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114 results on '"Eigenbrod S"'

3. MRI and clinical syndrome in dura materrelated Creutzfeldt-Jakob disease

Author

Meissner, B., Kallenberg, K., Sanchez-Juan, P., Ramljak, S., Krasnianski, A., Heinemann, U., Eigenbrod, S., Gelpi, E., Barsic, B., Kretzschmar, H., Schulz-Schaeffer, W., Knauth, M., Zerr, I., Meissner, B., Kallenberg, K., Sanchez-Juan, P., Ramljak, S., Krasnianski, A., Heinemann, U., Eigenbrod, S., Gelpi, E., Barsic, B., Kretzschmar, H., Schulz-Schaeffer, W., Knauth, M., and Zerr, I.

Abstract

Objective : Iatrogenic Creutzfeldt-Jakob disease (iCJD) is mainly associated with dura mater (DM) grafts and administration of human growth hormones (hGH). Data on disease course in DM-CJD are limited. We describe the clinical and diagnostic findings in this patient group with special emphasis on MRI signal alterations. Methods : Ten DM-CJD patients were studied for their clinical symptoms and diagnostic findings. The MRIs were evaluated for signal increase of the cortical and subcortical structures. Results : DM-CJD patients had a median incubation time of 18 years and median disease duration of 7 months. The majority of patients were MM homozygous at codon 129 of the prion protein gene (PRNP) and presented with gait ataxia and psychiatric symptoms. No correlation between the graft site and the initial disease course was found. The MRI showed cortical and basal ganglia signal increase each in eight out of ten patients and thalamic hyperintensity in five out of ten cases. Of interest, patients with thalamic signal increase were homozygous for methionine. Conclusion : The MRI findings in DM-CJD largely resemble those seen in sporadic CJD, as the cortex and basal ganglia are mainly affected

Published
2018

5. Quantifying prion disease penetrance using large population control cohorts

Author

Minikel, E.V. (Eric Vallabh), Vallabh, S.M. (Sonia M.), Lek, M. (Monkol), Estrada Gil, K. (Karol), Samocha, K.E. (Kaitlin E.), Sathirapongsasuti, J.F. (J. Fah), McLean, C.Y. (Cory Y.), Tung, J.Y. (Joyce Y.), Yu, L.P.C. (Linda P. C.), Gambetti, P. (Pierluigi), Blevins, J. (Janis), Zhang, S. (Shulin), Cohen, Y. (Yvonne), Chen, W. (Wei), Yamada, M., Hamaguchi, T. (Tsuyoshi), Sanjo, N. (Nobuo), Mizusawa, H. (Hidehiro), Nakamura, Y. (Yosikazu), Kitamoto, T. (Tetsuyuki), Collins, S.J. (Steven), Boyd, A. (Alison), Will, R.G. (Robert G.), Knight, R. (Richard), Ponto, C. (Claudia), Zerr, I. (Inga), Kraus, T.F.J. (Theo F.J.), Eigenbrod, S. (Sabina), Giese, A. (Armin), Calero, M. (Miguel), Pedro-Cuesta, J. (Jesús) de, Haik, S., Laplanche, J.-L. (Jean-Louis), Bouaziz-Amar, E. (Elodie), Brandel, J-P. (Jean-Philippe), Capellari, S. (Sabina), Parchi, P. (Piero), Poleggi, A. (Anna), Ladogana, A. (Anna), O'Donnell-Luria, A.H. (Anne H.), Karczewski, K.J. (Konrad), Marshall, J.L. (Jamie L.), Boehnke, M. (Michael), Laakso, M. (Markku), Mohlke, K.L. (Karen), Kähler, J. (Jan), Chambert, K. (Kimberly), McCarroll, S.A. (Steven), Sullivan, P.F. (Patrick F.), Hultman, C.M. (Christina), Purcell, S. (Shaun), Sklar, P. (Pamela), Lee, S.J. (Sven) van der, Rozemuller, A.J.M. (Annemieke), Jansen, C. (Casper), Hofman, A. (Albert), Kraaij, R. (Robert), Rooij, J.G.J. (Jeroen) van, Ikram, M.A. (Arfan), Uitterlinden, A.G. (André), Duijn, C.M. (Cornelia) van, Daly, M.J. (Mark), MacArthur, D.G. (Daniel G.), Minikel, E.V. (Eric Vallabh), Vallabh, S.M. (Sonia M.), Lek, M. (Monkol), Estrada Gil, K. (Karol), Samocha, K.E. (Kaitlin E.), Sathirapongsasuti, J.F. (J. Fah), McLean, C.Y. (Cory Y.), Tung, J.Y. (Joyce Y.), Yu, L.P.C. (Linda P. C.), Gambetti, P. (Pierluigi), Blevins, J. (Janis), Zhang, S. (Shulin), Cohen, Y. (Yvonne), Chen, W. (Wei), Yamada, M., Hamaguchi, T. (Tsuyoshi), Sanjo, N. (Nobuo), Mizusawa, H. (Hidehiro), Nakamura, Y. (Yosikazu), Kitamoto, T. (Tetsuyuki), Collins, S.J. (Steven), Boyd, A. (Alison), Will, R.G. (Robert G.), Knight, R. (Richard), Ponto, C. (Claudia), Zerr, I. (Inga), Kraus, T.F.J. (Theo F.J.), Eigenbrod, S. (Sabina), Giese, A. (Armin), Calero, M. (Miguel), Pedro-Cuesta, J. (Jesús) de, Haik, S., Laplanche, J.-L. (Jean-Louis), Bouaziz-Amar, E. (Elodie), Brandel, J-P. (Jean-Philippe), Capellari, S. (Sabina), Parchi, P. (Piero), Poleggi, A. (Anna), Ladogana, A. (Anna), O'Donnell-Luria, A.H. (Anne H.), Karczewski, K.J. (Konrad), Marshall, J.L. (Jamie L.), Boehnke, M. (Michael), Laakso, M. (Markku), Mohlke, K.L. (Karen), Kähler, J. (Jan), Chambert, K. (Kimberly), McCarroll, S.A. (Steven), Sullivan, P.F. (Patrick F.), Hultman, C.M. (Christina), Purcell, S. (Shaun), Sklar, P. (Pamela), Lee, S.J. (Sven) van der, Rozemuller, A.J.M. (Annemieke), Jansen, C. (Casper), Hofman, A. (Albert), Kraaij, R. (Robert), Rooij, J.G.J. (Jeroen) van, Ikram, M.A. (Arfan), Uitterlinden, A.G. (André), Duijn, C.M. (Cornelia) van, Daly, M.J. (Mark), and MacArthur, D.G. (Daniel G.)

Abstract

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Published
2016
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6. Integrin alpha v beta 3 (αvβ3) expression and MGMT promoter methylation in patients with glioblastoma

Author

Schnell, O, Pfirrmann, D, Albrecht, V, Eigenbrod, S, Tonn, JC, and Schichor, C

Subjects
MGMT promoter methylation, ddc: 610, Integrin alpha v beta 3, glioblastomas, 610 Medical sciences, Medicine, neoplasms, nervous system diseases
Abstract

Objective: Integrin alpha v beta 3 (αvβ3) is important for invasive tumor growth and angiogenesis in glioblastomas (GBM). In GBM patients with hypermethylation of the MGMT promoter, clinical studies have demonstrated a better prognosis when integrin-inhibitors were added to concommittant[for full text, please go to the a.m. URL], 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)

Published
2013
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7. Male gender is a risk factor for the clinical course of skull-base chordomas

Author

Rachinger, W, Simon, M, Dützmann, S, Feigl, G, Kremenevskaya, G,N, and Eigenbrod, S

Subjects
ddc: 610, skull base, gender, 610 Medical sciences, Medicine, chordoma
Abstract

Objective: Chordomas of the skull base are rare, locally invasive and have a poor prognosis. Aim of this retrospective multicentric study was to evaluate patterns of care, clinical course and prognostic factors of patients initially treated with open tumor resection. The prognostic influence of transmembrane[for full text, please go to the a.m. URL], 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)

Published
2013
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8. ALDH1A1 as a molecular marker with better prognosis for glioblastoma patients

Author

Schnell, O., Adam, S.A., Eigenbrod, S., Kretzschmar, H.A., Tonn, J.C., and Schüller, U.

Subjects
gliomas, Molekulare Marker, molecular markers, ddc: 610, 610 Medical sciences, Medicine, ALDH1A1, Gliome
Abstract

Objective: Aldehyde dehydrogenase 1A1 (ALDH1A1) has been identified in a variety of human cancers to be expressed by tumor cells and to serve as a reliable marker to predict patients clinical outcome. However, little is known so far about the function of ALDH1A1 in malignant brain tumors. Methods:[for full text, please go to the a.m. URL], 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS)

Published
2012

9. Cystic craniopharyngiomas: Microsurgical or stereotactic treatment?

Author

Rachinger, W., Kunz, M., Eigenbrod, S., Lutz, J., Tonn, J.C., and Kreth, F.W.

