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  • 1
    Language: English
    In: International journal of cancer, 2017-06-15, Vol.140 (12), p.2748-2757
    Description: To determine the sensitivity and specificity of HPV16 serology as diagnostic marker for HPV16‐driven oropharyngeal squamous cell carcinoma (OPSCC), 214 HNSCC patients from Germany and Italy with fresh‐frozen tumor tissues and sera collected before treatment were included in this study. Hundred and twenty cancer cases were from the oropharynx and 94 were from head and neck cancer regions outside the oropharynx (45 oral cavity, 12 hypopharynx and 35 larynx). Serum antibodies to early (E1, E2, E6 and E7) and late (L1) HPV16 proteins were analyzed by multiplex serology and were compared to tumor HPV RNA status as the gold standard. A tumor was defined as HPV‐driven in the presence of HPV16 DNA and HPV16 transformation‐specific RNA transcript patterns (E6*I, E1∧E4 and E1C). Of 120 OPSCC, 66 (55%) were HPV16‐driven. HPV16 E6 seropositivity was the best predictor of HPV16‐driven OPSCC (diagnostic accuracy 97% [95%CI 92–99%], Cohen's kappa 0.93 [95%CI 0.8–1.0]). Of the 66 HPV‐driven OPSCC, 63 were HPV16 E6 seropositive, compared to only one (1.8%) among the 54 non‐HPV‐driven OPSCC, resulting in a sensitivity of 96% (95%CI 88–98) and a specificity of 98% (95%CI 90–100). Of 94 HNSCC outside the oropharynx, six (6%) were HPV16‐driven. In these patients, HPV16 E6 seropositivity had lower sensitivity (50%, 95%CI 19–81), but was highly specific (100%, 95%CI 96–100). In conclusion, HPV16 E6 seropositivity appears to be a highly reliable diagnostic marker for HPV16‐driven OPSCC with very high sensitivity and specificity, but might be less sensitive for HPV16‐driven HNSCC outside the oropharynx. What's new? Human papillomavirus (HPV) infection is associated with a subset of oropharyngeal squamous cell carcinomas (OPSCC). HPV‐driven OPSCC patients have an improved survival, but a reliable marker that is applicable in clinical operations is still needed. Here, the authors analyzed HPV16 antibody levels to the oncoproteins E6 and E7 and to the regulatory proteins E1 and E2 in the serum of patients with molecularly‐defined tumor HPV status. HPV16 serology could identify HPV‐driven OPSCC patients with very high sensitivity [96% (95%CI 88–98)] and specificity [98% (95%CI 90–100)]. HPV16 serology may thus represent a powerful and accurate diagnostic marker for HPV‐driven OPSCC.
    Subject(s): human papillomavirus ; serology ; diagnosis ; early proteins ; oropharynx ; biomarker ; head and neck squamous cell carcinoma ; Oropharyngeal Neoplasms - immunology ; Human papillomavirus 16 - physiology ; Carcinoma, Squamous Cell - virology ; Humans ; Middle Aged ; Male ; Human papillomavirus 16 - immunology ; Antibodies, Viral - blood ; Host-Pathogen Interactions - immunology ; Carcinoma, Squamous Cell - diagnosis ; Sensitivity and Specificity ; Aged, 80 and over ; Papillomavirus Infections - immunology ; Adult ; Female ; Oncogene Proteins, Viral - genetics ; Papillomavirus Infections - virology ; Oropharyngeal Neoplasms - diagnosis ; Repressor Proteins - genetics ; Oropharyngeal Neoplasms - virology ; Carcinoma, Squamous Cell - immunology ; Repressor Proteins - immunology ; Antibodies, Viral - immunology ; Aged ; Oncogene Proteins, Viral - immunology ; Human papillomavirus 16 - genetics ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: The lancet oncology, 2015, Vol.16 (15), p.e534-e542
    Description: Summary Immunotherapy is a promising area of therapy in patients with neuro-oncological malignancies. However, early-phase studies show unique challenges associated with the assessment of radiological changes in response to immunotherapy reflecting delayed responses or therapy-induced inflammation. Clinical benefit, including long-term survival and tumour regression, can still occur after initial disease progression or after the appearance of new lesions. Refinement of the response assessment criteria for patients with neuro-oncological malignancies undergoing immunotherapy is therefore warranted. Herein, a multinational and multidisciplinary panel of neuro-oncology immunotherapy experts describe immunotherapy Response Assessment for Neuro-Oncology (iRANO) criteria based on guidance for the determination of tumour progression outlined by the immune-related response criteria and the RANO working group. Among patients who demonstrate imaging findings meeting RANO criteria for progressive disease within 6 months of initiating immunotherapy, including the development of new lesions, confirmation of radiographic progression on follow-up imaging is recommended provided that the patient is not significantly worse clinically. The proposed criteria also include guidelines for the use of corticosteroids. We review the role of advanced imaging techniques and the role of measurement of clinical benefit endpoints including neurological and immunological functions. The iRANO guidelines put forth in this Review will evolve successively to improve their usefulness as further experience from immunotherapy trials in neuro-oncology accumulate.
