanca, additional, Sánchez-Fernández, Paula, additional, López, Fernando, additional, Llorente, José Luis, additional, and Hermsen, Mario A., additional

Published
2023
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7. Characterization of a Preclinical In Vitro Model Derived from a SMARCA4-Mutated Sinonasal Teratocarcinosarcoma.

Author

Lorenzo-Guerra, Sara Lucila, Codina-Martínez, Helena, Suárez-Fernández, Laura, Cabal, Virginia N., García-Marín, Rocío, Riobello, Cristina, Vivanco, Blanca, Blanco-Lorenzo, Verónica, Sánchez-Fernández, Paula, López, Fernando, Llorente, Jóse Luis, and Hermsen, Mario A.

Subjects
SOMATIC mutation, PARANASAL sinuses, CYCLIN-dependent kinase inhibitors, ANIMAL models in research, NEUROENDOCRINE cells
Abstract

Sinonasal teratocarcinosarcoma (TCS) is a rare tumor that displays a variable histology with admixtures of epithelial, mesenchymal, neuroendocrine and germ cell elements. Facing a very poor prognosis, patients with TCS are in need of new options for treatment. Recently identified recurrent mutations in SMARCA4 may serve as target for modern therapies with EZH1/2 and CDK4/6 inhibitors. Here, we present the first in vitro cell line TCS627, established from a previously untreated primary TCS originating in the ethmoid sinus with invasion into the brain. The cultured cells expressed immunohistochemical markers, indicating differentiation of epithelial, neuroepithelial, sarcomatous and teratomatous components. Whole-exome sequencing revealed 99 somatic mutations including SMARCA4, ARID2, TET2, CDKN2A, WNT7A, NOTCH3 and STAG2, all present both in the primary tumor and in the cell line. Focusing on mutated SMARCA4 as the therapeutic target, growth inhibition assays showed a strong response to the CDK4/6 inhibitor palbociclib, but much less to the EZH1/2 inhibitor valemetostat. In conclusion, cell line TCS627 carries both histologic and genetic features characteristic of TCS and is a valuable model for both basic research and preclinical testing of new therapeutic options for treatment of TCS patients. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Biomarkers for Immunotherapy in Poorly Differentiated Sinonasal Tumors

Author

Villanueva-Fernández, Eva, primary, Hermsen, Mario A., additional, Suárez-Fernández, Laura, additional, Vivanco, Blanca, additional, Franchi, Alessandro, additional, García-Marín, Rocío, additional, Cabal, Virginia N., additional, Codina-Martínez, Helena, additional, Lorenzo-Guerra, Sara Lucila, additional, Llorente, José L., additional, and López, Fernando, additional

Published
2022
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14. International Multicenter Study of Clinical Outcomes of Sinonasal Melanoma Shows Survival Benefit for Patients Treated with Immune Checkpoint Inhibitors and Potential Improvements to the Current TNM Staging System

Author

Lechner, Matt, additional, Takahashi, Yoko, additional, Turri-Zanoni, Mario, additional, Ferrari, Marco, additional, Liu, Jacklyn, additional, Counsell, Nicholas, additional, Mattavelli, Davide, additional, Rampinelli, Vittorio, additional, Vermi, William, additional, Lombardi, Davide, additional, Saade, Rami, additional, Park, Ki Wan, additional, Schartinger, Volker H., additional, Franchi, Alessandro, additional, Facco, Carla, additional, Sessa, Fausto, additional, Battocchio, Simonetta, additional, Fenton, Tim R., additional, Vaz, Francis M., additional, O'Flynn, Paul, additional, Howard, David, additional, Stimpson, Paul, additional, Wang, Simon, additional, Hannan, S. Alam, additional, Unadkat, Samit, additional, Hughes, Jonathan, additional, Dwivedi, Raghav, additional, Forde, Cillian T., additional, Randhawa, Premjit, additional, Gane, Simon, additional, Joseph, Jonathan, additional, Andrews, Peter J., additional, Dave, Manas, additional, Fleming, Jason C., additional, Thomson, David, additional, Zhu, Tianyu, additional, Teschendorff, Andrew, additional, Royle, Gary, additional, Steele, Christopher, additional, Jimenez, Joaquin E., additional, Laco, Jan, additional, Wang, Eric W., additional, Snyderman, Carl, additional, Lacy, Peter D., additional, Woods, Robbie, additional, O'Neill, James P., additional, Saraswathula, Anirudh, additional, Kaur, Raman Preet, additional, Zhao, Tianna, additional, Ramanathan, Murugappan, additional, Gallia, Gary L., additional, London, Nyall R., additional, Le, Quynh-Thu, additional, West, Robert B., additional, Patel, Zara M., additional, Nayak, Jayakar V., additional, Hwang, Peter H., additional, Hermsen, Mario, additional, Llorente, Jose, additional, Facchetti, Fabio, additional, Nicolai, Piero, additional, Bossi, Paolo, additional, Castelnuovo, Paolo, additional, Jay, Amrita, additional, Carnell, Dawn, additional, Forster, Martin D., additional, Bell, Diana M., additional, Lund, Valerie J., additional, and Hanna, Ehab Y., additional