Subjects
Craniopharyngioma, ddc: 610, Mikrochirurgie, stereotactical, 610 Medical sciences, Medicine, microsurgical, Kraniopharyngeome, Stereotaxie
Abstract

Objective: The value of microsurgical and stereotactic treatment particularly in predominantly cystic craniopharyngiomas is poorly defined. We present the outcome data in terms of functional results and progression free survival (PFS) after individualized treatment strategies: Solid tumors were considered[for full text, please go to the a.m. URL], 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS)

Published
2012
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10. Spinal pilomyxoid astrocytoma developing a LOH 1p19q and cerebral metastasis

Author

Eigenbrod, S, Thon, N, Jansen, N, Janssen, H, Mielke, J, Ruiter, M, la Fougère, C, Peraud, A, Egensperger, R, and Kretzschmar, H

Subjects
ddc: 610, 610 Medical sciences, Medicine, nervous system diseases
Abstract

Background: Spinal glioma are rare and their biological behavior can differ from their cerebral counterparts. Pilomyxoid astrocytoma (PMA, WHO °II) typically occur in the hypothalamic/chiasmatic region of children. The few reported cases of pediatric spinal PMA displayed a particularly aggressive[for full text, please go to the a.m. URL], 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

Published
2012
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11. Tumor epigenetics: 5-Hydroxymethylcytosine in the human glioblastoma

Author

Kraus, T, Widmann, D, Greiner, A, Kolck, G, Eigenbrod, S, Globisch, D, Wagner, M, Carell, T, and Kretzschmar, H

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

The study of epigenetic changes that affect gene expression patterns seems of increasing importance during stem cell differentiation, ageing and tumorigenesis. Only 3 years ago a new modification has been found: 5-Hydroxymethylcytosine (5hmC). For a long time 5-methylcytosine (5mC) seemed to be the [for full text, please go to the a.m. URL], 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

Published
2012
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12. Unfavourable prognostic influence of IDH1 mutations in WHO Grade II astrocytomas turns into favourable predictive impact after malignant transformation

Author

Thon, N., Eigenbrod, S., Kreth, S., Lutz, J., Tonn, J.-C., Kretzschmar, H., Peraud, A., and Kreth, F.-W.

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Objective: The favourable impact of isocitrate dehydrogenases 1 (IDH1) mutations is well documented for malignant gliomas. Its influence on WHO grade II gliomas, however, remains unclear. Methods: IDH1 codon 132 pyrosequencing was performed in a mainly surgically treated series of 159 adult patients[for full text, please go to the a.m. URL], 62. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Polnischen Gesellschaft für Neurochirurgen (PNCH)

Published
2011

13. Biological tumor volume in 18FET-PET before radiochemotherapy correlates with survival in GBM

Author

Suchorska, B, Jansen, N L, Linn, J, Kretzschmar, H, Janssen, H, Eigenbrod, S, Simon, M, Pöpperl, G, Kreth, F W, la Fougere, C, Weller, M, Tonn, J C, Suchorska, B, Jansen, N L, Linn, J, Kretzschmar, H, Janssen, H, Eigenbrod, S, Simon, M, Pöpperl, G, Kreth, F W, la Fougere, C, Weller, M, and Tonn, J C

Abstract

OBJECTIVE The aim of this prospective longitudinal study was to identify static and dynamic O-(2-[(18)F]fluoroethyl)-l-tyrosine PET ((18)FET-PET)-derived imaging biomarkers in patients with glioblastoma (GBM). METHODS Seventy-nine patients with newly diagnosed GBM were included; 42 patients underwent stereotactic biopsy (unresectable tumors) and 37 patients microsurgical tumor resection. All patients were scheduled to receive radiotherapy plus concomitant and adjuvant temozolomide (RCx/TMZ). (18)FET-PET evaluation using static and dynamic analysis was done before biopsy/resection, after resection, 4 to 6 weeks following RCx, and after 3 cycles of TMZ. Endpoints were survival and progression-free-survival. Prognostic factors were obtained from proportional hazards models. RESULTS Biological tumor volume before RCx (BTVpreRCx) was the most important (18)FET-PET-derived imaging biomarker and was independent of MGMT promoter methylation and clinical prognostic factors: patients with smaller BTVpreRCx had significantly longer progression-free and overall survival (OS). (18)FET time-activity curves (TACs) before treatment and their changes after RCx were also related to outcome; patients with initially increasing TACs experienced longer OS. CONCLUSION BTVpreRCx and TAC represent important (18)FET-PET-derived imaging biomarkers in GBM. Increasing TACs are associated with prolonged OS. The BTVpreRCx is a strong prognostic factor for progression-free survival and OS independent of the mode of surgery. Our data furthermore suggest that patients harboring resectable GBM might benefit from maximal PET-guided tumor resection.

Published
2015

15. MGMT mRNA expression predicts clinical outcome in malignant glioma after radiotherapy and/or chemotherapy independent of MGMT promoter methylation

Author

Thon, N, Kreth, S, Eigenbrod, S, Kretzschmar, H, Tonn, JC, and Kreth, FW

Subjects
ddc: 610, 610 Medical sciences, Medicine, neoplasms
Abstract

Objective: Epigenetic silencing of the gene that encodes for O6-Methylguanine-DNA-methyltransferase (MGMT) has been correlated with favourable clinical outcome in patients with malignant gliomas after radio-/chemotherapy using alkylating agents such as temozolomide; It has been hypothesized that[for full text, please go to the a.m. URL], 61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010

Published
2010
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16. MGMT methylation status remains unchanged in recurrent malignant gliomas after radio-/chemotherapy

Author

Thon, N., Eigenbrod, S., Tonn, J.-C., and Kreth, F.-W.

Subjects
ddc: 610, 610 Medical sciences, Medicine, neoplasms
Abstract

Objective: Epigenetic silencing of the MGMT DNA-repair gene has been linked to a favourable prognosis in de-novo malignant gliomas treated with alkylating agents. In patients with recurrent tumors after radio-/chemotherapy, it has been hypothesized that tumor progression might be correlated with[for full text, please go to the a.m. URL], 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien

Published
2009

17. Prognostic relevance of MGMT promoter hypermethylation as demonstrated in serial stereotactic specimens from glioblastomas after primary concomitant radiochemo-therapy followed by adjuvant temozolomide

Author

Thon, N, Eigenbrod, S, Egensperger, R, Kretzschmar, H, Lutz, J, Tonn, JC, and Kreth, FW

Subjects
ddc: 610, 610 Medical sciences, Medicine, neoplasms
Abstract

Objective: Epigenetic silencing of the MGMT gene has been linked to favorable prognosis in glioblastomas (GBM) after treatment according to the EORTC protocol even when stratified for the extent of surgery except for patients who undergo biopsy only. Aim of this study was to evaluate the prognostic [for full text, please go to the a.m. URL], 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien

Published
2009
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18. RESULTS OF THE INTERNATIONAL INTERLABORATORY COMPARISON OF MGMT PROMOTER METHYLATION ANALYSIS INVOLVING TWENTY-THREE ACADEMIC CENTERS IN GERMANY, AUSTRIA AND THE NETHERLANDS

Author

Reifenberger, G., primary, Malzkorn, B., additional, Acker, T., additional, Bettstetter, M., additional, Buslei, R., additional, von Deimling, A., additional, Dietmaier, W., additional, Dubbink, H. J., additional, Eigenbrod, S., additional, Garvalov, B. K., additional, Gerstenmaier, U., additional, Giese, A., additional, Haase, D., additional, Hasselblatt, M., additional, Kirches, E., additional, Koch, A., additional, Marienfeld, R., additional, Mittelbronn, M., additional, Montesinos-Rongen, M., additional, Pagenstecher, A., additional, Riemenschneider, M. J., additional, Prinz, M., additional, Romeike, B., additional, Roos, A., additional, Spiegl-Kreinecker, S., additional, Schittenhelm, J., additional, Schlegel, J., additional, Thal, D. R., additional, Tops, B. B. J., additional, Weis, J., additional, Westphal, G., additional, Worm, K., additional, and Felsberg, J., additional

Published
2014
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24. Prediction of oligodendroglial histology and LOH 1p/19q using dynamic [18F]FET-PET imaging in intracranial WHO grade II and III gliomas

Author

Jansen, N. L., primary, Schwartz, C., additional, Graute, V., additional, Eigenbrod, S., additional, Lutz, J., additional, Egensperger, R., additional, Popperl, G., additional, Kretzschmar, H. A., additional, Cumming, P., additional, Bartenstein, P., additional, Tonn, J.-C., additional, Kreth, F.-W., additional, la Fougere, C., additional, and Thon, N., additional

Published
2012
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25. NEUROSURGICAL TREATMENTS