    Subject(s): Hematology, Oncology and Palliative Medicine ; Nervous System Neoplasms - diagnosis ; Algorithms ; Humans ; Immunotherapy ; Nervous System Neoplasms - therapy ; Disease Progression ; Practice Guidelines as Topic ; Medicine, Experimental ; Medical research ; Index Medicus ; pseudoprogression ; vaccine ; magnetic resonance imaging ; immunotherapy ; immune checkpoint
    ISSN: 1470-2045
    E-ISSN: 1474-5488
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: The EMBO journal, 2018-08-01, Vol.37 (15), p.n/a
    Description: Glioblastoma is the most common and aggressive brain tumor, with a subpopulation of stem‐like cells thought to mediate its recurring behavior and therapeutic resistance. The epithelial–mesenchymal transition (EMT) inducing factor Zeb1 was linked to tumor initiation, invasion, and resistance to therapy in glioblastoma, but how Zeb1 functions at molecular level and what genes it regulates remain poorly understood. Contrary to the common view that EMT factors act as transcriptional repressors, here we show that genome‐wide binding of Zeb1 associates with both activation and repression of gene expression in glioblastoma stem‐like cells. Transcriptional repression requires direct DNA binding of Zeb1, while indirect recruitment to regulatory regions by the Wnt pathway effector Lef1 results in gene activation, independently of Wnt signaling. Amongst glioblastoma genes activated by Zeb1 are predicted mediators of tumor cell migration and invasion, including the guanine nucleotide exchange factor Prex1, whose elevated expression is predictive of shorter glioblastoma patient survival. Prex1 promotes invasiveness of glioblastoma cells in vivo highlighting the importance of Zeb1/Lef1 gene regulatory mechanisms in gliomagenesis. Synopsis Genome‐wide characterization of Zeb1 transcriptional targets in glioblastoma stem cells reveals how Zeb1 coordinately regulates an EMT‐like program, simultaneously promoting gene activation and repression via two different mechanisms. ChIP‐seq mapping correlates transcriptional repression with direct Zeb1 binding to gene regulatory regions. Indirect recruitment mediated by Lef/Tcf factors potentiates gene expression independent of Wnt signaling. Activated genes include regulators of cell migration and invasion that correlate with Zeb1 expression in tumors. Zeb1 activates Prex1 to promote glioblastoma cell invasion in vivo. Genome‐wide binding reveals that the EMT‐inducer Zeb1, best‐known as a transcriptional repressor, can team up with a transcriptional activator to indirectly enhance gene expression.
