Search

Your search keyword '"Tihan T"' showing total 380 results
Start Over Author "Tihan T"
380 results on '"Tihan T"'

2. Centrally Reduced Diffusion Sign for Differentiation between Treatment-Related Lesions and Glioma Progression: A Validation Study

Author

Alcaide-Leon, P, Cluceru, J, Lupo, JM, Yu, TJ, Luks, TL, Tihan, T, Bush, NA, and Villanueva-Meyer, JE

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Clinical Trials and Supportive Activities, Rare Diseases, Biomedical Imaging, Brain Cancer, Brain Disorders, Clinical Research, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Adult, Aged, Aged, 80 and over, Brain, Brain Neoplasms, Combined Modality Therapy, Diffusion Magnetic Resonance Imaging, Disease Progression, Female, Glioma, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Necrosis, Neoplasm Recurrence, Local, ROC Curve, Sensitivity and Specificity, Clinical Sciences, Neurosciences, Nuclear Medicine & Medical Imaging, Clinical sciences, Physical chemistry
Abstract

Background and purposeDifferentiating between treatment-related lesions and tumor progression remains one of the greatest dilemmas in neuro-oncology. Diffusion MR imaging characteristics may provide useful information to help make this distinction. The aim of the study was to assess the diagnostic accuracy of the centrally reduced diffusion sign for differentiation of treatment-related lesions and true tumor progression in patients with suspected glioma recurrence.Materials and methodsThe images of 231 patients who underwent an operation for suspected glioma recurrence were reviewed. Patients with susceptibility artifacts or without central necrosis were excluded. The final diagnosis was established according to histopathology reports. Two neuroradiologists classified the diffusion patterns on preoperative MR imaging as the following: 1) reduced diffusion in the solid component only, 2) reduced diffusion mainly in the solid component, 3) no reduced diffusion, 4) reduced diffusion mainly in the central necrosis, and 5) reduced diffusion in the central necrosis only. Diagnostic accuracy metrics and the area under the receiver operating characteristic curve were estimated for the diffusion patterns.ResultsOne hundred three patients were included (22 with treatment-related lesions and 81 with tumor progression). The diagnostic accuracy results for the centrally reduced diffusion pattern as a predictor of treatment-related lesions ("mainly central" and "exclusively central" patterns versus all other patterns) were as follows: 64% sensitivity (95% CI, 41%-83%), 84% specificity (95% CI, 74%-91%), 52% positive predictive value (95% CI, 37%-66%), and 89% negative predictive value (95% CI, 83%-94%).ConclusionsThe centrally reduced diffusion sign is associated with the presence of treatment effect. The probability of a histologic diagnosis of a treatment-related lesion is low (11%) in the absence of centrally reduced diffusion.

Published
2020

3. A recurrent kinase domain mutation in PRKCA defines chordoid glioma of the third ventricle

Author

Goode, B, Mondal, G, Hyun, M, Ruiz, DG, Lin, YH, Van Ziffle, J, Joseph, NM, Onodera, C, Talevich, E, Grenert, JP, Hewedi, IH, Snuderl, M, Brat, DJ, Kleinschmidt-Demasters, BK, Rodriguez, FJ, Louis, DN, Yong, WH, Lopes, MB, Rosenblum, MK, Butowski, N, Tihan, T, Bollen, AW, Phillips, JJ, Wiita, AP, Yeh, I, Jacobson, MP, Bastian, BC, Perry, A, and Solomon, DA

Subjects
Neurosciences, Brain Cancer, Genetics, Rare Diseases, Human Genome, Brain Disorders, Clinical Research, Cancer, 2.1 Biological and endogenous factors
Abstract

Chordoid glioma is a rare brain tumor thought to arise from specialized glial cells of the lamina terminalis along the anterior wall of the third ventricle. Despite being histologically low-grade, chordoid gliomas are often associated with poor outcome, as their stereotypic location in the third ventricle makes resection challenging and efficacious adjuvant therapies have not been developed. Here we performed genomic profiling on 13 chordoid gliomas and identified a recurrent D463H missense mutation in PRKCA in all tumors, which localizes in the kinase domain of the encoded protein kinase C alpha (PKCα). Expression of mutant PRKCA in immortalized human astrocytes led to increased phospho-ERK and anchorage-independent growth that could be blocked by MEK inhibition. These studies define PRKCA as a recurrently mutated oncogene in human cancer and identify a potential therapeutic vulnerability in this uncommon brain tumor.

Published
2018

4. Differentiation of brain tumor-related edema based on 3D T1rho imaging

Author

Villanueva-Meyer, JE, Barajas, RF, Mabray, MC, Chen, W, Shankaranarayanan, A, Koon, P, Barani, IJ, Tihan, T, and Cha, S

Subjects
Brain Disorders, Clinical Research, Biomedical Imaging, Clinical Trials and Supportive Activities, Cancer, Rare Diseases, Brain Cancer, Neurosciences, Brain Edema, Brain Neoplasms, Diagnosis, Differential, Diffusion Magnetic Resonance Imaging, Glioblastoma, Glioma, Humans, Magnetic Resonance Imaging, T1rho, Metastasis, Peritumoral edema, Infiltrative edema, Vasogenic edema, Clinical Sciences, Nuclear Medicine & Medical Imaging
Abstract

Background and purposeCerebral edema associated with brain tumors is an important source of morbidity. Its type depends largely on the capillary ultra-structures of the histopathologic subtype of underlying brain tumor. The purpose of our study was to differentiate vasogenic edema associated with brain metastases and infiltrative edema related to diffuse gliomas using quantitative 3D T1 rho (T1ρ) imaging.Materials and methodsPreoperative MR examination including whole brain 3D T1ρ imaging was performed in 23 patients with newly diagnosed brain tumors (9 with metastasis, 8 with lower grade glioma, LGG, 6 with glioblastoma, GBM). Mean T1ρ values were measured in regions of peritumoral non-enhancing T2 signal hyperintensity, excluding both enhancing and necrotic or cystic component, and normal-appearing white matter.ResultsMean T1ρ values were significantly elevated in the vasogenic edema surrounding intracranial metastases when compared to the infiltrative edema associated with either LGG or GBM (p=0.02 and

Published
2017

7. Clinicopathologic features of pediatric oligodendrogliomas: A series of 50 patients

Author

Rodriguez, FJ, Tihan, T, Lin, D, McDonald, W, Nigro, J, Feuerstein, B, Jackson, S, Cohen, K, and Burger, PC

Subjects
Pathology, Clinical Sciences
Abstract

Oligodendrogliomas are an important adult form of diffuse gliomas with a distinctive clinical and genetic profile. Histologically similar tumors occurring rarely in children are incompletely characterized. We studied 50 patients with oligodendrogliomas (median age at diagnosis 8 y, range 7 mo to 20 y). Tumors resembling dysembryoplastic neuroepithelial tumors or pilocytic astrocytomas or those having a "mixed" histology were excluded. Tumors at first diagnosis were low grade (n=38) or anaplastic (n=12). Histologic features included uniform round cells with perinuclear halos (100%), secondary structures (predominantly perineuronal satellitosis) (90%), calcifications (46%), and microcysts (44%). Sequential surgical specimens were obtained in 8 low-grade oligodendroglioma patients, with only 1 progressing to anaplasia. Studies for 1p19q performed in 40 cases demonstrated intact 1p19q loci in 29 (73%), 1p19q codeletion in 10 (25%), and 1p deletion with intact 19q in 1 (2%). Except for 2 young patients (3 and 11 y of age), patients with 1p19q codeletion were older than 16 years at diagnosis. Mutant IDH1 (R132H) protein immunohistochemistry was positive in 4 (of 22) (18%) cases, 3 of which also had 1p19q codeletion, whereas 1p19q status was not available on the fourth case. There was a nonsignificant trend for worse overall survival in grade III tumors, but no significant association with age, extent of resection, or 1p19q status. In summary, oligodendrogliomas with classic histology occur in the pediatric population but lack 1p19q codeletion and IDH1 (R132H) mutations in most instances. They are predominantly low grade, recur/clinically progress in a subset, but demonstrate a relatively low frequency of histologic progression. © 2014 by Lippincott Williams & Wilkins.