Author

Nanney, A. D., primary, Adel, J. G., additional, Smith, T. R., additional, Chandler, J. P., additional, Kimmell, K. T., additional, Walter, K., additional, Zacharia, B. E., additional, Deibert, C., additional, Malone, H. R., additional, Sonabend, A. M., additional, Neugut, A. I., additional, Spencer, B., additional, Bruce, J. N., additional, Wang, Y., additional, Li, S., additional, Zhang, Z., additional, Chen, X., additional, You, G., additional, Yang, P., additional, Yan, W., additional, Bao, Z., additional, Yao, K., additional, Liu, Y., additional, Wang, L., additional, Jiang, T., additional, Farhoud, M. K., additional, Ruge, M. I., additional, Brandes, A. A., additional, Ermani, M., additional, Fioravanti, A., additional, Andreoli, A., additional, Pozzati, E., additional, Bacci, A., additional, Bartolini, S., additional, Poggi, R., additional, Crisi, G., additional, Franceschi, E., additional, Recinos, P. F., additional, Grabowski, M. M., additional, Nowacki, A. S., additional, Thompson, N., additional, Vogelbaum, M. A., additional, Sun, P., additional, Krueger, D., additional, Liu, Z., additional, Kohrman, M., additional, Dagens, A. B., additional, Rachinger, W., additional, Kunz, M., additional, Eigenbrod, S., additional, Lutz, J., additional, Tonn, J.-C., additional, Kreth, F.-W., additional, Duong, H. T., additional, Chaloner, C., additional, Bordo, G., additional, Eisenberg, A., additional, Rosenthal, K., additional, Sim, M.-S., additional, Boasberg, P., additional, Faries, M. B., additional, Hamid, O., additional, Kelly, D. F., additional, Thon, N., additional, Simon, M., additional, Westphal, M., additional, Schackert, G., additional, Nikkhah, G., additional, Hentschel, B., additional, Pietsch, T., additional, Reifenberger, G., additional, Weller, M., additional, Ironside, S., additional, Perry, J., additional, Tsao, M., additional, Mainprize, T., additional, Keith, J., additional, Laperrierre, N., additional, Paszat, L., additional, Sahgal, A., additional, Hoover, J. M., additional, Nwojo, M., additional, Puffer, R., additional, Parney, I. F., additional, Tanaka, S., additional, Nakada, M., additional, Hayashi, Y., additional, Hamada, J.-i., additional, Lee, I. Y., additional, Ekram, T., additional, Jain, R., additional, Scarpace, L., additional, Omodon, M., additional, Rock, J., additional, Rosenblum, M., additional, Kalkanis, S., additional, Amankulor, N. M., additional, Kim, J.-H., additional, Tabar, V., additional, Peck, K. K., additional, Holodny, A. I., additional, Gutin, P. H., additional, Kim, C.-Y., additional, Kim, Y.-H., additional, Kim, T., additional, Kim, I. K., additional, Kim, J. W., additional, Kim, Y. H., additional, Han, J. H., additional, Park, C.-K., additional, Kim, D. G., additional, Jung, H.-W., additional, Nonaka, M., additional, Bamba, Y., additional, Kanemura, Y., additional, and Nakajima, S., additional

Published
2012
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28. -OMICS AND PROGNOSTIC MARKERS

Author

Moriera, F., primary, So, K., additional, Gould, P., additional, Kamnasaran, D., additional, Jensen, R. L., additional, Hussain, I., additional, Gutmann, D. H., additional, Gorovets, D., additional, Kastenhuber, E. R., additional, Pentsova, E., additional, Nayak, L., additional, Huse, J. T., additional, van den Bent, M. J., additional, Gravendeel, L. A., additional, Gorlia, T., additional, Kros, J. M., additional, Wesseling, P., additional, Teepen, J., additional, Idbaih, A., additional, Sanson, M., additional, Smitt, P. A. S., additional, French, P. J., additional, Zhang, W., additional, Zhang, J., additional, Hoadley, K., additional, Carter, B., additional, Li, S., additional, Kang, C., additional, You, Y., additional, Jiang, C., additional, Song, S., additional, Jiang, T., additional, Chen, C., additional, Grimm, C., additional, Weiler, M., additional, Claus, R., additional, Weichenhan, D., additional, Hartmann, C., additional, Plass, C., additional, Weller, M., additional, Wick, W., additional, Jenkins, R. B., additional, Sicotte, H., additional, Xiao, Y., additional, Fridley, B. L., additional, Decker, P. A., additional, Kosel, M. L., additional, Kollmeyer, T. M., additional, Fink, S. R., additional, Rynearson, A. L., additional, Rice, T., additional, McCoy, L. S., additional, Smirnov, I., additional, Tehan, T., additional, Hansen, H. M., additional, Patoka, J. S., additional, Prados, M. D., additional, Chang, S. M., additional, Berger, M. S., additional, Lachance, D. H., additional, Wiencke, J. K., additional, Wiemels, J. L., additional, Wrensch, M. R., additional, Gephart, M. H., additional, Lee, E., additional, Kyriazopoulou-Panagiotopoulou, S., additional, Milenkovic, L., additional, Xun, X., additional, Hou, Y., additional, Kui, W., additional, Edwards, M., additional, Batzoglou, S., additional, Jun, W., additional, Scott, M., additional, Hobbs, J. E., additional, Tipton, J., additional, Zhou, T., additional, Kelleher, N. L., additional, Chandler, J. P., additional, Schwarzenberg, J., additional, Czernin, J., additional, Cloughesy, T., additional, Ellingson, B., additional, Geist, C., additional, Phelps, M., additional, Chen, W., additional, Nakada, M., additional, Hayashi, Y., additional, Obuchi, W., additional, Ohtsuki, S., additional, Watanabe, T., additional, Ikeda, C., additional, Misaki, K., additional, Kita, D., additional, Uchiyama, N., additional, Terasaki, T., additional, Hamada, J.-i., additional, Hiddingh, L., additional, Tops, B., additional, Hulleman, E., additional, Kaspers, G.-J. L., additional, Vandertop, W. P., additional, Noske, D. P., additional, Wurdinger, T., additional, Jeuken, J. W., additional, See, A. P., additional, Hwang, T., additional, Shin, D., additional, Shin, J. H., additional, Gao, Y., additional, Lim, M., additional, Hutterer, M., additional, Michael, M., additional, Gerold, U., additional, Karin, S., additional, Ingrid, G., additional, Florian, D., additional, Armin, M., additional, Eugen, T., additional, Eberhard, G., additional, Gunther, S., additional, Cook, R. W., additional, Oelschlager, K., additional, Sevim, H., additional, Chung, L., additional, Wheeler, H. T., additional, Baxter, R. C., additional, McDonald, K. L., additional, Chaturbedi, A., additional, Yu, L., additional, Zhou, Y.-H., additional, Wong, A., additional, Fatuyi, R., additional, Linskey, M. E., additional, Lavon, I., additional, Shahar, T., additional, Zrihan, D., additional, Granit, A., additional, Ram, Z., additional, Siegal, T., additional, Brat, D. J., additional, Cooper, L. A., additional, Gutman, D. A., additional, Chisolm, C. S., additional, Appin, C., additional, Kong, J., additional, Kurc, T., additional, Van Meir, E. G., additional, Saltz, J. H., additional, Moreno, C. S., additional, Abuhusain, H. J., additional, Don, A. S., additional, Nagarajan, R. P., additional, Johnson, B. E., additional, Olshen, A. B., additional, Xie, M., additional, Wang, J., additional, Sundaram, V., additional, Paris, P., additional, Wang, T., additional, Costello, J. F., additional, Sijben, A. E., additional, Boots-Sprenger, S. H., additional, Boogaarts, J., additional, Rijntjes, J., additional, Geitenbeek, J. M., additional, van der Palen, J., additional, Bernsen, H. J., additional, Schnell, O., additional, Adam, S. A., additional, Eigenbrod, S., additional, Kretzschmar, H. A., additional, Tonn, J.-C., additional, Schuller, U., additional, Sperduto, P. W., additional, Kased, N., additional, Roberge, D., additional, Xu, Z., additional, Shanley, R., additional, Luo, X., additional, Sneed, P. K., additional, Chao, S. T., additional, Weil, R. J., additional, Suh, J., additional, Bhatt, A., additional, Jensen, A. W., additional, Brown, P. D., additional, Shih, H. A., additional, Kirkpatrick, J., additional, Gaspar, L. E., additional, Fiveash, J. B., additional, Chiang, V., additional, Knisely, J. P., additional, Sperduto, C. M., additional, Lin, N., additional, Mehta, M. P., additional, Kwatra, M. M., additional, Porter, T. M., additional, Brown, K. E., additional, Herndon, J. E., additional, Bigner, D. D., additional, Dahlrot, R. H., additional, Kristensen, B. W., additional, Hansen, S., additional, Sulman, E. P., additional, Cahill, D. P., additional, Wang, M., additional, Won, M., additional, Hegi, M. E., additional, Aldape, K. D., additional, Gilbert, M. R., additional, Sadr, E. S., additional, Tessier, A., additional, Sadr, M. S., additional, Alshami, J., additional, Sabau, C., additional, Del Maestro, R., additional, Neal, M. L., additional, Rockne, R., additional, Trister, A. D., additional, Swanson, K. R., additional, Maleki, S., additional, Back, M., additional, Buckland, M., additional, Brazier, D., additional, McDonald, K., additional, Cook, R., additional, Parker, N., additional, Wheeler, H., additional, Jalbert, L., additional, Elkhaled, A., additional, Phillips, J. J., additional, Yoshihara, H. A., additional, Parvataneni, R., additional, Srinivasan, R., additional, Bourne, G., additional, Cha, S., additional, Nelson, S. J., additional, Gilbert, M., additional, Cahill, D., additional, Hegi, M., additional, Colman, H., additional, Mehta, M., additional, Sulman, E., additional, Constantin, A., additional, Phillips, J., additional, Yoshihara, H., additional, Nelson, S., additional, Gunn, S., additional, Reveles, X. T., additional, Tirtorahardjo, B., additional, Strecker, M. N., additional, and Fichtel, L., additional

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2011
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29. MEDICAL AND NEURO-ONCOLOGY