    Subject(s): cancer stem‐like cells ; Zeb1 ; glioblastoma multiforme ; Wnt signaling ; transcription ; Index Medicus ; Signal Transduction ; Cancer
    ISSN: 0261-4189
    E-ISSN: 1460-2075
    Source: HighWire Press (Free Journals)
    Source: PubMed Central
    Source: Alma/SFX Local Collection
    Source: EBSCOhost EJS
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 4
    Language: English
    In: International journal of cancer, 2020-03-01, Vol.146 (5), p.1281-1292
    Description: Tumor‐initiating cells are a subpopulation of cells that have self‐renewal capacity to regenerate a tumor. Here, we identify stem cell‐like chromatin features in human glioblastoma initiating cells (GICs) and link them to a loss of the repressive histone H3 lysine 9 trimethylation (H3K9me3) mark. Increasing H3K9me3 levels by histone demethylase inhibition led to cell death in GICs but not in their differentiated counterparts. The induction of apoptosis was accompanied by a loss of the activating H3 lysine 9 acetylation (H3K9ac) modification and accumulation of DNA damage and downregulation of DNA damage response genes. Upon knockdown of histone demethylases, KDM4C and KDM7A both differentiation and DNA damage were induced. Thus, the H3K9me3–H3K9ac equilibrium is crucial for GIC viability and represents a chromatin feature that can be exploited to specifically target this tumor subpopulation. What's new? Glioblastoma‐initiating cells (GICs) exhibit stem cell‐like properties, including the capacity for continuous self‐renewal. In this study, owing to the relevance of histone methylation and acetylation to DNA repair and self‐renewal in mouse and human embryonic stem cells, the authors investigated chromatin features in GICs. Analyses show that GICs possess an open chromatin structure, with enrichment of histone acetylation and reduced methylation. Inhibition of the histone demethylases KDM4C and KDM7A, leading to global restoration of H3K9me3 levels, reduced viability and induced differentiation in GICs. The findings suggest that selective targeting of histone demethylases is a promising strategy for eliminating GIC subpopulations.
    Subject(s): histone methylation ; cancer stem cells ; DNA repair ; histone acetylation ; heterochromatin ; Chromatin - metabolism ; Epigenesis, Genetic ; Humans ; Gene Expression Regulation, Neoplastic ; Apoptosis - genetics ; DNA Repair - genetics ; Jumonji Domain-Containing Histone Demethylases - genetics ; Promoter Regions, Genetic - genetics ; Gene Knockdown Techniques ; Cell Self Renewal - genetics ; Xenograft Model Antitumor Assays ; DNA Methylation ; Animals ; Glioblastoma - genetics ; Neoplastic Stem Cells - metabolism ; Glioblastoma - pathology ; HEK293 Cells ; Cell Line, Tumor ; Histones ; Lysine - metabolism ; Mice ; Acetylation ; Jumonji Domain-Containing Histone Demethylases - metabolism ; RNA, Small Interfering - metabolism ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 5
    Language: English
    In: International journal of cancer, 2014-12-01, Vol.135 (11), p.2727-2734
    Description: Proteoglycans are often overexpressed in tumors and can be found on several normal and neoplastic stem cells. In this study, we analyzed in‐depth the role of CSPG4 in head and neck squamous cell carcinomas (HNSCC). Analysis of CSPG4 in a homogeneous study sample of HPV‐negative stage IVa HNSCCs revealed overexpression of protein and mRNA levels in a subgroup of HNSCC tumors and a significant association of high CSPG4 protein levels with poor survival. This could be validated in three publicly available microarray datasets. As a potential cause for upregulated CSPG4 expression, we identified DNA hypomethylation in a CpG‐island of the promoter region. Accordingly, we found an inverse correlation of methylation and patient outcome. Finally, CSPG4 re‐expression was achieved by demethylating treatment of highly methylated HNSCC cell lines establishing a direct link between methylation and CSPG4 expression. In conclusion, we identified CSPG4 as a novel biomarker in HNSCC on several biological levels and established a causative link between DNA methylation and CSPG4 protein and mRNA expression. What's New? Head and neck squamous cell carcinoma (HNSCC) is a frequent cancer characterized by clinical and biological heterogeneity and poor disease outcome. Here, the authors examined the expression level of the stem cell‐associated proteoglycan CSPG4 as a potential novel biomarker in HNSCC. Studies were restricted to stage IVa tumors negative for human papilloma virus infection and showed increased expression of CSPG4 mRNA and protein expression accompanied by decreased promoter methylation. Promoter methylation was inversely correlated with disease outcome and could be reversed with demethylating agents, underscoring the therapeutic potential of CSPG4 targeting in the treatment of HNSCC patients.