Published
2014

8. Announcing the Asian Oceanian Society of Neuropathology guidelines for Adapting Diagnostic Approaches for Practical Taxonomy in Resource‐Restrained Regions (AOSNP‐ADAPTR).

Author

Buckland, M. E., Sarkar, C., Santosh, V., Al‐Hussaini, M., Park, S. H., Tihan, T., Ng, H. K., and Komori, T.

Subjects
NEUROLOGICAL disorders, CENTRAL nervous system tumors, FLUORESCENCE in situ hybridization
Abstract

The article discusses the challenges of implementing the World Health Organization (WHO) classification for central nervous system (CNS) tumors in resource-restrained regions, particularly in low- and middle-income countries in the Asian Oceanian region. The lack of molecular testing facilities and trained neuropathologists, as well as the limited therapeutic options for CNS tumors, pose significant obstacles. To address these challenges, the Asian Oceanian Society of Neuropathology (AOSNP) has developed the ADAPTR guidelines, which aim to adapt the WHO classification to suit the available diagnostic resources in each medical setting. The guidelines provide practical information for diagnosing CNS tumors in resource-limited settings, with a focus on benefiting patients. Different resource levels are defined, and recommendations are tailored to each level, allowing for clinically appropriate diagnoses regardless of the available technology. The guidelines also emphasize the importance of integrating radiological information and provide comprehensive lists of immunohistochemical markers for each tumor type. Diagnostic flowcharts and regular tumor board meetings are recommended for effective implementation. [Extracted from the article]

Published
2024
Full Text
View/download PDF

10. Title: Defining the clinical and prognostic landscape of embryonal tumors with multi-layered rosettes (ETMRs), a rare brain tumor registry (RBTC) study.

Author

Gajjar A., Leary S., Mulcahy Levy J.M., Lassaletta A., Rivas E., Reddy A., Gillespie G.Y., Gupta N., Yalon-Oren M., Amariglio L., Nakamura H., Wu K.-S., Wong T.-T., Ra Y.-S., Spina M.L., Emanuele P.V., Massimi L., Buccoliero A.M., Hansford J.R., Grundy R.G., Adamek D., Fangusaro J., Scharnhorst D., Johnston D., Lafay-Cousin L., Camelo-Piragua S., Kabbara N., Boutarbouch M., Da Costa M.J.G., Hanson D., Wood P., Al-Hussaini M., Amayiri N., Wang Y., Catchpoole D., Michaud J., Bendel A.E., Ellezam B., Gerber N., Plant A., Jeffery R., Dunham C., Moertel C., Walter A., Ziegler D., Dodgshun A., Gottardo N., Demir A., Ramanujachar R., Raabe E., Mary S., Dirks P., Taylor M., Eugene H., Lindsey H., Tihan T., Mette J., Dahl C., Low S., Smith A., Hazrati L.-N., Kresak J., Gino S., Tan E., Morales A., Santa-Maria V., Hawkins C., Bartels U., Stephens D., Nobusawa S., Dufour C., Bourdeaut F., Andre N., Bouffet E., Huang A., Khan S., Solano-Paez P., Suwal T., Al-Karmi S., Lu M., Ho B., Fouladi M., Gajjar A., Leary S., Mulcahy Levy J.M., Lassaletta A., Rivas E., Reddy A., Gillespie G.Y., Gupta N., Yalon-Oren M., Amariglio L., Nakamura H., Wu K.-S., Wong T.-T., Ra Y.-S., Spina M.L., Emanuele P.V., Massimi L., Buccoliero A.M., Hansford J.R., Grundy R.G., Adamek D., Fangusaro J., Scharnhorst D., Johnston D., Lafay-Cousin L., Camelo-Piragua S., Kabbara N., Boutarbouch M., Da Costa M.J.G., Hanson D., Wood P., Al-Hussaini M., Amayiri N., Wang Y., Catchpoole D., Michaud J., Bendel A.E., Ellezam B., Gerber N., Plant A., Jeffery R., Dunham C., Moertel C., Walter A., Ziegler D., Dodgshun A., Gottardo N., Demir A., Ramanujachar R., Raabe E., Mary S., Dirks P., Taylor M., Eugene H., Lindsey H., Tihan T., Mette J., Dahl C., Low S., Smith A., Hazrati L.-N., Kresak J., Gino S., Tan E., Morales A., Santa-Maria V., Hawkins C., Bartels U., Stephens D., Nobusawa S., Dufour C., Bourdeaut F., Andre N., Bouffet E., Huang A., Khan S., Solano-Paez P., Suwal T., Al-Karmi S., Lu M., Ho B., and Fouladi M.

Abstract

ETMR, an aggressive disease characterised by C19MC alterations, were previously categorised as various histologic diagnoses. The clinical spectrum and impact of conventional multi-modal therapy on this new WHO diagnostic category remains poorly understood as a majority of ~200 cases reported to date lack molecular confirmation. We undertook comprehensive clinico-pathologic studies of a large molecularly confirmed cohort to improve disease recognition and treatment approaches. Amongst 623 CNSPNETs patients enrolled in the RBTC registry, 159 primary ETMRs were confirmed based on a combination of FISH (125), methylation analysis (88), SNP and RNAseq (32) analyses; 91% had C19MC amplification/gains/fusions, 9% lacked C19MC alterations but had global methylation features of ETMR NOS. ETMRs arose in young patients (median age 26 months) predominantly as localized disease (M0-72%, M2-3 -18%) at multiple locations including cerebrum (60%) cerebellum (18%), midline structures (6%); notably 10% were brainstem primaries mimicking DIPG. Uni-and multivariate analyses of clinical and treatment details of curative regimens available for 110 patients identified metastatic disease (p=0.002), brainstem locations(p=0.005), extent of surgery, receipt of multi-modal therapy including high dose chemotherapy and radiation (P<0.001) as significant treatment prognosticators, while C19MC status, age and gender were nonsignificant risk factors. Analyses of events in all patients showed respective EFS at 3 and 12 months of 84%(95%CI:77-91) and 37%(95%CI:20-41) and 4yr OS of 27%(95%CI:18-37) indicating despite intensified therapies ETMR is a rapidly progressive and fatal disease. Our comprehensive data on the largest cohort of molecularly-confirmed ETMRs provides a critical framework to guide current clinical management and development of clinical trials.

Published
2021

11. Clinicopathologic and molecular features of intracranial desmoplastic small round cell tumors

Author

Lee, J.C., Villanueva-Meyer, J.E., Ferris, S.P., Cham, E.M., Zucker, J., Cooney, T., Gilani, A., Kleinschmidt-DeMasters, B.K., Trembath, D., Mafra, M., Chiang, J., Ellison, D.W., Cho, S.J., Horvai, A.E., Ziffle, J. Van, Onodera, C., Devine, P., Grenert, J.P., Voijs, C.M.A., Blokland, W.T.M. van, Leng, W.W.J. de, Ploegmakers, M.J., Flucke, U.E., Pekmezci, M., Bollen, A.W., Tihan, T., Koelsche, C., Deimling, A. von, Wesseling, P., Solomon, D.A., Perry, A., Lee, J.C., Villanueva-Meyer, J.E., Ferris, S.P., Cham, E.M., Zucker, J., Cooney, T., Gilani, A., Kleinschmidt-DeMasters, B.K., Trembath, D., Mafra, M., Chiang, J., Ellison, D.W., Cho, S.J., Horvai, A.E., Ziffle, J. Van, Onodera, C., Devine, P., Grenert, J.P., Voijs, C.M.A., Blokland, W.T.M. van, Leng, W.W.J. de, Ploegmakers, M.J., Flucke, U.E., Pekmezci, M., Bollen, A.W., Tihan, T., Koelsche, C., Deimling, A. von, Wesseling, P., Solomon, D.A., and Perry, A.