Author

Prithviraj, G. K., primary, Sommers, S. R., additional, Jump, R. L., additional, Halmos, B., additional, Chambless, L. B., additional, Parker, S. L., additional, Hassam-Malani, L., additional, McGirt, M. J., additional, Thompson, R. C., additional, Hunter, K., additional, Chamberlain, M. C., additional, Le, E. M., additional, Lee, E. L. T., additional, Sadighi, Z. S., additional, Pearlman, M. L., additional, Slopis, J. M., additional, Vats, T. S., additional, Khatua, S., additional, DeVito, N. C., additional, Yu, M., additional, Chen, R., additional, Pan, E., additional, Cloughesy, T., additional, Raizer, J., additional, Drappatz, J., additional, Gerena-Lewis, M., additional, Rogerio, J., additional, Yacoub, S., additional, Desjardin, A., additional, Groves, M. D., additional, DeGroot, J., additional, Loghin, M., additional, Conrad, C. A., additional, Hess, K., additional, Ni, J., additional, Ictech, S., additional, Yung, W. A., additional, Porter, A. B., additional, Dueck, A. C., additional, Karlin, N. J., additional, Olson, J., additional, Silber, J., additional, Reiner, A. S., additional, Panageas, K. S., additional, Iwamoto, F. M., additional, Cloughesy, T. F., additional, Aldape, K. D., additional, Rivera, A. L., additional, Eichler, A. F., additional, Louis, D. N., additional, Paleologos, N. A., additional, Fisher, B. J., additional, Ashby, L. S., additional, Cairncross, J. G., additional, Roldan, G. B., additional, Wen, P. Y., additional, Ligon, K. L., additional, Shiff, D., additional, Robins, H. I., additional, Rocque, B. G., additional, Mason, W. P., additional, Weaver, S. A., additional, Green, R. M., additional, Kamar, F. G., additional, Abrey, L. E., additional, DeAngelis, L. M., additional, Jhanwar, S. C., additional, Rosenblum, M. K., additional, Lassman, A. B., additional, Cachia, D., additional, Alderson, L., additional, Moser, R., additional, Smith, T., additional, Yunus, S., additional, Saito, K., additional, Mukasa, A., additional, Narita, Y., additional, Tabei, Y., additional, Shinoura, N., additional, Shibui, S., additional, Saito, N., additional, Flechl, B., additional, Ackerl, M., additional, Sax, C., additional, Dieckmann, K., additional, Crevenna, R., additional, Widhalm, G., additional, Preusser, M., additional, Marosi, C., additional, Ay, C., additional, Dunkler, D., additional, Pabinger, I., additional, Zielinski, C., additional, Belongia, M., additional, Jogal, S., additional, Schlingensiepen, K.-H., additional, Bogdahn, U., additional, Stockhammer, G., additional, Mahapatra, A. K., additional, Venkataramana, N. K., additional, Oliushine, V., additional, Parfenov, V., additional, Poverennova, I., additional, Hau, P., additional, Jachimczak, P., additional, Heinrichs, H., additional, Mammoser, A. G., additional, Shonka, N. A., additional, de Groot, J. F., additional, Shibahara, I., additional, Sonoda, Y., additional, Kumabe, T., additional, Saito, R., additional, Kanamori, M., additional, Yamashita, Y., additional, Watanabe, M., additional, Ishioka, C., additional, Tominaga, T., additional, Silvani, A., additional, Gaviani, P., additional, Lamperti, E., additional, Botturi, A., additional, DiMeco, F., additional, Broggi, G., additional, Fariselli, L., additional, Solero, C. L., additional, Salmaggi, A., additional, Woyshner, E. A., additional, Shu, F., additional, Oh, Y. S., additional, Iganej, S., additional, Singh, G., additional, Vemuri, S. L., additional, Theeler, B. J., additional, Ellezam, B., additional, Gilbert, M. R., additional, Aoki, T., additional, Kobayashi, H., additional, Takano, S., additional, Nishikawa, R., additional, Nagane, M., additional, Muragaki, Y., additional, Sugiyama, K., additional, Kuratsu, J., additional, Matsutani, M., additional, Langford, L. A., additional, Puduvalli, V. K., additional, Shen, D., additional, Chen, Z.-p., additional, Zhang, J.-p., additional, Bedekar, D., additional, Rand, S., additional, Connelly, J., additional, Malkin, M., additional, Paulson, E., additional, Mueller, W., additional, Schmainda, K., additional, Gallego, O., additional, Benavides, M., additional, Segura, P. P., additional, Balana, C., additional, Gil, M., additional, Berrocal, A., additional, Reynes, G., additional, Garcia, J. L., additional, Murata, P., additional, Bague, S., additional, Quintana, M. J., additional, Vasishta, V. G., additional, Kobayashi, K., additional, Tanaka, M., additional, Tsuchiya, K., additional, Shiokawa, Y., additional, Bavle, A. A., additional, Ayyanar, K., additional, Prado, M. P., additional, Hess, K. R., additional, Liu, V., additional, de Groot, J., additional, Loghin, M. E., additional, Colman, H., additional, Levin, V. A., additional, Alfred Yung, W. K., additional, Hackney, J. R., additional, Palmer, C. A., additional, Markert, J. M., additional, Cure, J., additional, Riley, K. O., additional, Fathallah-Shaykh, H., additional, Nabors, L. B., additional, Saria, M. G., additional, Corle, C., additional, Hu, J., additional, Rudnick, J., additional, Phuphanich, S., additional, Mrugala, M. M., additional, Lee, L. K., additional, Fu, B. D., additional, Bota, D. A., additional, Kim, R. Y., additional, Brown, T., additional, Feely, H., additional, Hu, A., additional, Lee, J. W., additional, Carter, B., additional, Kesari, S., additional, Kong, X.-T., additional, Sparagana, S., additional, Belousova, E., additional, Jozwiak, S., additional, Korf, B., additional, Frost, M., additional, Kuperman, R., additional, Kohrman, M., additional, Witt, O., additional, Wu, J., additional, Flamini, R., additional, Jansen, A., additional, Curtalolo, P., additional, Thiele, E., additional, Whittemore, V., additional, De Vries, P., additional, Ford, J., additional, Shah, G., additional, Cauwel, H., additional, Edrich, P., additional, Sahmoud, T., additional, Franz, D., additional, Khasraw, M., additional, Brown, C., additional, Ashley, D. M., additional, Rosenthal, M. A., additional, Jiang, X., additional, Mou, Y. g., additional, Chen, Z. p., additional, Oh, M., additional, kim, E., additional, Chang, J., additional, Juratli, T. A., additional, Kirsch, M., additional, Schackert, G., additional, Krex, D., additional, Wang, M., additional, Stupp, R., additional, Hegi, M., additional, Jaeckle, K. A., additional, Armstrong, T. S., additional, Wefel, J. S., additional, Won, M., additional, Blumenthal, D. T., additional, Mahajan, A., additional, Schultz, C. J., additional, Erridge, S. C., additional, Brown, P. D., additional, Chakravarti, A., additional, Curran, W. J., additional, Mehta, M. P., additional, Hofland, K. F., additional, Hansen, S., additional, Sorensen, M., additional, Schultz, H., additional, Muhic, A., additional, Engelholm, S., additional, Ask, A., additional, Kristiansen, C., additional, Thomsen, C., additional, Poulsen, H. S., additional, Lassen, U. N., additional, Zalatimo, O., additional, Weston, C., additional, Zoccoli, C., additional, Glantz, M., additional, Rahmanuddin, S., additional, Shiroishi, M. S., additional, Cen, S. Y., additional, Jones, J., additional, Chen, T., additional, Pagnini, P., additional, Go, J., additional, Lerner, A., additional, Gomez, J., additional, Law, M., additional, Ram, Z., additional, Wong, E. T., additional, Gutin, P. H., additional, Bobola, M. S., additional, Alnoor, M., additional, Silbergeld, D. L., additional, Rostomily, R. C., additional, Silber, J. R., additional, Martha, N., additional, Jacqueline, S., additional, Thaddaus, G., additional, Daniel, P., additional, Hans, M., additional, Armin, M., additional, Eugen, T., additional, Gunther, S., additional, Hutterer, M., additional, Tseng, H.-M., additional, Zoccoli, C. M., additional, Patel, A., additional, Rizzo, K., additional, Sheehan, J. M., additional, Sumrall, A. L., additional, Vredenburgh, J. J., additional, Desjardins, A., additional, Reardon, D. A., additional, Friiedman, H. S., additional, Peters, K. B., additional, Taylor, L. P., additional, Stewart, M., additional, Blondin, N. A., additional, Baehring, J. M., additional, Foote, T., additional, Laack, N., additional, Call, J., additional, Hamilton, M. G., additional, Walling, S., additional, Eliasziw, M., additional, Easaw, J., additional, Shirsat, N. V., additional, Kundar, R., additional, Gokhale, A., additional, Goel, A., additional, Moiyadi, A. A., additional, Wang, J., additional, Mutlu, E., additional, Oyan, A., additional, Yan, T., additional, Tsinkalovsky, O., additional, Jacobsen, H. K., additional, Talasila, K. M., additional, Sleire, L., additional, Pettersen, K., additional, Miletic, H., additional, Andersen, S., additional, Mitra, S., additional, Weissman, I., additional, Li, X., additional, Kalland, K.-H., additional, Enger, P. O., additional, Sepulveda, J., additional, Belda, C., additional, Sitt, R., additional, Phishniak, L., additional, Bokstein, F., additional, Philippe, M., additional, Carole, C., additional, Andre, M. d. P., additional, Marylin, B., additional, Olivier, C., additional, L'Houcine, O., additional, Dominique, F.-B., additional, Isabelle, N.-M., additional, Frederic, F., additional, Stephane, F., additional, Henry, D., additional, Errico, M. A., additional, Kunschner, L. J., additional, Soffietti, R., additional, Trevisan, E., additional, Ruda, R., additional, Bertero, L., additional, Bosa, C., additional, Fabrini, M. G., additional, Lolli, I., additional, Jalali, R., additional, Julka, P. K., additional, Anand, A. K., additional, Bhavsar, D., additional, Singhal, N., additional, Naik, R., additional, John, S., additional, Mathew, B. S., additional, Thaipisuttikul, I., additional, Graber, J., additional, Shirinian, M., additional, Fontebasso, A. M., additional, Jacob, K., additional, Gerges, N., additional, Montpetit, A., additional, Nantel, A., additional, Albrecht, S., additional, Jabado, N., additional, Shah, K., additional, Di, K., additional, Linskey, M., additional, Thon, N., additional, Eigenbrod, S., additional, Kreth, S., additional, Lutz, J., additional, Tonn, J.-C., additional, Kretzschmar, H., additional, Peraud, A., additional, Kreth, F.-W., additional, Muggeri, A. D., additional, Alderuccio, J. P., additional, Diez, B. D., additional, Jiang, P., additional, Chao, Y., additional, Gallagher, M., additional, Kim, R., additional, Pastorino, S., additional, Fogal, V., additional, Rudnick, J. D., additional, Bresee, C., additional, Rogatko, A., additional, Sakowsky, S., additional, Franco, M., additional, Lim, S., additional, Lopez, A., additional, Yu, L., additional, Ryback, K., additional, Tsang, V., additional, Lill, M., additional, Steinberg, A., additional, Sheth, R., additional, Grimm, S., additional, Helenowski, I., additional, Rademaker, A., additional, Nunes, F. P., additional, Merker, V., additional, Jennings, D., additional, Caruso, P., additional, Muzikansky, A., additional, Stemmer-Rachamimov, A., additional, Plotkin, S., additional, Spalding, A. C., additional, Vitaz, T. W., additional, Sun, D. A., additional, Parsons, S., additional, Welch, M. R., additional, Omuro, A., additional, Beal, K., additional, Correa, D., additional, Chan, T., additional, DeAngelis, L., additional, Gavrilovic, I., additional, Nolan, C., additional, Hormigo, A., additional, Kaley, T., additional, Mellinghoff, I., additional, Grommes, C., additional, Panageas, K., additional, Reiner, A., additional, Barradas, R., additional, Abrey, L., additional, Gutin, P., additional, Lee, S. Y., additional, Slagle-Webb, B., additional, Glantz, M. J., additional, Connor, J. R., additional, Schlimper, C. A., additional, Schlag, H., additional, Stoffels, G., additional, Weber, F., additional, Krueger, D. A., additional, Care, M. M., additional, Holland, K., additional, Agricola, K., additional, Tudor, C., additional, Byars, A., additional, Franz, D. N., additional, Rice, L., additional, Chandler, J., additional, Levy, R., additional, Muro, K., additional, Nayak, L., additional, Norden, A. D., additional, Kaley, T. J., additional, Thomas, A. A., additional, Fadul, C. E., additional, Meyer, L. P., additional, Lallana, E. C., additional, Gilbert, M., additional, Aldape, K., additional, De Groot, J., additional, Conrad, C., additional, Levin, V., additional, Groves, M., additional, Chris, P., additional, Puduvalli, V., additional, Nagpal, S., additional, Feroze, A., additional, Recht, L., additional, Rangarajan, H. G., additional, Kieran, M. W., additional, Scott, R. M., additional, Lew, S. M., additional, Firat, S. Y., additional, Segura, A. D., additional, Jogal, S. A., additional, Kumthekar, P. U., additional, Grimm, S. A., additional, Avram, M., additional, Patel, J., additional, Kaklamani, V., additional, McCarthy, K., additional, Cianfrocca, M., additional, Gradishar, W., additional, Mulcahy, M., additional, Von Roenn, J., additional, Galanis, E., additional, Anderson, S. K., additional, Lafky, J. M., additional, Kaufmann, T. J., additional, Uhm, J. H., additional, Giannini, C., additional, Kumar, S. K., additional, Northfelt, D. W., additional, Flynn, P. J., additional, Buckner, J. C., additional, Omar, A. I., additional, Schiff, D., additional, Delios, A., additional, Jakubowski, A., additional, Melguizo-Gavilanes, I., additional, Qiao, W., additional, Wang, X., additional, Hashemi-Sadraei, N., additional, Bawa, H., additional, Rahmathulla, G., additional, Patel, M., additional, Elson, P., additional, Stevens, G., additional, Peereboom, D., additional, Vogelbaum, M., additional, Weil, R., additional, Barnett, G., additional, Ahluwalia, M. S., additional, Alvord, E. C., additional, Rockne, R. C., additional, Rockhill, J. K., additional, Rostomily, R., additional, Lai, A., additional, Wardlaw, J., additional, Spence, A. M., additional, Swanson, K. R., additional, Zadeh, G., additional, Alahmadi, H., additional, Wilson, J., additional, Gentili, F., additional, Beumer, J. J., additional, Wright, J., additional, Takebe, N., additional, Gaur, R., additional, Werner-Wasik, M., additional, Gupta, A. J., additional, Campos-Gines, A., additional, Le, K., additional, Arango, C., additional, Richards, M., additional, Landeros, M., additional, Juan, H., additional, Chang, J. H., additional, Kim, J. S., additional, Cho, J. H., additional, Seo, C. O., additional, Baldock, A. L., additional, Rockne, R., additional, Canoll, P., additional, Born, D., additional, Yagle, K., additional, Alexandru, D., additional, Bota, D., additional, Linskey, M. E., additional, Nabeel, S., additional, Raval, S. N., additional, Rosenow, J., additional, Bredel, M., additional, New, P. Z., additional, Plotkin, S. R., additional, Supko, J. G., additional, Curry, W. T., additional, Chi, A. S., additional, Gerstner, E. R., additional, Batchelor, T. T., additional, Hashemi, N., additional, Chao, S. T., additional, Weil, R. J., additional, Suh, J. H., additional, Vogelbaum, M. A., additional, Stevens, G. H., additional, Barnett, G. H., additional, Corwin, D., additional, Holdsworth, C., additional, Stewart, R., additional, Swanson, K., additional, Graber, J. J., additional, Anderson, A. R., additional, Jeyapalan, S., additional, Goldman, M., additional, Boxerman, J., additional, Donahue, J., additional, Elinzano, H., additional, Evans, D., additional, O'Connor, B., additional, Puthawala, M. Y., additional, Oyelese, A., additional, Cielo, D., additional, Blitstein, M., additional, Dargush, M., additional, Santaniello, A., additional, Constantinou, M., additional, DiPetrillo, T., additional, Safran, H., additional, Halpin, C., additional, Barker, F. G., additional, Maher, E. A., additional, Ganji, S., additional, DeBerardinis, R., additional, Hatanpaa, K., additional, Rakheja, D., additional, Yang, X.-L., additional, Mashimo, T., additional, Raisanen, J., additional, Madden, C., additional, Mickey, B., additional, Malloy, C., additional, Bachoo, R., additional, Choi, C., additional, Ranjan, T., additional, Yono, N., additional, Han, S. J., additional, Sun, M., additional, Berger, M. S., additional, Aghi, M., additional, Gupta, N., additional, and Parsa, A. T., additional

