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Your search keyword '"Hegi, Monika"' showing total 55 results
Start Over Author "Hegi, Monika" Publisher oxford university press / usa
55 results on '"Hegi, Monika"'

2. Molecular diagnostic tools for the World Health Organization (WHO) 2021 classification of gliomas, glioneuronal and neuronal tumors; an EANO guideline.

Author

Sahm, Felix, Brandner, Sebastian, Bertero, Luca, Capper, David, French, Pim J, Figarella-Branger, Dominique, Giangaspero, Felice, Haberler, Christine, Hegi, Monika E, Kristensen, Bjarne W, Kurian, Kathreena M, Preusser, Matthias, Tops, Bastiaan B J, van den Bent, Martin, Wick, Wolfgang, Reifenberger, Guido, and Wesseling, Pieter

Published
2023
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3. EANO guideline on rational molecular testing of gliomas, glioneuronal, and neuronal tumors in adults for targeted therapy selection.

Author

Capper, David, Reifenberger, Guido, French, Pim J, Schweizer, Leonille, Weller, Michael, Touat, Mehdi, Niclou, Simone P, Euskirchen, Philipp, Haberler, Christine, Hegi, Monika E, Brandner, Sebastian, Rhun, Emilie Le, Rudà, Roberta, Sanson, Marc, Tabatabai, Ghazaleh, Sahm, Felix, Wen, Patrick Y, Wesseling, Pieter, Preusser, Matthias, and Bent, Martin J van den

Published
2023
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4. Towards more Diversity in Neuro-oncology Leadership—the DivINe Initiative.

Author

Kurz, Sylvia C, Stammberger, Anja, Rosahl, Steffen K, Abrey, Lauren E, Albert, Nathalie L, Baumgarten, Louisa von, Gempt, Jens, Grosu, Anca-L, Leidgens, Verena, McLean, Anna, Renovanz, Mirjam, Schwarzenberger, Julia, Sevenich, Lisa, Purkart, Tadeja Urbanic, Combs, Stephanie E, Tabatabai, Ghazaleh, Hegi, Monika, and Nowosielski, Martha

Published
2023
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7. Glioblastoma in adults: a Society for Neuro-Oncology (SNO) and European Society of Neuro-Oncology (EANO) consensus review on current management and future directions.

Author

Wen, Patrick Y, Weller, Michael, Lee, Eudocia Quant, Alexander, Brian M, Barnholtz-Sloan, Jill S, Barthel, Floris P, Batchelor, Tracy T, Bindra, Ranjit S, Chang, Susan M, Chiocca, E Antonio, Cloughesy, Timothy F, DeGroot, John F, Galanis, Evanthia, Gilbert, Mark R, Hegi, Monika E, Horbinski, Craig, Huang, Raymond Y, Lassman, Andrew B, Rhun, Emilie Le, and Lim, Michael

Published
2020
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14. Is more better? The impact of extended adjuvant temozolomide in newly diagnosed glioblastoma: a secondary analysis of EORTC and NRG Oncology/RTOG.

Author

Blumenthal, Deborah T., Gorlia, Thierry, Gilbert, Mark R., Kim, Michelle M., Nabors, L. Burt, Mason, Warren P., Hegi, Monika E., Zhang, Peixin, Golfinopoulos, Vassilis, Perry, James R., Nam, Do Hyun, Erridge, Sara C., Corn, Benjamin W., Mirimanoff, René O., Brown, Paul D., Baumert, Brigitta G., Mehta, Minesh P., van den Bent, Martin J., Reardon, David A., and Weller, Michael

Published
2017
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23. Two cilengitide regimens in combination with standard treatment for patients with newly diagnosed glioblastoma and unmethylated MGMT gene promoter: results of the open-label, controlled, randomized phase II CORE study.

Author

Nabors, L. Burt, Fink, Karen L., Mikkelsen, Tom, Grujicic, Danica, Tarnawski, Rafal, Do Hyun Nam, Mazurkiewicz, Maria, Salacz, Michael, Ashby, Lynn, Zagonel, Vittorina, Depenni, Roberta, Perry, James R., Hicking, Christine, Picard, Martin, Hegi, Monika E., Lhermitte, Benoit, and Reardon, David A.

Published
2015
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40. Characterization of p53 mutations in methylene chloride-induced lung tumors from B6C3F1 mice.

Author

Hegi, Monika E., Söderkvist, Peter, Foley, Julie F., Schoonhoven, Robert, Swenberg, James A., Kari, Frank, Maronpot, Robert, Anderson, Marshall W., and Wiseman, Roger W.