Abstract

Contains fulltext : 219243.pdf (Publisher’s version ) (Closed access), Desmoplastic small round cell tumors (DSRCTs) are highly aggressive sarcomas that most commonly occur intra-abdominally, and are defined by EWSR1-WT1 gene fusion. Intracranial DSRCTs are exceptionally rare with only seven previously reported fusion-positive cases. Herein, we evaluate the clinical, morphologic, immunohistochemical and molecular features of five additional examples. All patients were male (age range 6-25 years; median 11 years), with four tumors located supratentorially and one within the posterior fossa. The histologic features were highly variable including small cell, embryonal, clear cell, rhabdoid, anaplastic and glioma-like appearances. A prominent desmoplastic stroma was seen in only two cases. The mitotic index ranged from <1 to 12/10 HPF (median 5). While all tumors showed strong desmin positivity, epithelial markers such as EMA, CAM 5.2 and other keratins were strongly positive in only one, focally positive in two and negative in two cases. EWSR1-WT1 gene fusion was present in all cases, with accompanying mutations in the TERT promoter or STAG2 gene in individual cases. Given the significant histologic diversity, in the absence of genetic evaluation these cases could easily be misinterpreted as other entities. Desmin immunostaining is a useful initial screening method for consideration of a DSRCT diagnosis, prompting confirmatory molecular testing. Demonstrating the presence of an EWSR1-WT1 fusion provides a definitive diagnosis of DSRCT. Genome-wide methylation profiles of intracranial DSRCTs matched those of extracranial DSRCTs. Thus, despite the occasionally unusual histologic features and immunoprofile, intracranial DSRCTs likely represent a similar, if not the same, entity as their soft tissue counterpart based on the shared fusion and methylation profiles.

Published
2020

13. Diffuse Midline Gliomas with Histone H3-K27M Mutation: A Series of 47 Cases Assessing the Spectrum of Morphologic Variation and Associated Genetic Alterations

Author

Solomon, DA, Wood, MD, Tihan, T, Bollen, AW, Gupta, N, Phillips, JJJ, and Perry, A

Subjects
Male, Histones, Methionine, histone H3, 2.1 Biological and endogenous factors, Aetiology, Child, Cancer, Brain Neoplasms, Glioma, Middle Aged, Isocitrate Dehydrogenase, Gene Expression Regulation, Neoplastic, ErbB Receptors, diffuse midline glioma, Child, Preschool, DIPG, Female, Adult, X-linked Nuclear Protein, Pediatric Research Initiative, Adolescent, Clinical Sciences, Glycine, histone H3.1, histone H3.3, Article, Young Adult, Rare Diseases, HIST1H3B, Genetics, Humans, Preschool, astrocytoma, Genetic Association Studies, Aged, Neoplastic, Neurology & Neurosurgery, PTEN Phosphohydrolase, glioblastoma, Neurosciences, diffuse intrinsic pontine glioma, Brain Disorders, K27M mutation, Brain Cancer, Gene Expression Regulation, Mutation, Tumor Suppressor Protein p53, H3F3A
Abstract

© 2015 International Society of Neuropathology Somatic mutations of the H3F3A and HIST1H3B genes encoding the histone H3 variants, H3.3 and H3.1, were recently identified in high-grade gliomas arising in the thalamus, pons and spinal cord of children and young adults. However, the complete range of patients and locations in which these tumors arise, as well as the morphologic spectrum and associated genetic alterations remain undefined. Here, we describe a series of 47 diffuse midline gliomas with histone H3-K27M mutation. The 25 male and 22 female patients ranged in age from 2 to 65 years (median = 14). Tumors were centered not only in the pons, thalamus, and spinal cord, but also in the third ventricle, hypothalamus, pineal region and cerebellum. Patients with pontine tumors were younger (median = 7 years) than those with thalamic (median = 24 years) or spinal (median = 25 years) tumors. A wide morphologic spectrum was encountered including gliomas with giant cells, epithelioid and rhabdoid cells, primitive neuroectodermal tumor (PNET)-like foci, neuropil-like islands, pilomyxoid features, ependymal-like areas, sarcomatous transformation, ganglionic differentiation and pleomorphic xanthoastrocytoma (PXA)-like areas. In this series, histone H3-K27M mutation was mutually exclusive with IDH1 mutation and EGFR amplification, rarely co-occurred with BRAF-V600E mutation, and was commonly associated with p53 overexpression, ATRX loss (except in pontine gliomas), and monosomy 10.

Published
2016

14. Well-differentiated pediatric glial neoplasms with features of oligodendroglioma, angiocentric glioma and dysembryoplastic neuroepithelial tumors: A morphological diagnostic challenge [Oligodendrogliom, anjiosentrik gliom ve disembriyoplastik nöroepitelyal tümör özellikleri taşi{dotless}yan İyi diferansiye pediatrik glial tümörler: Morfolojik bir tani{dotless}sal sorun]

Author

Keser H., Barnes M., Moes G., Lee H.S., Tihan T., and Keser, H., Department of Pathology, Cumhuriyet University, Sivas, Turkey -- Barnes, M., University of California, San Francisco, United States -- Moes, G., Kaiser Permanente Oakland Medical Center, Oakland, United States -- Lee, H.S., University of California, San Francisco, United States -- Tihan, T., University of California, San Francisco, United States

Subjects
Oligodendroglioma, Glioma, Pediatric brain neoplasms
Abstract

Objective: Oligodendrogliomas are rare in the pediatric population, and most oligodendroglioma-like tumors in this age group may belong to other entities. In addition, accurate diagnosis and grading of such lesions using criteria developed for adult oligodendrogliomas prove difficult, and often controversial. Material and Method: During a study of tumors previously diagnosed as pediatric oligodendroglioma, we identified four tumors displayed features of that resembled oligodendroglioma, angiocentric glioma and dysembryoplastic neuroepithelial tumor but could not be classified as either one of these entities. Ther clinical, histological and immunohistochemical features of these cases were investigated in this study. Results: Two male (both 9 years old) and two female (ages 4 years and 20 months) patients presented with new onset of seizures. All patients were treated surgically, and two required reoperation. Histologically, the tumors were well-differentiated glial neoplasms with focal angiocentric pattern, delicate vascularity, diffuse growth, infiltrative margins, cortical nodules, focal myxoid areas, and leptomeningeal extension. Immunohistochemical studies showed diffuse nuclear positivity with Olig-2 and GFAP antibodies, whereas staining with neuronal markers, EMA, p53, and IDH1 were negative. Fluorescent in-situ hybridization analysis demonstrated intact 1p/19q in all tumors, and there was no ultrastructural evidence of ependymal differentiation. All patients were alive with disease with a mean follow-up of 112 months. Conclusion: These four cases illustrate the morphological diversity of well-differentiated, oligodendroglioma-like glial neoplasms and the uncertainty in their classification among pediatric tumors., Tihan, T.; University of California, San Francisco, Department of Pathology, San Francisco, United States; email: tarik.tihan@ucsf.edu