Published
2011
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30. Hot spots in dynamic18FET-PET delineate malignant tumor parts within suspected WHO grade II gliomas

Author

Kunz, M., primary, Thon, N., additional, Eigenbrod, S., additional, Hartmann, C., additional, Egensperger, R., additional, Herms, J., additional, Geisler, J., additional, la Fougere, C., additional, Lutz, J., additional, Linn, J., additional, Kreth, S., additional, von Deimling, A., additional, Tonn, J. C., additional, Kretzschmar, H. A., additional, Popperl, G., additional, and Kreth, F. W., additional

Published
2011
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32. Cerebral angiitis in four patients with chronic GVHD

Author

Sostak, P, primary, Padovan, C S, additional, Eigenbrod, S, additional, Roeber, S, additional, Segerer, S, additional, Schankin, C, additional, Siegert, S, additional, Saam, T, additional, Theil, D, additional, Kolb, H-J, additional, Kretzschmar, H, additional, and Straube, A, additional

Published
2009
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37. MRI and clinical syndrome in dura materrelated Creutzfeldt-Jakob disease

Author

Meissner, B., Kallenberg, K., Sanchez-Juan, P., Ramljak, S., Krasnianski, A., Heinemann, U., Eigenbrod, S., Gelpi, E., Barsic, B., Kretzschmar, H., Schulz-Schaeffer, W., Knauth, M., Zerr, I., Meissner, B., Kallenberg, K., Sanchez-Juan, P., Ramljak, S., Krasnianski, A., Heinemann, U., Eigenbrod, S., Gelpi, E., Barsic, B., Kretzschmar, H., Schulz-Schaeffer, W., Knauth, M., and Zerr, I.