    Subject(s): CSPG4 methylation and expression ; HNSCC ; survival ; Prognosis ; Chondroitin Sulfate Proteoglycans - genetics ; Follow-Up Studies ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Humans ; Gene Expression Regulation, Neoplastic ; Promoter Regions, Genetic - genetics ; Case-Control Studies ; Immunoenzyme Techniques ; Young Adult ; DNA Methylation ; Carcinoma, Squamous Cell - mortality ; Membrane Proteins - metabolism ; Tumor Cells, Cultured ; Real-Time Polymerase Chain Reaction ; Membrane Proteins - genetics ; RNA, Messenger - genetics ; Chondroitin Sulfate Proteoglycans - metabolism ; Survival Rate ; Reverse Transcriptase Polymerase Chain Reaction ; Head and Neck Neoplasms - pathology ; CpG Islands ; Head and Neck Neoplasms - genetics ; Head and Neck Neoplasms - mortality ; Neoplasm Staging ; Squamous cell carcinoma ; RNA ; Analysis ; Patient outcomes ; Stem cells ; Genetic research ; Methylation ; Papillomavirus infections ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 6
    Language: English
    In: Acta neurochirurgica, 2009-11, Vol.151 (11), p.1359-1365
    Description: The appropriate management of low-grade gliomas is still a matter of debate. So far, there are no randomized studies that analyze the impact of surgical resection on patient outcome. The value of the data obtained from the few retrospective reports available is often limited. In the present study, we performed an analysis on data of 130 adult low-grade glioma patients. Extent of the resection was evaluated in correlation to the overall survival (OS) and progression-free survival (PFS) using Cox regression multivariate analysis. Extended surgery was shown to prolong OS and PFS significantly. Re-surgery in the case of a tumor relapse has a significant impact on OS and PFS, too. In summary, we could retrospectively evaluate a large case series of well-defined low-grade gliomas patients with a long follow-up period showing that extended surgery would be the most effective therapy for low-grade glioma patients even in recurrent diseases.
    Subject(s): Prognosis ; Age Factors ; Humans ; Middle Aged ; Neoplasm Invasiveness - prevention & control ; Brain Neoplasms - pathology ; Neuronavigation ; Male ; Neoplasm Recurrence, Local - surgery ; Brain Neoplasms - surgery ; Young Adult ; Glioma - pathology ; Adult ; Female ; Retrospective Studies ; Brain Neoplasms - mortality ; Glioma - surgery ; Combined Modality Therapy - statistics & numerical data ; Monitoring, Intraoperative ; Neurosurgical Procedures - statistics & numerical data ; Glioma - mortality ; Neoplasm Recurrence, Local - prevention & control ; Survival Rate ; Treatment Outcome ; Radiotherapy - statistics & numerical data ; Preoperative Care ; Stereotaxic Techniques ; Neoplasm Invasiveness - physiopathology ; Magnetic Resonance Imaging ; Drug Therapy - methods ; Adolescent ; Radiotherapy - methods ; Aged ; Combined Modality Therapy - methods ; Neoplasm Recurrence, Local - epidemiology ; Neurosurgical Procedures - methods ; Drug Therapy - statistics & numerical data ; Care and treatment ; Gliomas ; Brain tumors ; Patient outcomes ; Analysis ; Oncology, Experimental ; Universities and colleges ; Research ; Cancer ; Index Medicus
    ISSN: 0001-6268
    E-ISSN: 0942-0940
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 7
    Language: English
    In: International journal of cancer, 2016-10-15, Vol.139 (8), p.1776-1787
    Description: In a previous study, Protein Kinase C iota (PRKCI) emerged as an important candidate gene for glioblastoma (GBM) stem‐like cell (GSC) survival. Here, we show that PKCι is overexpressed and activated in patient derived GSCs compared with normal neural stem cells and normal brain lysate, and that silencing of PRKCI in GSCs causes apoptosis, along with loss of clonogenicity and reduced proliferation. Notably, PRKCI silencing reduces tumor growth in vivo in a xenograft mouse model. PKCι has been intensively studied as a therapeutic target in non‐small cell lung cancer, resulting in the identification of an inhibitor, aurothiomalate (ATM), which disrupts the PKCι/ERK signaling axis. However, we show that, although sensitive to pharmacological inhibition via a pseudosubstrate peptide inhibitor, GSCs are much less sensitive to ATM, suggesting that PKCι acts along a different signaling axis in GSCs. Gene expression profiling of PRKCI‐silenced GSCs revealed a novel role of the Notch signaling pathway in PKCι mediated GSC survival. A proximity ligation assay showed that Notch1 and PKCι are in close proximity in GSCs. Targeting PKCι in the context of Notch signaling could be an effective way of attacking the GSC population in GBM. What's new? Increased understanding of gene expression patterns in glioblastoma (GBM) has led to the identification of genes involved in survival, among them protein kinase C iota (PRKCI). PRKCI is classified as an oncogene in several human cancer types. In this study, PRKCI was found to be overexpressed in patient‐derived GBM stem‐like cells (GSCs) and to play a crucial role in GSC survival through Notch signaling. Its silencing slowed tumor growth and prolonged survival in a xenograft GBM mouse model. The findings highlight the therapeutic promise of PKCι and its potential to provide a new avenue for GSC‐targeted GBM therapies.