Published
2014

18. Integrated (epi)-Genomic Analyses Identify Subgroup-Specific Therapeutic Targets in CNS Rhabdoid Tumors.

Author

Torchia, J, Golbourn, B, Feng, S, Ho, KC, Sin-Chan, P, Vasiljevic, A, Norman, JD, Guilhamon, P, Garzia, L, Agamez, NR, Lu, M, Chan, TS, Picard, D, de Antonellis, P, Khuong-Quang, D-A, Planello, AC, Zeller, C, Barsyte-Lovejoy, D, Lafay-Cousin, L, Letourneau, L, Bourgey, M, Yu, M, Gendoo, DMA, Dzamba, M, Barszczyk, M, Medina, T, Riemenschneider, AN, Morrissy, AS, Ra, Y-S, Ramaswamy, V, Remke, M, Dunham, CP, Yip, S, Ng, H-K, Lu, J-Q, Mehta, V, Albrecht, S, Pimentel, J, Chan, JA, Somers, GR, Faria, CC, Roque, L, Fouladi, M, Hoffman, LM, Moore, AS, Wang, Y, Choi, SA, Hansford, JR, Catchpoole, D, Birks, DK, Foreman, NK, Strother, D, Klekner, A, Bognár, L, Garami, M, Hauser, P, Hortobágyi, T, Wilson, B, Hukin, J, Carret, A-S, Van Meter, TE, Hwang, EI, Gajjar, A, Chiou, S-H, Nakamura, H, Toledano, H, Fried, I, Fults, D, Wataya, T, Fryer, C, Eisenstat, DD, Scheinemann, K, Fleming, AJ, Johnston, DL, Michaud, J, Zelcer, S, Hammond, R, Afzal, S, Ramsay, DA, Sirachainan, N, Hongeng, S, Larbcharoensub, N, Grundy, RG, Lulla, RR, Fangusaro, JR, Druker, H, Bartels, U, Grant, R, Malkin, D, McGlade, CJ, Nicolaides, T, Tihan, T, Phillips, J, Majewski, J, Montpetit, A, Bourque, G, Bader, GD, Reddy, AT, Gillespie, GY, Warmuth-Metz, M, Rutkowski, S, Tabori, U, Lupien, M, Brudno, M, Schüller, U, Pietsch, T, Judkins, AR, Hawkins, CE, Bouffet, E, Kim, S-K, Dirks, PB, Taylor, MD, Erdreich-Epstein, A, Arrowsmith, CH, De Carvalho, DD, Rutka, JT, Jabado, N, Huang, A, Torchia, J, Golbourn, B, Feng, S, Ho, KC, Sin-Chan, P, Vasiljevic, A, Norman, JD, Guilhamon, P, Garzia, L, Agamez, NR, Lu, M, Chan, TS, Picard, D, de Antonellis, P, Khuong-Quang, D-A, Planello, AC, Zeller, C, Barsyte-Lovejoy, D, Lafay-Cousin, L, Letourneau, L, Bourgey, M, Yu, M, Gendoo, DMA, Dzamba, M, Barszczyk, M, Medina, T, Riemenschneider, AN, Morrissy, AS, Ra, Y-S, Ramaswamy, V, Remke, M, Dunham, CP, Yip, S, Ng, H-K, Lu, J-Q, Mehta, V, Albrecht, S, Pimentel, J, Chan, JA, Somers, GR, Faria, CC, Roque, L, Fouladi, M, Hoffman, LM, Moore, AS, Wang, Y, Choi, SA, Hansford, JR, Catchpoole, D, Birks, DK, Foreman, NK, Strother, D, Klekner, A, Bognár, L, Garami, M, Hauser, P, Hortobágyi, T, Wilson, B, Hukin, J, Carret, A-S, Van Meter, TE, Hwang, EI, Gajjar, A, Chiou, S-H, Nakamura, H, Toledano, H, Fried, I, Fults, D, Wataya, T, Fryer, C, Eisenstat, DD, Scheinemann, K, Fleming, AJ, Johnston, DL, Michaud, J, Zelcer, S, Hammond, R, Afzal, S, Ramsay, DA, Sirachainan, N, Hongeng, S, Larbcharoensub, N, Grundy, RG, Lulla, RR, Fangusaro, JR, Druker, H, Bartels, U, Grant, R, Malkin, D, McGlade, CJ, Nicolaides, T, Tihan, T, Phillips, J, Majewski, J, Montpetit, A, Bourque, G, Bader, GD, Reddy, AT, Gillespie, GY, Warmuth-Metz, M, Rutkowski, S, Tabori, U, Lupien, M, Brudno, M, Schüller, U, Pietsch, T, Judkins, AR, Hawkins, CE, Bouffet, E, Kim, S-K, Dirks, PB, Taylor, MD, Erdreich-Epstein, A, Arrowsmith, CH, De Carvalho, DD, Rutka, JT, Jabado, N, and Huang, A

Abstract

We recently reported that atypical teratoid rhabdoid tumors (ATRTs) comprise at least two transcriptional subtypes with different clinical outcomes; however, the mechanisms underlying therapeutic heterogeneity remained unclear. In this study, we analyzed 191 primary ATRTs and 10 ATRT cell lines to define the genomic and epigenomic landscape of ATRTs and identify subgroup-specific therapeutic targets. We found ATRTs segregated into three epigenetic subgroups with distinct genomic profiles, SMARCB1 genotypes, and chromatin landscape that correlated with differential cellular responses to a panel of signaling and epigenetic inhibitors. Significantly, we discovered that differential methylation of a PDGFRB-associated enhancer confers specific sensitivity of group 2 ATRT cells to dasatinib and nilotinib, and suggest that these are promising therapies for this highly lethal ATRT subtype.

Published
2016

19. Pitfalls in the use of whole slide imaging for the diagnosis of central nervous system tumors: a pilot study in surgical neuropathology

Author

Uysal, Sanem Pınar; Orhan Yelda Ceren, Pekmezci M.; Tihan T.; Lee H. S., School of Medicine, Uysal, Sanem Pınar; Orhan Yelda Ceren, Pekmezci M.; Tihan T.; Lee H. S., and School of Medicine

Abstract

Background: Whole slide imaging (WSI) finds increasingly higher value in everyday surgical pathology in addition to its well-established use for educational and research purposes. However, its diagnostic utility, especially in subspecialty settings such as neuropathology, is not fully validated. Neuropathology practice is unique with smaller overall tissue size and frequent need for high-power evaluation. In addition, tumor grade is an integral part of the initial diagnosis. The purpose of this study is to assess the feasibility of primary pathology diagnosis of surgical neuropathology specimens using WSI. Materials and Methods: We reviewed consecutive surgical neuropathology cases diagnosed in our institution during a 2-month period and identified a single diagnostic slide, which was scanned at 40× magnification. Two neuropathologists who were blinded to the original diagnoses reviewed the whole slide image and rendered a diagnosis including tumor grade when applicable. They reviewed the single diagnostic slide after a wash-out period. Intra- and inter-observer discrepancies, as well as reasons for discrepancies, were evaluated. Results: The concordance rates were 94.9% and 88% for two neuropathologists. Two critical issues leading to discrepancies were identified: (1) identification of mitoses and (2) recognition of nuclear details. Conclusions: Given the current study is exclusively for surgical neuropathology cases, an all-encompassing conclusion about the utility of WSI for diagnostic purposes may not be available. Nevertheless, pathologists should be aware of the potential pitfalls due to identification of mitotic figures and nuclear details. We recommend independent validation for each subspecialty of pathology to identify subspecialty-specific concerns, so they can be properly addressed. © 2016 Journal of Pathology Informatics | Published by Wolters Kluwer -Medknow., NA

Published
2016

20. INHERITED VARIANTS NEAR TERC AND TERT ARE ASSOCIATED WITH LONGER TELOMERES AND INCREASED GLIOMA RISK: GENOME-WIDE ASSOCIATION RESULTS FROM THE UCSF ADULT GLIOMA STUDY AND THE ENGAGE CONSORTIUM TELOMERE GROUP