Abstract

Objective : Iatrogenic Creutzfeldt-Jakob disease (iCJD) is mainly associated with dura mater (DM) grafts and administration of human growth hormones (hGH). Data on disease course in DM-CJD are limited. We describe the clinical and diagnostic findings in this patient group with special emphasis on MRI signal alterations. Methods : Ten DM-CJD patients were studied for their clinical symptoms and diagnostic findings. The MRIs were evaluated for signal increase of the cortical and subcortical structures. Results : DM-CJD patients had a median incubation time of 18 years and median disease duration of 7 months. The majority of patients were MM homozygous at codon 129 of the prion protein gene (PRNP) and presented with gait ataxia and psychiatric symptoms. No correlation between the graft site and the initial disease course was found. The MRI showed cortical and basal ganglia signal increase each in eight out of ten patients and thalamic hyperintensity in five out of ten cases. Of interest, patients with thalamic signal increase were homozygous for methionine. Conclusion : The MRI findings in DM-CJD largely resemble those seen in sporadic CJD, as the cortex and basal ganglia are mainly affected

38. MiRNA expression patterns predict survival in glioblastoma

Author

Niyazi Maximilian, Zehentmayr Franz, Niemöller Olivier M, Eigenbrod Sabina, Kretzschmar Hans, Osthoff Klaus-Schulze, Tonn Jörg-Christian, Atkinson Mike, Mörtl Simone, and Belka Claus

Subjects
radiotherapy, glioblastoma, microRNA, methylation, prognosis, Medical physics. Medical radiology. Nuclear medicine, R895-920, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background In order to define new prognostic subgroups in patients with glioblastoma a miRNA screen (> 1000 miRNAs) from paraffin tissues followed by a bio-mathematical analysis was performed. Methods 35 glioblastoma patients treated between 7/2005 - 8/2008 at a single institution with surgery and postoperative radio(chemo)therapy were included in this retrospective analysis. For microarray analysis the febit biochip "Geniom® Biochip MPEA homo-sapiens" was used. Total RNA was isolated from FFPE tissue sections and 1100 different miRNAs were analyzed. Results It was possible to define a distinct miRNA expression pattern allowing for a separation of distinct prognostic subgroups. The defined miRNA pattern was significantly associated with early death versus long-term survival (split at 450 days) (p = 0.01). The pattern and the prognostic power were both independent of the MGMT status. Conclusions At present, this is the first dataset defining a prognostic role of miRNA expression patterns in patients with glioblastoma. Having defined such a pattern, a prospective validation of this observation is required.

Published
2011
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39. Brain-derived proteins in the CSF, do they correlate with brain pathology in CJD?

Author

Eigenbrod Sabina, Varges Daniela, Heinemann Uta, Bartl Mario, Krasnianski Anna, Meissner Bettina, Ciesielczyk Barbara, Bodemer Monika, Schulz-Schaeffer Walter J, Boesenberg-Grosse Constanze, Kretzschmar Hans A, Green Alison, and Zerr Inga

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background Brain derived proteins such as 14-3-3, neuron-specific enolase (NSE), S 100b, tau, phosphorylated tau and Aβ1–42 were found to be altered in the cerebrospinal fluid (CSF) in Creutzfeldt-Jakob disease (CJD) patients. The pathogenic mechanisms leading to these abnormalities are not known, but a relation to rapid neuronal damage is assumed. No systematic analysis on brain-derived proteins in the CSF and neuropathological lesion profiles has been performed. Methods CSF protein levels of brain-derived proteins and the degree of spongiform changes, neuronal loss and gliosis in various brain areas were analyzed in 57 CJD patients. Results We observed three different patterns of CSF alteration associated with the degree of cortical and subcortical changes. NSE levels increased with lesion severity of subcortical areas. Tau and 14-3-3 levels increased with minor pathological changes, a negative correlation was observed with severity of cortical lesions. Levels of the physiological form of the prion protein (PrPc) and Aβ1–42 levels correlated negatively with cortical pathology, most clearly with temporal and occipital lesions. Conclusion Our results indicate that the alteration of levels of brain-derived proteins in the CSF does not only reflect the degree of neuronal damage, but it is also modified by the localization on the brain pathology. Brain specific lesion patterns have to be considered when analyzing CSF neuronal proteins.

Published
2006
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41. Sphingosine-kinase and sphingosine-1-phosphate regulate migration of immature dendritic cells.

Author

Jakl, V., Eigenbrod, S., Derwand, R., Dauer, M., Endres, S., and Eigler, A.

Subjects
*DENDRITIC cells, *SPHINGOSINE, *CELL migration, *ANTIGENS, *CANCER treatment, *IMMUNOTHERAPY
Abstract

The examines the role of SphK and S1P in migration of dendritic cells (DC). It suggests a role for Sphingosinekinase/Sphingosine-1- phosphate (SphK/S1P) in accumulation of peripheral immature (iDC) at sites of antigen invasion. The article provides a new approach to optimize DC-based cancer immunotherapy by therapeutic modulation of SphK/S1P and have to be verified in an animal model in the next step.

Published
2004
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42. The number of methylated CpG sites within the MGMT promoter region linearly correlates with outcome in glioblastoma receiving alkylating agents.

Author

Siller S, Lauseker M, Karschnia P, Niyazi M, Eigenbrod S, Giese A, and Tonn JC

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Base Sequence, Cohort Studies, Female, Humans, Male, Middle Aged, Polymerase Chain Reaction methods, Prognosis, Survival Analysis, Temozolomide therapeutic use, Antineoplastic Agents, Alkylating therapeutic use, Brain Neoplasms genetics, CpG Islands, DNA Methylation, DNA Modification Methylases genetics, DNA Repair Enzymes genetics, Glioblastoma drug therapy, Glioblastoma genetics, Promoter Regions, Genetic, Tumor Suppressor Proteins genetics
Abstract

MGMT-promoter methylation is associated with favorable outcome in glioblastoma. The aim of this study was to determine whether the absolute number of methylated Cytosine-Guanine-dinucleotide-(CpG-)sites within the DMR-2 island of the MGMT-promoter may correlate with outcome in a qualitative or quantitative fashion. In a cohort of newly diagnosed glioblastoma patients treated with stereotactic biopsy or open tumor resection plus concomitant chemoradiotherapy, we assessed MGMT-promoter methylation by methylation-specific polymerase-chain-reaction (MSP). Methylation of the CpG-sites 74-98 within the MGMT-promoter region was additionally analysed by Sanger sequencing, and the total number of methylated CpG-sites was correlated with outcome using proportional hazards models. 215 patients with glioblastoma were identified and stratified per MSP (positive: 53%, negative: 47%). Among MSP-positive tumors, hierarchical clustering identified three subgroups with different methylation rates (median: 80% vs. 52% vs. 47%), indicating a site-dependent methylation propagation. The methylation status of a given CpG-site indicated a neighborhood-dependent methylation propagation. Survival was linearly associated with the cumulative number of methylated CpG-sites. This was particularly true in patients who received at least one adjuvant cycle of temozolomide. Notably, all CpG-sites analyzed contributed similarly to effect size; this enabled a further predictive substratification of MSP-positive tumors with median OS ranging from as low as 17.1 months (< 18 methylated CpG-sites) to as high as 26.2 months (≥ 18 methylated CpG-sites) in the overall cohort. All in all, total number of methylated CpG-sites may correlate with outcome in a linear fashion. Such analysis may therefore add further predictive value to conventional methods of determining the MGMT-promoter status.

Published
2021
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43. MGMT promoter methylation is not correlated with integrin expression in malignant gliomas: clarifying recent clinical trial results.

Author

Schnell O, Albrecht V, Pfirrmann D, Eigenbrod S, Krebs B, Romagna A, Siller S, Giese A, Tonn JC, and Schichor C

Subjects
Biomarkers, Tumor genetics, Biomarkers, Tumor metabolism, Brain Neoplasms genetics, Brain Neoplasms pathology, Clinical Trials as Topic, Enzyme-Linked Immunosorbent Assay, Glioblastoma genetics, Glioblastoma pathology, Humans, Immunohistochemistry, Brain Neoplasms metabolism, DNA Methylation, DNA Modification Methylases genetics, DNA Repair Enzymes genetics, Glioblastoma metabolism, Integrin alphaVbeta3 metabolism, Promoter Regions, Genetic, Tumor Suppressor Proteins genetics
Abstract

Integrin alpha-v-beta-3 (α v β 3 ) is important for invasive tumor growth and angiogenesis in glioblastomas (GBM). However, recent clinical trials on inhibition of this integrin led to ambiguous results whether patients with methylated or unmethylated 6 O-methylguanine methyltransferase (MGMT) promoter might profit from this kind of therapy. Therefore, we addressed the still unanswered question about a possible correlation between integrin α v β 3 expression and MGMT promoter methylation in GBM. For this purpose, tumor samples from newly diagnosed and untreated GBM patients with methylated (n = 22) or unmethylated (n = 17) MGMT promoter were simultaneously analyzed for integrin α v β 3 expression by an automated immunohistochemical staining platform. Interestingly, subsequent semi-quantitative analysis by a special imaging software did not show any difference in integrin expression between patients with methylated or unmethylated MGMT promoter status. Moreover, further analysis of the integrin subunits via ELISA from histologic sections revealed that there is no difference in integrin subunit expression between these patients. Hence, our results are important for designing future clinical trials with respect to treatment stratification, while it still has to be identified which other molecular factors determine differential responses to targeted anti-integrin α v β 3 treatment.