Published
2022
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15. Multicenter Analysis of Clinical Outcomes of Sinonasal Mucosal Melanoma

Author

Lechner, Matt, additional, Takahashi, Yoko, additional, Turri-Zanoni, Mario, additional, Ferrari, Marco, additional, Liu, Jacklyn, additional, Counsell, Nicholas, additional, Mattavelli, Davide, additional, Rampinelli, Vittorio, additional, Lombardi, Davide, additional, Saade, Rami, additional, Park, Ki Wan, additional, Schartinger, Volker H., additional, Franchi, Alessandro, additional, Maragliano, Roberta, additional, Battocchio, Simonetta, additional, Emanuel, Oscar, additional, Fenton, Tim, additional, Vaz, Francis M., additional, O'Flynn, Paul, additional, Howard, David, additional, Stimpson, Paul, additional, Wang, Simon, additional, Hannan, S. Alam, additional, Unadkat, Samit, additional, Hughes, Jonathan, additional, Dwivedi, Raghav, additional, Forde, Cillian T., additional, Randhawa, Premjit, additional, Gane, Simon, additional, Joseph, Jonathan, additional, Andrews, Peter J., additional, Zhu, Tianyu, additional, Teschendorff, Andrew, additional, Royle, Gary, additional, Bewicke-Copley, Helen, additional, Steele, Christopher, additional, Williams, Luke, additional, Jimenez-Garcia, Joaquin E., additional, Wang, Eric W., additional, Snyderman, Carl, additional, Lacy, Peter, additional, Woods, Robbie, additional, O'Neill, James P., additional, Le, Quynh-Thu, additional, West, Robert B., additional, Patel, Zara M., additional, Nayak, Jayakar, additional, Hwang, Peter H., additional, Hermsen, Mario, additional, Llorente, Jose, additional, Facchetti, Fabio, additional, Nicolai, Piero, additional, Bossi, Paolo, additional, Castelnuovo, Paolo, additional, Jay, Amrita, additional, Carnell, Dawn, additional, Forster, Martin D., additional, Bell, Diana M., additional, Lund, Valerie J., additional, and Hanna, Ehab Y., additional

Published
2022
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19. Aberrant Signaling Pathways in Sinonasal Intestinal-Type Adenocarcinoma

Author

Riobello, Cristina, primary, Sánchez-Fernández, Paula, additional, Cabal, Virginia N., additional, García-Marín, Rocío, additional, Suárez-Fernández, Laura, additional, Vivanco, Blanca, additional, Blanco-Lorenzo, Verónica, additional, Álvarez Marcos, César, additional, López, Fernando, additional, Llorente, José Luis, additional, and Hermsen, Mario A., additional

Published
2021
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24. Abstract 1470: Preclinical activity of the first reversible, potent and selective inhibitor of EGFR exon 20 insertions

Author

Siegel, Franziska, primary, Siegel, Stephan, additional, Graham, Keith, additional, Kaplan, Bethany, additional, Petersen, Kirstin, additional, Boemer, Ulf, additional, Eberspaecher, Uwe, additional, Korr, Daniel, additional, Moenning, Ursula, additional, Suelzle, Detlev, additional, Schroeder, Jens, additional, Prinz, Florian, additional, Zitzmann-Kolbe, Sabine, additional, Karsli-Uzunbas, Gizem, additional, Lewis, Timothy, additional, Hermsen, Mario, additional, Cherniack, Andrew, additional, von Nussbaum, Franz, additional, Eis, Knut, additional, Meyerson, Matthew, additional, and Greulich, Heidi, additional

Published
2021
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25. Prognostic and Therapeutic Implications of Immune Classification by CD8+ Tumor-Infiltrating Lymphocytes and PD-L1 Expression in Sinonasal Squamous Cell Carcinoma