Abstract

Mutations of the tumor suppressor gene are the most common defined genetic alterations seen in a wide variety of human cancers. In contrast, little is known about the importance of the gene in chemically induced tumors of rodents, which are widely used as models for the evaluation of human health risks. In this study we examined 54 methylene chloride-induced and seven spontaneously arising lung tumors from female B6C3F1 mice for losses of heterozygosity (LOH) at markers near the gene on chromosome 11. LOH was detected in seven methylene chloride-induced lung carcinomas by Southern analysis of a restriction fragment length polymorphism and PCR analysis of five simple sequence length polymorphisms. In each case allele loss was observed at all six markers; thus, these chromosomal alterations were likely to have resulted from mitotic nondisjunction. In contrast, LOH was not detected in 20 liver tumors from methylene chloride-treated mice at the locus, which is tightly linked to the gene on chromosome 11. In addition single strand conformation polymorphism analysis was performed to screen for mutations in the most conserved regions of the gene (exons 5 to 8). Consequently, potential mutations identified by direct sequencing, were only detected in four of the seven tumor samples with LOH, but not in any of the remaining lung tumors. Overexpression of the protein by immuno-histochemical staining was detected only in the four tumors that contained point mutations and in a focal area of another tumor. Finally, using a simple sequence length polymorphism within the retinoblastoma tumor suppressor gene, LOH on mouse chromosome 14 was also detected in three lung carcinomas and one liver tumor. Inactivation of and possibly the retinoblastoma tumor suppressor gene appear to be infrequent events in lung and liver tumors from methylene chloride treated mice. [ABSTRACT FROM PUBLISHER]

Published
1993

41. Analysis of activated protooncogenes in B6C3F1 mouse liver tumors induced by ciprofibrate, a potent peroxisome proliferator.

Author

Hegi, Monika E., Fox, Tony R., Belinsky, Steven A., Devereux, Theodora R., and Anderson, Marshall W.

Abstract

Liver tumors from B6C3F1 mice induced by the potent peroxisome proliferator ciprofibrate, a hypolipidemic drug, were evaluated for the presence of transforming genes by the nude mouse tumorigenicity assay. As reported earlier, the tumors were not activated by a point mutation in codon 61 of H-. Two of the eight tumors examined contained a mutation in codon 13 or an H- gene mutated in codon 117. Screening of another 23 ciprofibrate-induced liver tumors by oligonucleotide hybridization analysis and direct DNA sequencing resulted in the identification of three tumor DNA samples with point mutations in codon 117 of the H- gene. In addition, another tumor sample contained a K- gene with a mutation in codon 61. Mutations in these codons have been seen only rarely in chemically induced liver tumors from this mouse strain. Of 15 spontaneous B6C3F1 liver tumors screened in the same manner, one exhibited a K- gene activated by a mutation in codon 13 and a second contained an H- gene activated by a mutation in codon 117. These gene mutations have not been reported previously from spontaneous liver tumors. The frequency and spectrum of oncogene mutations characterized in ciprofibrate-induced liver tumors differ significantly from the frequency and pattern identified in spontaneously occurring liver tumors. The results of this study with a limited number of samples suggest that protooncogene activation or activation of other protooncogenes that can be detected by the nude mouse tumorigenicity assay are not frequent events in the mechanism of carcinogenicity of the peroxisome proliferator ciprofibrate. However, the lower frequency and distinct pattern of H- mutations observed in these tumors disprove the assumption of promotion of spontaneous hepatocarcinogenesis by ciprofibrate. [ABSTRACT FROM PUBLISHER]

Published
1993

42. Detection by P-postlabeling of thymidine glycol in γ-irradiated DNA.

Author

Hegi, Monika E., Sagelsdorff, Peter, and Lutz, Werner K.

Abstract

The P-postlabeling method has been adapted for the analysis of thymidine--glycol-3′-phosphate (-dTGp, -5,6-dihydroxy-5,6-dihydrothymidine-3′-phosphate). -dTGp was isolated and purified from normal nucleotides by phenylboronate affinity chromatography and phosphorylated by T4 polynucleotide kinase in presence of 1 mM BeCl at pH 7.5. These modifications of the postlabeling method resulted in a 5′-phosphorylation of dTGp with a labeling efficiency of up to 20% whereas the natural nucleotides were almost completely dephosphorylated at the 3′ position under these conditions. The reaction products, containing radio-labeled thymidine--glycol-3′ ,5′-bis-[5′-P]phosphate (-pdTGp), were separated by two-dimensional anion-exchange TLC on polyethyleneimine cellulose sheets. Boric acid was added in the second dimension in order to selectively retard -glycols. The method was applied to γ-irradiated nucleotides and calf thymus DNA. In the nucleotide mixture, 330–99 000 thymine glycol (TG) moieties were detected per 10 thymines (T) in a dose range of 14–1000 Gy respectively. In DNA, these values ranged from 400 to 2700 TG/10 T. The data are in good agreement with methods using radiochemical and immunological techniques. Non-irradiated DNA showed a background level of 1OTG/10 T. This practical limit of detection was higher than can be achieved with the postlabeling technique, indicating that the present method might be a sensitive alternative for a determination of oxidative DNA damage. [ABSTRACT FROM PUBLISHER]

Published
1989

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