Published
2018
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44. Substitutions of PrP N-terminal histidine residues modulate scrapie disease pathogenesis and incubation time in transgenic mice.

Author

Eigenbrod S, Frick P, Bertsch U, Mitteregger-Kretzschmar G, Mielke J, Maringer M, Piening N, Hepp A, Daude N, Windl O, Levin J, Giese A, Sakthivelu V, Tatzelt J, Kretzschmar H, and Westaway D

Subjects
Animals, Mice, Mice, Transgenic, Histidine chemistry, Prion Proteins chemistry, Scrapie pathology
Abstract

Prion diseases have been linked to impaired copper homeostasis and copper induced-oxidative damage to the brain. Divalent metal ions, such as Cu2+ and Zn2+, bind to cellular prion protein (PrPC) at octapeptide repeat (OR) and non-OR sites within the N-terminal half of the protein but information on the impact of such binding on conversion to the misfolded isoform often derives from studies using either OR and non-OR peptides or bacterially-expressed recombinant PrP. Here we created new transgenic mouse lines expressing PrP with disrupted copper binding sites within all four histidine-containing OR's (sites 1-4, H60G, H68G, H76G, H84G, "TetraH>G" allele) or at site 5 (composed of residues His-95 and His-110; "H95G" allele) and monitored the formation of misfolded PrP in vivo. Novel transgenic mice expressing PrP(TetraH>G) at levels comparable to wild-type (wt) controls were susceptible to mouse-adapted scrapie strain RML but showed significantly prolonged incubation times. In contrast, amino acid replacement at residue 95 accelerated disease progression in corresponding PrP(H95G) mice. Neuropathological lesions in terminally ill transgenic mice were similar to scrapie-infected wt controls, but less severe. The pattern of PrPSc deposition, however, was not synaptic as seen in wt animals, but instead dense globular plaque-like accumulations of PrPSc in TgPrP(TetraH>G) mice and diffuse PrPSc deposition in (TgPrP(H95G) mice), were observed throughout all brain sections. We conclude that OR and site 5 histidine substitutions have divergent phenotypic impacts and that cis interactions between the OR region and the site 5 region modulate pathogenic outcomes by affecting the PrP globular domain.

Published
2017
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45. Overexpression of cytosolic, plasma membrane bound and extracellular heat shock protein 70 (Hsp70) in primary glioblastomas.

Author

Thorsteinsdottir J, Stangl S, Fu P, Guo K, Albrecht V, Eigenbrod S, Erl J, Gehrmann M, Tonn JC, Multhoff G, and Schichor C

Subjects
AC133 Antigen metabolism, Biomarkers metabolism, Brain metabolism, Brain pathology, Brain surgery, Brain Neoplasms genetics, Brain Neoplasms pathology, Brain Neoplasms therapy, Cell Membrane pathology, Cohort Studies, Cytosol pathology, Endothelial Cells metabolism, Endothelial Cells pathology, Epilepsy metabolism, Epilepsy pathology, Epilepsy surgery, Female, Glioblastoma genetics, Glioblastoma pathology, Glioblastoma therapy, Humans, Isocitrate Dehydrogenase genetics, Isocitrate Dehydrogenase metabolism, Male, Middle Aged, Neoplasm Grading, ROC Curve, Sarcoma, Small Cell, Brain Neoplasms metabolism, Cell Membrane metabolism, Cytosol metabolism, Extracellular Space metabolism, Glioblastoma metabolism, HSP70 Heat-Shock Proteins metabolism
Abstract

A unique feature in several non-CNS-tumors is the overexpression of heat shock protein 70 (Hsp70, HSPA1A) in the cytosol, but also its unusual plasma membrane expression and release. Although in gliomas, cytosolic Hsp70 levels are not associated with histological grading, the role of membrane bound and released Hsp70 is still completely unknown. Membrane bound as well as cytosolic Hsp70 can be detected in viable tumor cells with the monoclonal antibody (mAb) cmHsp70.1. Herein, we analysed membrane bound Hsp70 levels in primary and secondary gliomas of different grades and on isolated glioma subpopulations (endothelial cells, CD133-positive cells, primary cultures) by immunohistochemistry and flow cytometry using cmHsp70.1 mAb. Extracellular Hsp70 was determined by a commercial Hsp70 sandwich ELISA (R&D) in plasma samples of glioblastoma patients and healthy volunteers. We found an overexpression of Hsp70 in primary glioblastomas compared to low-grade, anaplastic, or secondary gliomas as determined by immunohistochemistry. Especially in flow cytometry, a strong plasma membrane Hsp70 expression was only observed in primary but not secondary glioblastomas. Within the heterogeneous tumor mass, CD133-positive tumor-initiating and primary glioblastoma cells showed a high membrane Hsp70 expression density, whereas endothelial cells, isolated from glioblastoma tissues only showed a weak staining pattern. Also in plasma samples, secreted Hsp70 protein was significantly increased in patients harbouring primary glioblastomas compared to those with secondary and low grade glioblastomas. Taken together, we show for the first time that cytosolic, membrane bound and extracellular Hsp70 is uniquely overexpressed in primary glioblastomas.

Published
2017
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46. Outcome in unresectable glioblastoma: MGMT promoter methylation makes the difference.

Author

Thon N, Thorsteinsdottir J, Eigenbrod S, Schüller U, Lutz J, Kreth S, Belka C, Tonn JC, Niyazi M, and Kreth FW

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Antineoplastic Agents, Alkylating therapeutic use, Biopsy, Central Nervous System Neoplasms diagnosis, Central Nervous System Neoplasms drug therapy, Central Nervous System Neoplasms radiotherapy, Chemoradiotherapy, Dacarbazine analogs & derivatives, Dacarbazine therapeutic use, Drug Resistance, Neoplasm genetics, Female, Follow-Up Studies, Glioblastoma diagnosis, Glioblastoma drug therapy, Glioblastoma radiotherapy, Humans, Longitudinal Studies, Male, Middle Aged, Prognosis, Prospective Studies, Salvage Therapy, Temozolomide, Young Adult, Central Nervous System Neoplasms genetics, DNA Methylation, DNA Modification Methylases genetics, DNA Repair Enzymes genetics, Glioblastoma genetics, Promoter Regions, Genetic, Tumor Suppressor Proteins genetics
Abstract

In 2011, we reported a predominant prognostic/predictive role of MGMT promoter methylation status on progression-free survival (PFS) in unresectable glioblastoma patients undergoing upfront radiotherapy plus concomitant and maintenance temozolomide (RTX/TMZ → TMZ). We, here, present the final results of this prospective study focussing on the prognostic/predictive value of MGMT promoter methylation status for death risk stratification. Overall, 56 adult patients with unresectable, biopsy proven glioblastoma were prospectively assigned to upfront RTX/TMZ → TMZ treatment between March 2006 and August 2008. Last follow-up was performed in June 2016. MGMT promoter methylation was determined using methylation-specific PCR (MSP) and sodium bisulfite sequencing. Analyses were done by intention to treat. Prognostic factors were obtained from proportional hazard models. At the time of the final analysis 55 patients showed progressive disease and 53 patients had died. MGMT promoter was methylated (unmethylated) in 30 (26) patients. Methylation of the MGMT promoter was the strongest favorable predictor for overall survival (OS, median: 20.3 vs. 7.3 months, p < 0.001, HR 0.30, 95% CI 0.16-0.55), and PFS (median: 15.0 vs. 6.1 months, p < 0.001, HR 0.31, 95% CI 0.17-0.57) and was also associated with higher frequencies of treatment response and prolonged post-recurrence survival (PRS, median: 4.5 vs. 1.4 months, p < 0.002, HR 0.39, 95% CI 0.21-0.71). Knowledge of MGMT promoter methylation status is essential for patients' counseling, prognostic evaluation, and for the design of future trials dealing with unresectable glioblastomas.

Published
2017
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47. Quantifying prion disease penetrance using large population control cohorts.

Author

Minikel EV, Vallabh SM, Lek M, Estrada K, Samocha KE, Sathirapongsasuti JF, McLean CY, Tung JY, Yu LP, Gambetti P, Blevins J, Zhang S, Cohen Y, Chen W, Yamada M, Hamaguchi T, Sanjo N, Mizusawa H, Nakamura Y, Kitamoto T, Collins SJ, Boyd A, Will RG, Knight R, Ponto C, Zerr I, Kraus TF, Eigenbrod S, Giese A, Calero M, de Pedro-Cuesta J, Haïk S, Laplanche JL, Bouaziz-Amar E, Brandel JP, Capellari S, Parchi P, Poleggi A, Ladogana A, O'Donnell-Luria AH, Karczewski KJ, Marshall JL, Boehnke M, Laakso M, Mohlke KL, Kähler A, Chambert K, McCarroll S, Sullivan PF, Hultman CM, Purcell SM, Sklar P, van der Lee SJ, Rozemuller A, Jansen C, Hofman A, Kraaij R, van Rooij JG, Ikram MA, Uitterlinden AG, van Duijn CM, Daly MJ, and MacArthur DG

Subjects
Case-Control Studies, Cohort Studies, Genetic Predisposition to Disease, Humans, Mutation genetics, Prions genetics, Risk Factors, Penetrance, Prion Diseases genetics
Abstract

More than 100,000 genetic variants are reported to cause Mendelian disease in humans, but the penetrance-the probability that a carrier of the purported disease-causing genotype will indeed develop the disease-is generally unknown. We assess the impact of variants in the prion protein gene (PRNP) on the risk of prion disease by analyzing 16,025 prion disease cases, 60,706 population control exomes, and 531,575 individuals genotyped by 23andMe Inc. We show that missense variants in PRNP previously reported to be pathogenic are at least 30 times more common in the population than expected on the basis of genetic prion disease prevalence. Although some of this excess can be attributed to benign variants falsely assigned as pathogenic, other variants have genuine effects on disease susceptibility but confer lifetime risks ranging from <0.1 to ~100%. We also show that truncating variants in PRNP have position-dependent effects, with true loss-of-function alleles found in healthy older individuals, a finding that supports the safety of therapeutic suppression of prion protein expression., (Copyright © 2016, American Association for the Advancement of Science.)