Author

García-Marín, Rocío, primary, Reda, Sara, additional, Riobello, Cristina, additional, Cabal, Virginia N., additional, Suárez-Fernández, Laura, additional, Vivanco, Blanca, additional, Álvarez-Marcos, César, additional, López, Fernando, additional, Llorente, José L., additional, and Hermsen, Mario A., additional

Published
2021
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27. Mismatch Repair Deficiency and Somatic Mutations in Human Sinonasal Tumors

Author

Hieggelke, Lena, Heydt, Carina, Castiglione, Roberta, Rehker, Jan, Merkelbach-Bruse, Sabine, Riobello, Cristina, Llorente, Jose Luis, Hermsen, Mario A., Buettner, Reinhard, Hieggelke, Lena, Heydt, Carina, Castiglione, Roberta, Rehker, Jan, Merkelbach-Bruse, Sabine, Riobello, Cristina, Llorente, Jose Luis, Hermsen, Mario A., and Buettner, Reinhard

Abstract

Simple Summary Sinonasal carcinomas are rare tumors with an overall poor prognosis. Due to limitations in local therapeutic approaches, systemic neo-adjuvant or adjuvant therapies are becoming increasingly important in order to improve patient outcome. This study aimed to examine potentially therapeutic targetable molecular alterations in different sinonasal tumors, including deficiency in mismatch repair proteins and microsatellite instability as well as driver mutations. According to our results, immunohistochemical (IHC) analysis of mismatch repair (MMR) proteins and sequencing-based panel analysis should be integrated into the diagnostics of clinically aggressive inverted sinonasal papilloma (ISP) and sinonasal squamous cell carcinoma (SNSCC) in order to enable the therapeutic possibility of a targeted therapy. Due to limitations in local therapy approaches for sinonasal tumors, improvement in systemic therapies plays a pivotal role for prolongation of the patient's survival. The aim of this study was to examine potential biomarkers, including deficiency in mismatch repair proteins (dMMR)/microsatellite instability (MSI-H) in sinonasal cancers and their precancerous lesions. A comprehensive analysis of 10 sinonasal cancer cell lines by whole exome sequencing, screening 174 sinonasal tumors by immunohistochemistry (IHC) for mismatch repair deficiency and next generation sequencing (NGS) of 136 tumor samples revealed a dMMR/MSI-H sinonasal squamous cell carcinoma (SNSCC) cell line based on a somatic missense mutation in MLH1 and an overall frequency of dMMR/MSI-H SNSCC of 3.2% (4/125). Targetable EGFR mutations were found in 89.3% (25/28) of inverted sinonasal papilloma (ISP) and in 60% (6/10) of ISP-associated carcinomas. While PIK3CA and EGFR mutations were not mutually exclusive, KRAS mutated tumors were an EGFR-wildtype. The effect of potential driver mutations in FGFR2, FGFR3, BRAF, HRAS, MAP2K1, PTEN, NOTCH1 and CARD11 need further investigation. Our results

Published
2021

34. Multicenter Analysis of Clinical Outcomes and Biomarkers of Esthesioneuroblastoma

Author

Lechner, Matt, additional, Hermsen, Mario, additional, Turri-Zanoni, Mario, additional, Schartinger, Volker H., additional, Helman, Sam, additional, Varghese, Jordan, additional, Solares, C. Arturo, additional, Magliocca, Kelly, additional, Wang, Simon, additional, Sprung, Susanne, additional, Howard, David, additional, Engel, Nils, additional, Capper, David, additional, Schueller, Ulrich, additional, Forster, Martin, additional, Jay, Amrita, additional, Forde, Cillian, additional, Dudas, Jozsef, additional, Riechelmann, Herbert, additional, Manes, R. Peter, additional, Yarbrough, Wendell G., additional, Llorente, Jose L., additional, Wise, Sarah K., additional, Castelnuovo, Paolo, additional, and Lund, Valerie J., additional

Published
2020
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39. Factors Secreted by Cancer-Associated Fibroblasts that Sustain Cancer Stem Properties in Head and Neck Squamous Carcinoma Cells as Potential Therapeutic Targets

Author

Álvarez-Teijeiro, Saúl, primary, García-Inclán, Cristina, additional, Villaronga, M., additional, Casado, Pedro, additional, Hermida-Prado, Francisco, additional, Granda-Díaz, Rocío, additional, Rodrigo, Juan, additional, Calvo, Fernando, additional, del-Río-Ibisate, Nagore, additional, Gandarillas, Alberto, additional, Morís, Francisco, additional, Hermsen, Mario, additional, Cutillas, Pedro, additional, and García-Pedrero, Juana, additional

Published
2018
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40. Genetic profiling of poorly differentiated sinonasal tumours