Author

Walsh, K, Codd, V, Smirnov, I, Rice, T, Decker, P, Hansen, H, Molinaro, A, Pekmezci, M, Tihan, T, Berger, M, Chang, S, Prados, M, Lachance, D, O'Neill, BP, van der Harst, P, Wiencke, J, Samani, N, Jenkins, R, Wrensch, M, and Grp, ENGAGECT

Subjects
Oncology and Carcinogenesis, Neurosciences, Oncology & Carcinogenesis
Published
2014

24. Clinical Outcomes and Prognostic Factors for Central Neurocytoma

Author

Imber, B.S., primary, Braunstein, S.E., additional, Wu, F.Y., additional, Nabavizadeh, N., additional, Boehling, N., additional, Weinberg, V.K., additional, Tihan, T., additional, Chang, S., additional, McDermott, M.W., additional, Prados, M., additional, Berger, M.S., additional, and Haas-Kogan, D.A., additional

Published
2015
Full Text
View/download PDF

28. GE-09 * TERT PROMOTER MUTATION, IDH MUTATION AND 1p/19q CODELETION DEFINE FIVE GLIOMA MOLECULAR GROUPS WITH SPECIFIC CLINICAL CHARACTERISTICS AND GERMLINE VARIANT ASSOCIATIONS

Author

Eckel-Passow, J., primary, Lachance, D., additional, Walsh, K., additional, Decker, P., additional, Sicotte, H., additional, Pekmezci, M., additional, Molinaro, A., additional, Rice, T., additional, Kosel, M., additional, Smirnov, I., additional, Sarkar, G., additional, Caron, A., additional, Kollmeyer, T., additional, Giannini, C., additional, Huse, J., additional, Tihan, T., additional, Wiemels, J., additional, Wiencke, J., additional, Wrensch, M., additional, and Jenkins, R., additional

Published
2014
Full Text
View/download PDF

29. MUTATION-BASED MOLECULAR GLIOMA CLASSIFICATION: PREVALENCE AND ASSOCIATION WITH GERMLINE RISK SNPS

Author

Jenkins, R. B., primary, Decker, P., additional, Kosel, M., additional, Eckel-Passow, J., additional, Walsh, K. M., additional, Smirnov, I. V., additional, Caron, A., additional, Kollmeyer, T., additional, Rice, T., additional, Hansen, H. M., additional, Molinaro, A. M., additional, McCoy, L. S., additional, Bracci, P. M., additional, Cabriga, B. S., additional, Marshall, R., additional, Pekmezci, M., additional, Zheng, S., additional, O'Neill, B., additional, Buckner, J., additional, Giannini, C., additional, Perry, A., additional, Tihan, T., additional, Berger, M. S., additional, Chang, S. M., additional, Prados, M., additional, Wiemels, J., additional, Wiencke, J., additional, Wrensch, M., additional, and Lachance, D., additional

Published
2014
Full Text
View/download PDF

30. SINGLE NUCLEOTIDE POLYMORPHISMS (SNPS) ASSOCIATED WITH GLIOMA SURVIVAL

Author

Wrensch, M., primary, Walsh, K. M., additional, Smirnov, I. V., additional, Rice, T., additional, Hansen, H. M., additional, Molinaro, A. M., additional, McCoy, L. S., additional, Bracci, P. M., additional, Cabriga, B. S., additional, Perry, A., additional, Marshall, R., additional, Pekmezci, M., additional, Zheng, S., additional, Wiemels, J. L., additional, Tihan, T., additional, Berger, M. S., additional, Chang, S. M., additional, Prados, M. D., additional, Wiencke, J. K., additional, Decker, P., additional, Kosel, M., additional, Eckel-Passow, J., additional, Caron, A., additional, Kollmeyer, T., additional, O'Neill, B., additional, Giannini, C., additional, Buckner, J., additional, Lachance, D., additional, and Jenkins, R., additional

Published
2014
Full Text
View/download PDF

31. Brain tumor epidemiology : Consensus from the Brain Tumor Epidemiology Consortium

Author

Bondy, M L, Scheurer, M E, Malmer, Beatrice, Barnholtz-Sloan, J S, Davis, F G, Il'yasova, D, Kruchko, C, McCarthy, B J, Rajaraman, P, Schwartzbaum, J A, Sadetzki, S, Schlehofer, B, Tihan, T, Wiemels, J L, Wrensch, M, Buffler, P A, Bondy, M L, Scheurer, M E, Malmer, Beatrice, Barnholtz-Sloan, J S, Davis, F G, Il'yasova, D, Kruchko, C, McCarthy, B J, Rajaraman, P, Schwartzbaum, J A, Sadetzki, S, Schlehofer, B, Tihan, T, Wiemels, J L, Wrensch, M, and Buffler, P A

Abstract

Epidemiologists in the Brain Tumor Epidemiology Consortium (BTEC) have prioritized areas for further research. Although many risk factors have been examined over the past several decades, there are few consistent findings, possibly because of small sample sizes in individual studies and differences between studies in patients, tumor types, and methods of classification. Individual studies generally have lacked samples of sufficient size to examine interactions. A major priority based on available evidence and technologies includes expanding research in genetics and molecular epidemiology of brain tumors. BTEC has taken an active role in Promoting understudied groups, such as pediatric brain tumors; the etiology of rare glioma subtypes, such as oligodendroglioma; and meningioma, which, although it is not uncommon, has only recently, been registered systematically in the United States. There also is a pressing need for more researchers, especially junior investigators, to study brain tumor epidemiology. However, relatively poor funding for brain tumor research has made it difficult to encourage careers in this area. In this report, BTEC epidemiologists reviewed the groups Consensus oil the Current state of scientific findings, and they present a consensus oil research priorities to identify which important areas the science should move to address.

Published
2008
Full Text
View/download PDF

32. Genetic variants in telomerase-related genes are associated with an older age at diagnosis in glioma patients: evidence for distinct pathways of gliomagenesis

Author

Walsh, K. M., primary, Rice, T., additional, Decker, P. A., additional, Kosel, M. L., additional, Kollmeyer, T., additional, Hansen, H. M., additional, Zheng, S., additional, McCoy, L. S., additional, Bracci, P. M., additional, Anderson, E., additional, Hsuang, G., additional, Wiemels, J. L., additional, Pico, A. R., additional, Smirnov, I., additional, Molinaro, A. M., additional, Tihan, T., additional, Berger, M. S., additional, Chang, S. M., additional, Prados, M. D., additional, Lachance, D. H., additional, Sicotte, H., additional, Eckel-Passow, J. E., additional, Wiencke, J. K., additional, Jenkins, R. B., additional, and Wrensch, M. R., additional

Published
2013
Full Text
View/download PDF

33. Inherited variant on chromosome 11q23 increases susceptibility to IDH-mutated but not IDH-normal gliomas regardless of grade or histology

Author

Rice, T., primary, Zheng, S., additional, Decker, P. A., additional, Walsh, K. M., additional, Bracci, P., additional, Xiao, Y., additional, McCoy, L. S., additional, Smirnov, I., additional, Patoka, J. S., additional, Hansen, H. M., additional, Hsuang, G., additional, Wiemels, J. L., additional, Tihan, T., additional, Pico, A. R., additional, Prados, M. D., additional, Chang, S. M., additional, Berger, M. S., additional, Caron, A., additional, Fink, S., additional, Kollmeyer, T., additional, Rynearson, A., additional, Voss, J., additional, Kosel, M. L., additional, Fridley, B. L., additional, Lachance, D. H., additional, Eckel-Passow, J. E., additional, Sicotte, H., additional, O'Neill, B. P., additional, Giannini, C., additional, Wiencke, J. K., additional, Jenkins, R. B., additional, and Wrensch, M. R., additional