    Subject(s): atypical protein kinase C iota ; glioblastoma ; notch signaling ; glioblastoma stem‐like cells ; Protein Kinase C - genetics ; Glioblastoma - enzymology ; Neoplastic Stem Cells - drug effects ; Receptors, Notch - metabolism ; Humans ; Brain Neoplasms - pathology ; Apoptosis - genetics ; Gene Expression Profiling ; Molecular Targeted Therapy ; Glioblastoma - genetics ; Isoenzymes - metabolism ; Protein Kinase C - metabolism ; HEK293 Cells ; Neoplastic Stem Cells - pathology ; Brain Neoplasms - enzymology ; Isoenzymes - genetics ; Gene Silencing ; Neural Stem Cells - drug effects ; Brain Neoplasms - genetics ; Protein Kinase C - antagonists & inhibitors ; Brain Neoplasms - drug therapy ; Mice, SCID ; Neural Stem Cells - enzymology ; Neural Stem Cells - pathology ; Animals ; Glioblastoma - pathology ; Protein Kinase C - biosynthesis ; Mice, Inbred NOD ; Mice ; Protein Kinase Inhibitors - pharmacology ; Enzyme Activation ; Glioblastoma - drug therapy ; Isoenzymes - biosynthesis ; Neoplastic Stem Cells - enzymology ; Isoenzymes - antagonists & inhibitors ; Analysis ; Stem cells ; Automated teller machines ; Lung cancer, Non-small cell ; Gene expression ; Glioblastoma multiforme ; Protein kinases ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 8
    Language: English
    In: Genes chromosomes & cancer, 2019-06, Vol.58 (6), p.392-395
    Description: Chromosomal instability is one of the hallmarks of cancer and caused by chromosome missegregation during mitosis, a process frequently associated with micronucleus formation. Micronuclei are formed when chromosomes fail to join a daughter nucleus during cell division and are surrounded by their own nuclear membrane. Although it has been commonly assumed that the gain or loss of specific chromosomes is random during compromised cell division, recent data suggest that the size of chromosomes can impact on chromosome segregation fidelity. To test whether chromosome missegregation rates scale with chromosome size in primary human cancer cells, we assessed chromosome sequestration into micronuclei in patient‐derived primary NCH149 glioblastoma cells, which display high‐level numerical chromosome instability (CIN), pronounced spontaneous micronucleus formation but virtually no structural CIN. The cells were analyzed by interphase fluorescence in situ hybridization using chromosome‐specific painting probes for all chromosomes. Overall, 33% of early passage NCH149 cells harbored micronuclei. Entrapment within a micronucleus clearly correlated with chromosome size with larger chromosomes being significantly more frequently missegregated into micronuclei than smaller chromosomes in primary glioblastoma cells. These findings extend the concept that chromosome size determines segregation fidelity by implying that size‐specific micronucleus entrapment occurs in primary human cancer cells as well.