Published
2016
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48. Dynamic 18F-FET PET in suspected WHO grade II gliomas defines distinct biological subgroups with different clinical courses.

Author

Thon N, Kunz M, Lemke L, Jansen NL, Eigenbrod S, Kreth S, Lutz J, Egensperger R, Giese A, Herms J, Weller M, Kretzschmar H, Tonn JC, la Fougère C, and Kreth FW

Subjects
Adult, Aged, Aged, 80 and over, Disease-Free Survival, Female, Glioma metabolism, Humans, Isocitrate Dehydrogenase metabolism, Male, Middle Aged, O(6)-Methylguanine-DNA Methyltransferase metabolism, Positron-Emission Tomography methods, Prognosis, Promoter Regions, Genetic genetics, Prospective Studies, Young Adult, Glioma diagnosis, Glioma pathology, Radiopharmaceuticals, Tyrosine analogs & derivatives
Abstract

In suspected grade II gliomas, three distinct patterns of time-activity curves (TAC) on O-(2-[(18)F]fluoroethyl)-1-tyrosine ((18)F-FET) positron emission tomography (PET) have been delineated (i) increasing TAC homogeneously throughout the tumor, and decreasing TAC, (ii) either homogeneously throughout the tumor or (iii) only focally within otherwise increasing TAC patterns. Increasing TAC was associated with low-grade histology and decreasing TAC with high-grade histology. This prospective study analyzed whether these patterns correlate with distinct biological tumor subtypes and differential outcome. (18)F-FET PET-guided biopsies were used for stepwise histopathological evaluation. Molecular-genetic evaluation included O(6)-methylguanine-DNA methyltransferase (MGMT) promoter methylation, isocitrate dehydrogenase (IDH1/2) mutational and 1p/19q codeletion status. Progression-free survival (PFS) was estimated with the Kaplan-Meier method. Prognostic factors were obtained from multivariate regression models. 98 adult patients were included. Homogeneous increasing, focal decreasing and homogeneous decreasing TAC were seen in 51, 19 and 28 patients. The corresponding 1-year (2-years) PFS were 92% (85%), 89% (51%) and 50% (28%; p = 0.002). IDH1/2 mutations were more frequent in tumors with homogeneous increasing (90%) and focal decreasing (79%) TAC, but were rare in those exhibiting homogeneous decreasing TAC (25%; p < 0.001). Overall, TAC patterns, IDH1/2 mutational and 1p/19q codeletion status were powerful and independent prognostic factors. Dynamic (18)F-FET PET might be an important and independent imaging biomarker for patients with suspected WHO grade II gliomas and offers perspectives for stratified diagnostic and therapeutic strategies. Tumors with focal decreasing TAC need highly targeted surgical interventions to avoid undergrading and undertreatment., (© 2014 UICC.)

Published
2015
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49. Biological tumor volume in 18FET-PET before radiochemotherapy correlates with survival in GBM.

Author

Suchorska B, Jansen NL, Linn J, Kretzschmar H, Janssen H, Eigenbrod S, Simon M, Pöpperl G, Kreth FW, la Fougere C, Weller M, and Tonn JC

Subjects
Adult, Aged, Antineoplastic Agents, Alkylating therapeutic use, Brain diagnostic imaging, Brain pathology, Brain Neoplasms pathology, Chemoradiotherapy, Combined Modality Therapy, Dacarbazine analogs & derivatives, Dacarbazine therapeutic use, Disease-Free Survival, Female, Glioblastoma pathology, Humans, Longitudinal Studies, Male, Microsurgery, Middle Aged, Neurosurgical Procedures, Prospective Studies, Temozolomide, Treatment Outcome, Tyrosine analogs & derivatives, Brain Neoplasms diagnostic imaging, Brain Neoplasms therapy, Glioblastoma diagnostic imaging, Glioblastoma therapy, Positron-Emission Tomography, Tumor Burden
Abstract

Objective: The aim of this prospective longitudinal study was to identify static and dynamic O-(2-[(18)F]fluoroethyl)-L-tyrosine PET ((18)FET-PET)-derived imaging biomarkers in patients with glioblastoma (GBM)., Methods: Seventy-nine patients with newly diagnosed GBM were included; 42 patients underwent stereotactic biopsy (unresectable tumors) and 37 patients microsurgical tumor resection. All patients were scheduled to receive radiotherapy plus concomitant and adjuvant temozolomide (RCx/TMZ). (18)FET-PET evaluation using static and dynamic analysis was done before biopsy/resection, after resection, 4 to 6 weeks following RCx, and after 3 cycles of TMZ. Endpoints were survival and progression-free-survival. Prognostic factors were obtained from proportional hazards models., Results: Biological tumor volume before RCx (BTV(preRCx)) was the most important (18)FET-PET-derived imaging biomarker and was independent of MGMT promoter methylation and clinical prognostic factors: patients with smaller BTV(preRCx) had significantly longer progression-free and overall survival (OS). (18)FET time-activity curves (TACs) before treatment and their changes after RCx were also related to outcome; patients with initially increasing TACs experienced longer OS., Conclusion: BTV(preRCx) and TAC represent important (18)FET-PET-derived imaging biomarkers in GBM. Increasing TACs are associated with prolonged OS. The BTV(preRCx) is a strong prognostic factor for progression-free survival and OS independent of the mode of surgery. Our data furthermore suggest that patients harboring resectable GBM might benefit from maximal PET-guided tumor resection., (© 2015 American Academy of Neurology.)

Published
2015
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50. Prognostic significance of dynamic 18F-FET PET in newly diagnosed astrocytic high-grade glioma.

Author

Jansen NL, Suchorska B, Wenter V, Schmid-Tannwald C, Todica A, Eigenbrod S, Niyazi M, Tonn JC, Bartenstein P, Kreth FW, and la Fougère C

Subjects
Astrocytoma metabolism, Biological Transport, Female, Humans, Kinetics, Male, Middle Aged, Neoplasm Grading, Prognosis, Retrospective Studies, Tyrosine metabolism, Astrocytoma diagnostic imaging, Astrocytoma pathology, Positron-Emission Tomography, Tyrosine analogs & derivatives
Abstract

Unlabelled: Despite advances in diagnosis and the use of different therapeutic regimens in astrocytic high-grade glioma (HGG), the prognosis for patients remains grim. Additional pretherapeutic information is needed to tailor management. To gain additional prognostic information at primary diagnosis, we investigated the value of dynamic O-(2-(18)F-fluoroethyl)-L-tyrosine ((18)F-FET) PET., Methods: We retrospectively evaluated 121 patients who had a primary diagnosis of astrocytic HGG (51 World Health Organization [WHO] grade III; 70 WHO IV) and underwent dynamic (18)F-FET PET before histopathologic assessment. We assessed static parameters (maximal and mean tumoral standardized uptake value corrected for mean background activity in the contralateral hemisphere [SUV(max)/BG and SUV(mean)/BG, respectively], biologic tumor volume) and dynamic time-activity curves, including minimal time to peak (TTP(min)). The prognostic influence of PET parameters and other clinical parameters on progression-free and overall survival was evaluated using uni- and multivariate Cox regression and Kaplan-Meier survival estimates., Results: In the group overall, median progression-free survival and overall survival were 12.2 and 21.9 mo. SUV(max)/BG, SUV(mean)/BG, and biologic tumor volume were significantly higher in WHO IV than in WHO III gliomas; median TTP(min) was 12.5 min in both groups. On univariate analysis, the factors age, WHO grade, O6-methylguanine-DNA methyltransferase promoter methylation status, contrast enhancement, initial treatment, and TTP(min) showed prognostic significance, with WHO grade, O6-methylguanine-DNA methyltransferase status, age, and TTP(min) remaining significant in the multivariate analysis. WHO grade and TTP(min) reached a similar fit for the prognostic evaluation. The prognosis of WHO III astrocytoma with an early TTP(min) of 12.5 min or less did not differ significantly from that of glioblastoma., Conclusion: Early TTP(min) is associated with worse outcome in patients with newly diagnosed astrocytic HGG. In the preoperative setting, TTP(min) can be a valuable noninvasive prognostic marker with comparable significance to WHO grade. Additionally, TTP(min) can help identify highly aggressive WHO III astrocytoma tumors and may help in adjusting standard treatment toward an individualized, risk-adapted therapy regime., (© 2015 by the Society of Nuclear Medicine and Molecular Imaging, Inc.)

Published
2015
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