Published
2013
Full Text
View/download PDF

34. CLIN-PATHOLOGY

Author

Alexandru, D., primary, Satyadev, R., additional, So, W., additional, Lee, S. H., additional, Lee, Y. S., additional, Hong, Y.-K., additional, Kang, C. S., additional, Rodgers, S. D., additional, Marascalchi, B. J., additional, Strom, R. G., additional, Riina, H., additional, Samadani, U., additional, Frempong-Boadu, A., additional, Babu, R., additional, Sen, C., additional, Zagzag, D., additional, Anderson, M. D., additional, Abel, T. W., additional, Moots, P. L., additional, Odia, Y., additional, Orr, B. A., additional, Eberhart, C. G., additional, Rodriguez, F., additional, Sweis, R. T., additional, Lavingia, J., additional, Connelly, J., additional, Cochran, E., additional, van den Bent, M., additional, Hartmann, C., additional, Preusser, M., additional, Strobel, T., additional, Dubbink, H. J., additional, Kros, J. M., additional, von Deimling, A., additional, Boisselier, B., additional, Sanson, M., additional, Halling, K. C., additional, Diefes, K. L., additional, Aldape, K., additional, Giannini, C., additional, Rodriguez, F. J., additional, Ligon, A. H., additional, Horkayne-Szakaly, I., additional, Rushing, E. J., additional, Ligon, K. L., additional, Vena, N., additional, Garcia, D. I., additional, Douglas Cameron, J., additional, Raghunathan, A., additional, Wani, K., additional, Armstrong, T. S., additional, Vera-Bolanos, E., additional, Fouladi, M., additional, Gajjar, A., additional, Goldman, S., additional, Lehman, N. L., additional, Metellus, P., additional, Mikkelsen, T., additional, Necesito-Reyes, M. J. T., additional, Omuro, A., additional, Packer, R. J., additional, Partap, S., additional, Pollack, I. F., additional, Prados, M. D., additional, Ian Robbins, H., additional, Soffietti, R., additional, Wu, J., additional, Gilbert, M. R., additional, Aldape, K. D., additional, Prosniak, M., additional, Harshyne, L. A., additional, Andrews, D. W., additional, Craig Hooper, D., additional, Kagawa, N., additional, Hosen, N., additional, Kijima, N., additional, Hirayama, R., additional, Chiba, Y., additional, Yamamoto, F., additional, Kinoshita, M., additional, Hashimoto, N., additional, Fujimoto, Y., additional, Yoshimine, T., additional, Hu, J., additional, Nuno, M., additional, Patil, C., additional, Rudnick, J., additional, Phuphanich, S., additional, Bannykh, S., additional, Chu, R., additional, Yu, J., additional, Black, K., additional, Choi, J., additional, Kim, D., additional, Shim, K. W., additional, Kim, S. H., additional, Kanno, H., additional, Nishihara, H., additional, Tanaka, S., additional, Yanagi, T., additional, Buczkowicz, P., additional, Khuong-Quang, D.-A., additional, Rakopoulos, P., additional, Bouffet, E., additional, Morrison, A., additional, Bartels, U., additional, Pfister, S. M., additional, Jabado, N., additional, Hawkins, C., additional, Weinberg, B. D., additional, Newell, K. L., additional, Kumar, P., additional, Wang, F., additional, Venneti, S., additional, Madden, M., additional, Coyne, T., additional, Phillips, J., additional, Gorovets, D., additional, Huse, J., additional, Kofler, J., additional, Lu, C., additional, Tihan, T., additional, Sullivan, L., additional, Santi, M., additional, Judkins, A., additional, Thompson, C., additional, Perry, A., additional, Iorgulescu, J. B., additional, Laufer, I., additional, Hameed, M., additional, Lis, E., additional, Boland, P., additional, Komotar, R., additional, Bilsky, M., additional, Amato-Watkins, A. C., additional, Neal, J., additional, Rees, A. D., additional, Davies, J. S., additional, Hayhurst, C., additional, Lu-Emerson, C., additional, Snuderl, M., additional, Davidson, C., additional, Kirkpatrick, N. D., additional, Huang, Y., additional, Duda, D. G., additional, Ancukiewicz, M., additional, Stemmer-Rachamimov, A., additional, Batchelor, T. T., additional, Jain, R. K., additional, Ellezam, B., additional, Theeler, B. J., additional, Sadighi, Z. S., additional, Mehta, V., additional, Tran, M.-D. T., additional, Adesina, A. M., additional, Puduvalli, V. K., additional, and Bruner, J. M., additional