    Subject(s): micronucleus ; cancer cells ; size ; chromosome ; Medical research ; Gliomas ; Analysis ; Cancer cells ; Genetic research ; Medicine, Experimental ; Genetic aspects ; Chromosomes ; Cancer ; Index Medicus
    ISSN: 1045-2257
    E-ISSN: 1098-2264
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 9
    Language: English
    In: The Journal of pathology, 2014-09, Vol.234 (1), p.23-33
    Description: Cancer cells with enhanced self‐renewal capacity influence tumour growth in glioblastoma. So far, a variety of surrogate markers have been proposed to enrich these cells, emphasizing the need to devise new characterization methods. Here, we screen a large panel of glioblastoma cultures (n = 21) cultivated under stem cell‐permissive conditions and identify several cell lines with enhanced self‐renewal capacity. These cell lines are capable of matrix‐independent growth and form fast‐growing, orthotopic tumours in mice. Employing isolation, re‐plating, and label‐retention techniques, we show that self‐renewal potential of individual cells is partitioned asymmetrically between daughter cells in a robust and cell line‐specific fashion. This yields populations of fast‐ and slow‐cycling cells, which differ in the expression of cell cycle‐associated transcripts. Intriguingly, fast‐growing cells keep their slow‐cycling counterparts in a reversible state of quiescence associated with high chemoresistance. Our results suggest that two different subpopulations of tumour cells contribute to aberrant growth and tumour recurrence after therapy in glioblastoma. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Subject(s): self‐renewal; glioblastoma; label retention; quiescence ; Gene Dosage - genetics ; Cell Proliferation ; Oligonucleotide Array Sequence Analysis ; Humans ; Brain Neoplasms - pathology ; Gene Expression Profiling ; Brain Neoplasms - metabolism ; Neoplasm Recurrence, Local - pathology ; Animals ; Comparative Genomic Hybridization ; Neoplastic Stem Cells - metabolism ; Glioblastoma - pathology ; Cell Line, Tumor ; Neoplastic Stem Cells - pathology ; Glioblastoma - metabolism ; Mice ; Disease Models, Animal ; Glioblastoma multiforme ; Analysis ; Stem cells ; Index Medicus
    ISSN: 0022-3417
    E-ISSN: 1096-9896
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Language: English
    In: Neuropathology and applied neurobiology, 2015-10, Vol.41 (6), p.733-742
    Description: Aims The differential diagnosis of cystic epithelial masses of the sellar region, especially the histopathological differentiation of craniopharyngiomas and Rathke's cleft cysts, poses a challenge even to experienced diagnosticians. Recently, BRAF V600E mutations have been described as a genetic hallmark of papillary craniopharyngiomas. We investigated a series of 33 Rathke's cleft cysts to determine the frequency of BRAF V600E mutations and its suitability as an additional diagnostic marker for the differentiation of cystic lesions of the sellar region. Methods Thirty‐three Rathke's cleft cysts and 18 papillary craniopharyngiomas were analysed for BRAF mutational status by immunohistochemistry using a monoclonal antibody (VE1) that selectively recognizes the BRAF V600E mutant epitope and additional BRAF pyrosequencing in a subset of samples. Results Thirty of 33 specimens diagnosed as Rathke's cleft cysts were negative by VE1 immunohistochemistry and pyrosequencing, whereas in three cysts and in all the 18 papillary craniopharyngiomas, a BRAF V600E mutation was detected. Clinical and histological re‐evaluation of the three BRAF V600E mutated cases formerly diagnosed as Rathke's cleft cysts revealed unusual presentations. Two of them were rediagnosed as papillary craniopharyngiomas. The patient of the third case had a history of craniopharyngioma operated 14 years before, and reoperation showed a cystic epithelial lesion with unclear histology. Conclusions The determination of BRAF mutational status is recommended in any cystic sellar lesion and can in most cases be provided by VE1 immunohistochemistry even in specimens of low cellularity. Confirmation by (pyro‐)sequencing should be attempted whenever sufficient epithelium is available due to variable staining results. BRAF V600E mutation, a marker of papillary craniopharyngioma, can distinguish this cystic lesion from Rathke's cleft cyst.
    Subject(s): VE1 immunohistochemistry ; pyrosequencing ; papillary craniopharyngioma ; Rathke's cleft cysts ; BRAF V600E mutation ; Diagnosis, Differential ; Craniopharyngioma - pathology ; Humans ; Middle Aged ; Male ; Antibodies, Monoclonal ; Central Nervous System Cysts - pathology ; Central Nervous System Cysts - genetics ; Young Adult ; Craniopharyngioma - genetics ; Proto-Oncogene Proteins B-raf - genetics ; Proto-Oncogene Proteins B-raf - immunology ; Adult ; Female ; Aged ; Mutation ; Immunohistochemistry ; Monoclonal antibodies ; Cysts ; Gene mutations ; Analysis ; Antigenic determinants ; Index Medicus
    ISSN: 0305-1846
    E-ISSN: 1365-2990
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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