Author

López-Hernández, Alejandro, primary, Vivanco, Blanca, additional, Franchi, Alessandro, additional, Bloemena, Elisabeth, additional, Cabal, Virginia N., additional, Potes, Sira, additional, Riobello, Cristina, additional, García-Inclán, Cristina, additional, López, Fernando, additional, Llorente, José L., additional, and Hermsen, Mario, additional

Published
2018
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41. Genetic profiling of poorly differentiated sinonasal tumours

Author

Lopez-Hernandez, A., Vivanco, B., Franchi, A., Bloemena, E., Cabal, V.N., Potes, S., Riobello, C., Garcia-Inclan, C., Lopez, F., Llorente, J.L., Hermsen, Mario, Lopez-Hernandez, A., Vivanco, B., Franchi, A., Bloemena, E., Cabal, V.N., Potes, S., Riobello, C., Garcia-Inclan, C., Lopez, F., Llorente, J.L., and Hermsen, Mario

Abstract

Contains fulltext : 191237.pdf (publisher's version ) (Open Access), The sinonasal cavities harbour a variety of rare tumour types. Many carry a poor prognosis while therapeutic options are limited. Histopathological classification can be difficult, especially for poorly differentiated tumours such as olfactory neuroblastoma (ONB), sinonasal neuroendocrine carcinoma (SNEC) and sinonasal undifferentiated carcinoma (SNUC). We analysed Affymetrix OncoScan genome-wide copy number profiles of these three tumour types, both as originally diagnosed and as regrouped by their cytokeratin (Ck) and neuroendocrine (Ne) expression pattern, aiming to find a relation between phenotype and genotype. According to the original histopathological classification our series consisted of 24 ONB, 11 SNEC and 19 SNUC, while immunohistochemistry indicated 11 Ck-Ne+/ONB, 18 Ck+Ne+/SNEC, 24 Ck+Ne-/SNUC, and 1 Ck-Ne-/unclassified. As originally diagnosed, the three tumour types showed similar copy number profiles. However, when regrouped by Ck/Ne immunostaining we found a distinct set of gains and losses; Ck-Ne+/ONB harboured few and predominantly whole chromosomes abnormalities, Ck+Ne+/SNEC carried both gains and losses in high frequency, and Ck+Ne-/SNUC showed mostly gains. In addition, each tumour carried a number of unique chromosomal deletions. Genome-wide copy number profiling supports the value of immunohistochemical CkNe staining of ONB, SNEC and SNUC for tumour classification, which is important for prognosis and therapeutic decision-making.

Published
2018

42. Factors Secreted by Cancer-Associated Fibroblasts that Sustain Cancer Stem Properties in Head and Neck Squamous Carcinoma Cells as Potential Therapeutic Targets

Author

Instituto de Salud Carlos III, Centro de Investigación Biomédica en Red Cáncer (España), Principado de Asturias, European Commission, Álvarez-Teijeiro, Saúl, García-Inclán, Cristina, Villaronga, M. Ángeles, Casado, Pedro, Hermida-Prado, Francisco, Granda-Díaz, Rocío, Rodrigo, Juan P., Calvo, Fernando, Río Ibisate, Nagore Del, Gandarillas, Alberto, Morís, Francisco, Hermsen, Mario, Cutillas, Pedro, García-Pedrero, Juana M., Instituto de Salud Carlos III, Centro de Investigación Biomédica en Red Cáncer (España), Principado de Asturias, European Commission, Álvarez-Teijeiro, Saúl, García-Inclán, Cristina, Villaronga, M. Ángeles, Casado, Pedro, Hermida-Prado, Francisco, Granda-Díaz, Rocío, Rodrigo, Juan P., Calvo, Fernando, Río Ibisate, Nagore Del, Gandarillas, Alberto, Morís, Francisco, Hermsen, Mario, Cutillas, Pedro, and García-Pedrero, Juana M.