Published
2012
Full Text
View/download PDF

35. LAB-CELL BIOLOGY AND SIGNALING

Author

Kijima, N., primary, Hosen, N., additional, Kagawa, N., additional, Hashimoto, N., additional, Chiba, Y., additional, Kinoshita, M., additional, Sugiyama, H., additional, Yoshimine, T., additional, Kim, Y. Z., additional, Kim, K. H., additional, Lee, E. H., additional, Hu, B., additional, Sim, H., additional, Mohan, N., additional, Agudelo-Garcia, P., additional, Nuovo, G., additional, Cole, S., additional, Viapiano, M. S., additional, McFarland, B. C., additional, Hong, S. W., additional, Rajbhandari, R., additional, Twitty, G. B., additional, Kenneth Gray, G., additional, Yu, H., additional, Langford, C. P., additional, Yancey Gillespie, G., additional, Benveniste, E. N., additional, Nozell, S. E., additional, Nitta, R., additional, Mitra, S., additional, Bui, T., additional, Li, G., additional, Munoz, J. L., additional, Rodriguez-Cruz, V., additional, Rameshwar, P., additional, See, W. L., additional, Mukherjee, J., additional, Shannon, K. M., additional, Pieper, R. O., additional, Floyd, D. H., additional, Xiao, A., additional, Purow, B. W., additional, Lavon, I., additional, Zrihan, D., additional, Refael, M., additional, Bier, A., additional, Canello, T., additional, Siegal, T., additional, Granit, A., additional, Xie, Q., additional, Wang, X., additional, Gong, Y., additional, Mao, Y., additional, Chen, X., additional, Zhou, L., additional, Lee, S. X., additional, Tunkyi, A., additional, Wong, E. T., additional, Swanson, K. D., additional, Zhang, K., additional, Chen, L., additional, Zhang, J., additional, Shi, Z., additional, Han, L., additional, Pu, P., additional, Kang, C., additional, Cho, W. H., additional, Ogawa, D., additional, Godlewski, J., additional, Bronisz, A., additional, Antonio Chiocca, E., additional, Mustafa, D. A. M., additional, Sieuwerts, A. M., additional, Smid, M., additional, de Weerd, V., additional, Martens, J. W., additional, Foekens, J. A., additional, Kros, J. M., additional, McCulloch, C., additional, Graff, J., additional, Sui, Y., additional, Dinn, S., additional, Huang, Y., additional, Li, Q., additional, Fiona, G., additional, Nakashima, H., additional, Leiss, L., additional, Manini, I., additional, Enger, P. O., additional, Yang, C., additional, Iyer, R., additional, Yu, A. C. H., additional, Li, S., additional, Ikejiri, B. L., additional, Zhuang, Z., additional, Lonser, R., additional, Massoud, T. F., additional, Paulmurugan, R., additional, Gambhir, S. S., additional, Merrill, M. J., additional, Sun, M., additional, Chen, M., additional, Edwards, N. A., additional, Shively, S. B., additional, Lonser, R. R., additional, Baia, G. S., additional, Caballero, O. L., additional, Orr, B. A., additional, Lal, A., additional, Ho, J. S., additional, Cowdrey, C., additional, Tihan, T., additional, Mawrin, C., additional, Riggins, G. J., additional, Lu, D., additional, Leo, C., additional, Wheeler, H., additional, McDonald, K., additional, Schulte, A., additional, Zapf, S., additional, Stoupiec, M., additional, Kolbe, K., additional, Riethdorf, S., additional, Westphal, M., additional, Lamszus, K., additional, Timmer, M., additional, Rohn, G., additional, Koch, A., additional, Goldbrunner, R., additional, Ruggieri, R., additional, Vanan, I., additional, Dong, Z., additional, Sarkaria, J. N., additional, Tran, N. L., additional, Berens, M. E., additional, Symons, M., additional, Rowther, F. B., additional, Dawson, T., additional, Ashton, K., additional, Darling, J., additional, Warr, T., additional, Okamoto, M., additional, Palanichamy, K., additional, Gordon, N., additional, Patel, D., additional, Walston, S., additional, Krishanan, T., additional, Chakravarti, A., additional, Kalinina, J., additional, Carroll, A., additional, Wang, L., additional, Yu, Q., additional, Mancheno, D. E., additional, Wu, S., additional, Liu, F., additional, Ahn, J., additional, He, M., additional, Mao, H., additional, Van Meir, E. G., additional, Debinski, W., additional, Gonzales, O., additional, Beauchamp, A., additional, Gibo, D. M., additional, Seals, D. F., additional, Speranza, M. C., additional, Frattini, V., additional, Kapetis, D., additional, Pisati, F., additional, Eoli, M., additional, Pellegatta, S., additional, Finocchiaro, G., additional, Maherally, Z., additional, Smith, J. R., additional, Pilkington, G. J., additional, Zhu, W., additional, Wang, Q., additional, Clark, P. A., additional, Yang, S.-S., additional, Lin, S.-H., additional, Kahle, K. T., additional, Kuo, J. S., additional, Sun, D., additional, Hossain, M. B., additional, Cortes-Santiago, N., additional, Gururaj, A., additional, Thomas, J., additional, Gabrusiewicz, K., additional, Gumin, J., additional, Xipell, E., additional, Lang, F., additional, Fueyo, J., additional, Yung, W. K. A., additional, Gomez-Manzano, C., additional, Cook, N. J., additional, Lawrence, J. E., additional, Rovin, R. A., additional, Belton, R. J., additional, Winn, R. J., additional, Ferluga, S., additional, Lee, S.-H., additional, Khwaja, F. W., additional, Zerrouqi, A., additional, Devi, N. S., additional, Drucker, K. L., additional, Lee, H. K., additional, Finniss, S., additional, Cazacu, S., additional, Poisson, L., additional, Xiang, C., additional, Rempel, S. A., additional, Mikkelsen, T., additional, Brodie, C., additional, Shen, J., additional, Kenchappa, R. S., additional, Valadez, J. G., additional, Cooper, M. K., additional, Carter, B. D., additional, Forsyth, P. A., additional, Lee, J. S., additional, Erdreich-Epstein, A., additional, Song, H.-R., additional, Lawn, S., additional, Kenchappa, R., additional, Forsyth, P., additional, Lim, K. J., additional, Bar, E. E., additional, Eberhart, C. G., additional, Blough, M., additional, Alnajjar, M., additional, Chesnelong, C., additional, Weiss, S., additional, Chan, J., additional, Cairncross, G., additional, Wykosky, J., additional, Cavenee, W., additional, Furnari, F., additional, Brown, K. E., additional, Keir, S. T., additional, Sampson, J. H., additional, Bigner, D. D., additional, Kwatra, M. M., additional, Kotipatruni, R. P., additional, Thotala, D. K., additional, Jaboin, J., additional, Taylor, T. E., additional, Schinzel, A. C., additional, Hahn, W. C., additional, Cavenee, W. K., additional, Furnari, F. B., additional, Kapoor, G. S., additional, Macyszyn, L., additional, Bi, Y., additional, Fetting, H., additional, Poptani, H., additional, Ittyerah, R., additional, Davuluri, R. V., additional, O'Rourke, D., additional, Pitter, K. L., additional, Hosni-Ahmed, A., additional, Colevas, K., additional, Holland, E. C., additional, Jones, T. S., additional, Malhotra, A., additional, Potts, C., additional, Fernandez-Lopez, A., additional, Kenney, A. M., additional, Cheng, S., additional, Feng, H., additional, Jarzynka, M. J., additional, Li, Y., additional, Keezer, S., additional, Johns, T. G., additional, Hamilton, R. L., additional, Vuori, K., additional, Nishikawa, R., additional, Fenton, T., additional, Cheng, T., additional, Mikheev, A. M., additional, Mikheeva, S. A., additional, Silber, J. R., additional, Horner, P. J., additional, Rostomily, R., additional, Henson, E. S., additional, Brown, M., additional, Eisenstat, D. D., additional, Gibson, S. B., additional, Price, R. L., additional, Song, J., additional, Bingmer, K., additional, Oglesbee, M., additional, Cook, C., additional, Kwon, C.-H., additional, Nguyen, T. T., additional, Chiocca, E. A., additional, Lukiw, W. J., additional, Culicchia, F., additional, Jones, B. M., additional, Zhao, Y., additional, and Bhattacharjee, S., additional

Published
2012
Full Text
View/download PDF

36. EPIDEMIOLOGY

Author

Nagasawa, D. T., primary, Bergsneider, M., additional, Kelly, D., additional, Shafa, B., additional, Duong, D., additional, Ausman, J., additional, Liau, L., additional, McBride, D., additional, Yang, I., additional, Mann, B. S., additional, Yabroff, R., additional, Harlan, L., additional, Zeruto, C., additional, Abrams, J., additional, Gondi, V., additional, Eickhoff, J., additional, Tome, W. A., additional, Kozak, K. R., additional, Mehta, M. P., additional, Field, K. M., additional, Drummond, K., additional, Yilmaz, M., additional, Gibbs, P., additional, Rosenthal, M. A., additional, Allaei, R., additional, Johnson, K. J., additional, Hooten, A. J., additional, Kaste, E., additional, Ross, J. A., additional, Largaespada, D. A., additional, Johnson, D. R., additional, O'Neill, B. P., additional, Rice, T., additional, Zheng, S., additional, Xiao, Y., additional, Decker, P. A., additional, McCoy, L. S., additional, Smirnov, I., additional, Patoka, J. S., additional, Hansen, H. M., additional, Wiemels, J. L., additional, Tihan, T., additional, Prados, M. D., additional, Chang, S. M., additional, Berger, M. S., additional, Pico, A., additional, Rynearson, A., additional, Voss, J., additional, Caron, A., additional, Kosel, M. L., additional, Fridley, B. L., additional, Lachance, D. H., additional, Giannini, C., additional, Wiencke, J. K., additional, Jenkins, R. B., additional, Wrensch, M. R., additional, Buckner, J. C., additional, Burch, P. A., additional, Thompson, R. C., additional, Nabors, L. B., additional, Olson, J. J., additional, Brem, S., additional, Madden, M. H., additional, Browning, J. E., additional, Egan, K. M., additional, Pereira, E. A., additional, Livermore, J., additional, Alexe, D. M., additional, Ma, R., additional, Ansorge, O., additional, Cadoux-Hudson, T. A., additional, Wang, M., additional, Dignam, J., additional, Won, M., additional, Curran, W., additional, Mehta, M., additional, Gilbert, M., additional, Terry, A. R., additional, Barker, F. G., additional, Leffert, L. R., additional, Bateman, B., additional, Souter, I., additional, Plotkin, S. R., additional, Ishaq, O., additional, Montgomery, J., additional, Terezakis, S., additional, Wharam, M., additional, Lim, M., additional, Holdhoff, M., additional, Kleinberg, L., additional, Redmond, K., additional, Kruchko, C., additional, Paker, A. M., additional, Chi, T. L., additional, Kamiya-Matsuoka, C., additional, Loghin, M. E., additional, Lautenschlaeger, T., additional, Dedousi-Huebner, V., additional, and Chakravarti, A., additional

