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561 results on '"Hermsen, Mario"'

108. 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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115. Intragenic NF1 deletions in sinonasal mucosal malignant melanoma.

Author

Riobello, Cristina, Casanueva Muruais, Rodrigo, Suárez‐Fernández, Laura, García‐Marín, Rocío, Cabal, Virginia N., Blanco‐Lorenzo, Verónica, Franchi, Alessandro, Laco, Jan, López, Fernando, Llorente, José Luis, and Hermsen, Mario A.

Subjects
MELANOMA, PARANASAL sinuses, CANCER relapse, IMMUNE checkpoint inhibitors, NUCLEOTIDE sequencing, BRAF genes
Abstract

Mucosal malignant melanoma (MMM) is a rare and aggressive tumor. Despite effective local therapies, tumor recurrence and metastasis remain frequent. The genetics of MMM remain incompletely understood. This study is aimed to identify actionable genetic alterations by next‐generation sequencing. Fifteen MMM samples were analyzed by next‐generation and Sanger sequencing. Gene copy number alterations were analyzed by MLPA. Mutation status was correlated with pERK, pAKT, and Ki‐67 expression and follow‐up data. Inactivating mutations and intragenic deletions in neurofibromatosis type‐1 (NF1) were identified in 3 and 2 cases, respectively, (in total 5/15, 33%) and activating mutations in NRAS and KRAS (3/15, 20%) cases. Other mutated genes included CDKN2A, APC, ATM, MITF, FGFR1, and FGFR2. BRAF and KIT mutations were not observed. Cases with NF1 alterations tended to have worse overall survival. The mutational status was not associated with pERK, pAKT, or Ki‐67 immunostaining. MMM carries frequent gene mutations activating the MAPK pathway, similar to cutaneous melanoma. In contrast, NF1 is the most frequently affected gene. Intragenic NF1 deletions have not been described before and may go undetected by sequencing studies. This finding is clinically relevant as NF1‐mutated melanomas have worse survival and could benefit from therapy with immune checkpoint and MEK inhibitors. [ABSTRACT FROM AUTHOR]

Published
2022
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116. Comparative genomic hybridization in primary sinonasal adenocarcinomas

Author

Ariza, Manuela, Llorente, Jose Luis, Alvarez-Marcas, Cesar, Baragano, Lucia, Salas, Ana, Prado, Nuria Rodriguez, Hermsen, Mario, Suarez, Carlos, and Sampedro, Andres

Subjects
Adenocarcinoma -- Care and treatment, Paranasal sinus diseases -- Care and treatment, Cell hybridization -- Research, Genomics -- Research, Health
Published
2004

117. IDH2 Mutation Analysis in Undifferentiated and Poorly Differentiated Sinonasal Carcinomas for Diagnosis and Clinical Management

Author

Riobello, Cristina, primary, López-Hernández, Alejandro, additional, Cabal, Virginia N., additional, García-Marín, Rocío, additional, Suárez-Fernández, Laura, additional, Sánchez-Fernández, Paula, additional, Vivanco, Blanca, additional, Blanco, Verónica, additional, López, Fernando, additional, Franchi, Alessandro, additional, Llorente, José L., additional, and Hermsen, Mario A., additional

Published
2019
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119. Abstract 2125: Genetic analysis for classification and treatment of poorly differentiated sinonasal cancer

Author

Hermsen, Mario, primary, Riobello, Cristina, additional, Cabal, Virginia N., additional, García-Marín, Rocío, additional, Potes-Ares, Sira, additional, Suárez-Fernández, Laura, additional, Vivanco, Blanca, additional, Franchi, Alessandro, additional, Büttner, Reinhard, additional, López, Fernando, additional, and Llorente, José Luis, additional

Published
2019
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127. 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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128. 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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129. 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

130. 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

132. Genomic profiling of intestinal-type sinonasal adenocarcinoma reveals subgroups of patients with distinct clinical outcomes

Author

López-Hernández, Alejandro, primary, Pérez-Escuredo, Jhudit, additional, Vivanco, Blanca, additional, García-Inclán, Cristina, additional, Potes-Ares, Sira, additional, Cabal, Virginia N., additional, Riobello, Cristina, additional, Costales, María, additional, López, Fernando, additional, Llorente, José Luis, additional, and Hermsen, Mario A., additional

Published
2017
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136. 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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138. 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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140. Comparative Genomic Hybridisation in Pathology

Author

Weiss, Marjan M., primary, Hermsen, Mario A. J. A., additional, Snijders, Antoine, additional, Buerger, Horst, additional, Boecker, Werner, additional, Kuipers, Ernst J., additional, van Diest, Paul J., additional, and Meijer, Gerrit A., additional

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150. 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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