Abstract

This study investigates for the first time the crosstalk between stromal fibroblasts and cancer stem cell (CSC) biology in head and neck squamous cell carcinomas (HNSCC), with the ultimate goal of identifying effective therapeutic targets. The effects of conditioned media from cancer-associated fibroblasts (CAFs) and normal fibroblasts (NFs) on the CSC phenotype were assessed by combining functional and expression analyses in HNSCC-derived cell lines. Further characterization of CAFs and NFs secretomes by mass spectrometry was followed by pharmacologic target inhibition. We demonstrate that factors secreted by CAFs but not NFs, in the absence of serum/supplements, robustly increased anchorage-independent growth, tumorsphere formation, and CSC-marker expression. Modulators of epidermal growth factor receptor (EGFR), insulin-like growth factor receptor (IGFR), and platelet-derived growth factor receptor (PDGFR) activity were identified as paracrine cytokines/factors differentially secreted between CAFs and NFs, in a mass spectrometry analysis. Furthermore, pharmacologic inhibition of EGFR, IGFR, and PDGFR significantly reduced CAF-induced tumorsphere formation and anchorage-independent growth suggesting a role of these receptor tyrosine kinases in sustaining the CSC phenotype. These findings provide novel insights into tumor stroma–CSC communication, and potential therapeutic targets to effectively block the CAF-enhanced CSC niche signaling circuit.

Published
2018

45. Current Concepts on Dedifferentiation/High-Grade Transformation in Salivary Gland Tumors

Author

Costa, Ana Flávia, Altemani, Albina, and Hermsen, Mario

Subjects
Article Subject
Abstract

The concept of dedifferentiation had previously been used in salivary gland carcinomas. Recently, the term “high-grade transformation” was introduced for adenoid cystic carcinoma, acinic cell carcinoma, epithelial-myoepithelial carcinoma, and polymorphous low-grade adenocarcinoma and may better reflect this phenomenon, although transformation into moderately differentiated adenocarcinoma (i.e., not “high grade”) has also been described. Among the immunohistochemical markers, Ki-67 seems to be the only one that can help distinguish between the conventional and transformed components; however, the combination of morphological criteria is still sovereign. The overexpression of p53 was observed in the transformed component in all tumor types studied, despite few cases having been demonstrated to carry mutations or deletions in TP53 gene. Genetic studies in salivary gland tumors with dedifferentiation/high-grade transformation are rare and deserve further investigation. This paper aims at providing an overview on the recent concepts in histopathological classification of salivary gland tumors, complemented by immunohistochemical and genetic findings.

Published
2011
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46. High-Frequency Targetable EGFR Mutations in Sinonasal Squamous Cell Carcinomas Arising from Inverted Sinonasal Papilloma

Author

Udager, Aaron M., primary, Rolland, Delphine C.M., additional, McHugh, Jonathan B., additional, Betz, Bryan L., additional, Murga-Zamalloa, Carlos, additional, Carey, Thomas E., additional, Marentette, Lawrence J., additional, Hermsen, Mario A., additional, DuRoss, Kathleen E., additional, Lim, Megan S., additional, Elenitoba-Johnson, Kojo S.J., additional, and Brown, Noah A., additional

Published
2015
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48. Integrated Human Papillomavirus Type 16 and Loss of Heterozygosity at 11q22 and 18q21 in an Oral Carcinoma and Its Derivative Cell Line

Author

Steenbergen, Renske D.M., Walboomers, Jan M.M., Meijer, Chris J.L.M., Snijders, Peter J.F., Hermsen, Mario A.J.A., Joenje, Hans, Arwert, Fré, Pathology, Amsterdam Neuroscience - Cellular & Molecular Mechanisms, CCA - Cancer biology and immunology, CCA - Imaging and biomarkers, CCA - Cancer Treatment and quality of life, AII - Cancer immunology, and Human genetics

Abstract

A human papillomavirus (HPV) type 16 containing oral squamous cell carcinoma cell line 93VU147T at early passage was demonstrated to match its primary tumor with regard to HPV status and loss of heterozygosity at loci potentially involved in HPV-mediated carcinogenesis. DNA in situ hybridization of the cell line and the primary tumor revealed the presence of HPV 16 DNA clonally associated with the neoplastic cells. One- and two-dimensional Southern blot hybridization suggested HPV 16 to be integrated in the host genome at over hundred copies/cell. An identical restriction enzyme profile was observed for the tumor and the cell line. Viral DNA integration was confirmed by fluorescence in situ hybridization on metaphase spreads of the cell line, which revealed six stained loci comprising one at 15q14-15 and five at cytogenetically unidentifiable chromosomes. In addition, the tumor and the cell line displayed mRNA expression of the E6/E7 region encoding the viral oncoproteins, as determined by reverse transcription-PCR. Northern blot analysis of the cell line revealed three major and three minor transcripts harboring E67E7 sequences. Both the primary tumor and cell line showed loss of heterozygosity at the 11q22 (D11S35) and 18q21 (DCC) loci. These data support a role for HPV 16 in the development of a subset of oral cancers, presumably in concert with loss of function of tumor suppressor genes at 11q and 18q.

Published
1995

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