Published
2011
Full Text
View/download PDF

37. Immunotherapy

Author

Fujita, M., primary, Kohanbash, G., additional, McDonald, H. A., additional, Delamarre, L., additional, Decker, S. A., additional, Ohlfest, J. R., additional, Okada, H., additional, Kalinski, P., additional, Ueda, R., additional, Hoji, A., additional, Donegan, T. E., additional, Mintz, A. H., additional, Engh, J. A., additional, Bartlett, D. L., additional, Brown, C. K., additional, Zeh, H., additional, Holtzman, M. P., additional, Reinhart, T. A., additional, Whiteside, T. L., additional, Butterfield, L. H., additional, Hamilton, R. L., additional, Potter, D. M., additional, Pollack, I. F., additional, Salazar, A. M., additional, Lieberman, F. S., additional, Olin, M. R., additional, Andersen, B. M., additional, Grogan, P. T., additional, Hunt, M., additional, Popescu, F. E., additional, Xiong, Z. L., additional, Seiler, C., additional, Forster, C. L., additional, SantaCruz, K. S., additional, Chen, W., additional, Blazar, B. R., additional, Hu, J., additional, Wheeler, C. J., additional, Phuphanich, S., additional, Rudnick, J., additional, Nuno, M., additional, Serrano, N., additional, Dantis, J., additional, Richardson, J., additional, Mazer, M., additional, Wang, H. Q., additional, Chu, R., additional, Black, K. L., additional, Yu, J., additional, Li, Y. M., additional, Vallera, D. A., additional, Hall, W. A., additional, Rudnick, J. D., additional, Chu, R. M., additional, Wang, H., additional, Yu, J. S., additional, Yang, I., additional, Han, S., additional, Tihan, T., additional, Wrensch, M., additional, Parsa, A. T., additional, Hunt, M. A., additional, Gallardo, J. L., additional, Pluhar, G. E., additional, Brown, C. E., additional, Starr, R., additional, Martinez, C., additional, Bading, J., additional, Ressler, J. A., additional, Badie, B., additional, Jensen, M. C., additional, Glick, R. P., additional, Ksendzovsky, A., additional, Zengou, R., additional, Polak, P., additional, Simonini, V., additional, Lichtor, T., additional, Feinstein, D., additional, Chow, K. K., additional, Ahmed, N., additional, Salsman, V. S., additional, Kew, Y., additional, Powell, S., additional, Grossman, R., additional, Heslop, H. E., additional, Gottschalk, S., additional, Barnett, F. H., additional, Marchetti, V., additional, Wang, M., additional, Johnson, A., additional, Scheppke, L., additional, Jacobson, R., additional, Nemerow, G., additional, Friedlander, M., additional, Salsman, V., additional, Leen, A. M., additional, Bollard, C. M., additional, Rooney, C., additional, New, P. Z., additional, Salvoldo, B., additional, and Heslop, H., additional

Published
2010
Full Text
View/download PDF

38. Reply

Author

Aiken, A.H., primary, Tihan, T., additional, and Glastonbury, C., additional

Published
2010
Full Text
View/download PDF

40. High-Resolution CT Imaging of Carotid Artery Atherosclerotic Plaques

Author

Wintermark, M., primary, Jawadi, S.S., additional, Rapp, J.H., additional, Tihan, T., additional, Tong, E., additional, Glidden, D.V., additional, Abedin, S., additional, Schaeffer, S., additional, Acevedo-Bolton, G., additional, Boudignon, B., additional, Orwoll, B., additional, Pan, X., additional, and Saloner, D., additional

Published
2008
Full Text
View/download PDF

41. Pediatric astrocytomas with monomorphous pilomyxoid features and a less favorable outcome

Author

UCL - Cliniques universitaires Saint-Luc, UCL, Tihan, T, Godfraind, Catherine, Fisher, PG, Kepner, JL, McComb, RD, Goldthwaite, PT, Burger, PC, UCL - Cliniques universitaires Saint-Luc, UCL, Tihan, T, Godfraind, Catherine, Fisher, PG, Kepner, JL, McComb, RD, Goldthwaite, PT, and Burger, PC

Abstract

Among tumors classified as pilocytic astrocytoma (PA) in the Johns Hopkins Hospital Department of Pathology files, we identified 18 cases with a distinctive monomorphous pilomyxoid histological pattern and a higher recurrence rate than that of PA with classical histological features (classical PA). The majority of the tumors occurred in infants and young children and involved the hypothalamic/chiasmatic region. The tumors were histologically similar to PA, but they were more monomorphous and more myxoid. Rosenthal fibers were not seen and only 1 of 18 tumors had eosinophilic granular bodies. At the end of the follow-up period, 6 patients were dead and 12 were alive with evidence of disease. Progression free survival (PFS) at 1 year was 38.7%. In comparison, we identified a control group of 13 classical PAs in the same age range and location as the study group. In this group, PFS at 1 year was 69.2%, which was significantly better than that for pilomyxoid tumors (p = 0.04). There was no CSF dissemination or death due to tumor progression among patients with classical PA. Eight of these patients are alive with recurrent disease, and 4 have no evidence of disease. While the monomorphous pilomyxoid tumors have some resemblance to classical PA, our results suggest that the former is a more aggressive variant or a separate entity that needs to be recognized for prognostic purposes.

Published
1999

47. Solitary fibrous tumors in the central nervous system.

Author

Tihan T, Viglione M, Rosenblum MK, Olivi A, and Burger PC

Abstract

Context.--Solitary fibrous tumors (SFTs) of the central nervous system are rare neoplasms that usually present as dura-based masses and clinically resemble meningiomas. Histologically, they can be similar to fibrous meningioma or hemangiopericytoma (HPC). In particular, densely cellular regions seen in some SFTs can be indistinguishable from HPC. Little is known about the biological behavior of SFTs, although most seem amenable to total resection. Objectives.--To define the clinicopathologic spectrum of SFTs in the central nervous system and to outline their differences from HPC and meningioma. Design.--We present the clinicopathologic features of 18 patients with SFT and compare them with those of an age- and sex-matched cohort of HPCs. Results.--Eleven SFTs were supratentorial, 3 were infratentorial, and 4 were intraspinal. Four of the 18 tumors were intra-axial (2 in the lateral ventricles and 2 within the spinal cord). Histologically, SFTs were similar to their soft tissue counterparts. Six tumors (6/18) had densely cellular regions, and 1 tumor showed frankly anaplastic features. All but 3 patients underwent gross total resection, and there were no metastases or tumor-related mortalities during the median follow-up of 40 months. In contrast, there were 15 local recurrences (83%), 5 extracranial metastases (27%), and 4 tumor-related deaths (22%) in the HPC cohort. Conclusions.--Our study presents the clinicopathologic features of SFT as a distinct entity from both meningioma and HPC. We also present unusual examples of anaplastic, intraventricular, and intramedullary spinal SFTs that expand the clinicopathologic spectrum of these uncommon and sometimes diagnostically difficult neoplasms. [ABSTRACT FROM AUTHOR]

Published
2003
Full Text
View/download PDF

49. A clinicopathologic reappraisal of brain stem tumor classification. Identification of pilocystic astrocytoma and fibrillary astrocytoma as distinct entities.

Author

Fisher, Paul G., Breiter, Steven N., Carson, Benjamin S., Wharam, Moody D., Williams, Jeffery A., Weingart, Jon D., Foer, Dana R., Goldthwaite, Patricia T., Tihan, Tarik, Burger, Peter C., Fisher, P G, Breiter, S N, Carson, B S, Wharam, M D, Williams, J A, Weingart, J D, Foer, D R, Goldthwaite, P T, Tihan, T, and Burger, P C

Published
2000
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results