Journal articles: 'Gliome diffus'

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Hofer. "Neuroonkologie - neue Therapiestrategien." Therapeutische Umschau 69, no. 10 (October 1, 2012): 597–604. http://dx.doi.org/10.1024/0040-5930/a000336.

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Die jährliche Inzidenz der häufigsten primären Hirntumoren, der Gliome, beträgt 5-6 /100'000 (www.cbtrus.org). In der Schweiz werden etwa 500 Neuerkrankungen bei Erwachsenen pro Jahr diagnostiziert. Etablierte Risikofaktoren für die Entwicklung von Gliomen sind frühere Exposition mit ionisierenden Strahlen und selten eine genetische Prädisposition (i.R. von familiären Tumorsyndromen). Ein Risiko durch den Gebrauch von mobilen Telefonen wird zwar vermutet, ist aber bislang noch nicht durch epidemiologische Langzeituntersuchungen bewiesen. Die Prognose und Therapieindikationen richten sich weitgehend nach klinischen Faktoren wie Alter und Performance Status des Patienten. Die Primärtherapie von Glioblastomen (GBM, WHO-Grad IV) ist international standardisiert und beinhaltet größtmögliche Resektion, postoperative Radiotherapie des Teilhirns mit konkomitierender Chemotherapie (Temozolomid über 6 Wochen) gefolgt von Temozolomid über 6 Monate. Glioblastome rezidivieren immer innerhalb weniger Monate bis Jahre. Zur Behandlung eines Rezidivs stehen dem Patienten verschiedene individuelle Therapieoptionen zur Verfügung. Je nach Lage und Größe kann sich ein Rezidiv für eine zweite Resektion, für eine stereotaktische Re-Bestrahlung oder für eine Zweitlinienchemotherapie und/oder für die Behandlung mit einer Angiogenesehemmung eignen. Gliome sind diffus infiltrierende Krankheiten des Gehirns und daher von Anfang an nicht kurativ behandelbar, das mittlere Überleben liegt für GBM bei 15 Monaten. Bei Patienten über 70 Jahren und einem guten Allgemeinzustand ist nach der Stratifizierung für den Methylierungsstatus des MGMT Promoter Gens eine alleinige Radiotherapie oder bei methyliertem MGMT Status eine alleinige Chemotherapie als Erstlinientherapie gerechtfertigt. Anaplastische Gliome (WHO-Grad III) können postoperativ mit Radiotherapie oder Chemotherapie behandelt werden und beim Auftreten eines Rezidives mit der entsprechend anderen Modalität. Falls ein WHO-Grad III-Gliom aber eine 1p,19q Co-Deletion aufweist, sollte die Primärtherapie nach neuesten Erkenntnissen immer eine Chemo- und Radiotherapie beinhalten. Das mittlere Überleben variiert je nach prognostischen Faktoren von 3 bis > 7 Jahren. Für WHO-Grad II-Gliomen gibt es bislang keine standardisierte Therapie. Neben einer primären "wait and see" Strategie, stehen bei Tumorprogress die Chemotherapie oder die Radiotherapie zur Verfügung. Die Studienresultate der EORTC Studie (22033/26033), welche die beiden Therapieoptionen in der Erstlinientherapie prüft, stehen noch aus.

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Mandonnet, E. "Conduite à tenir devant un gliome diffus de bas grade." Pratique Neurologique - FMC 5, no. 3 (September 2014): 177–83. http://dx.doi.org/10.1016/j.praneu.2014.07.002.

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Wostrack, Maria, and Bernhard Meyer. "Intradurale intramedulläre Tumoren: Epidemiologie, Diagnostik und Therapie." Die Wirbelsäule 04, no. 02 (April 2020): 84–90. http://dx.doi.org/10.1055/a-0968-8240.

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ZusammenfassungIntramedulläre Tumoren sind ausgesprochen selten. Die häufigsten Entitäten sind Ependymome (überwiegend im Erwachsenenalter), Astrozytome (überwiegend im Kindesalter) und Hämangioblastome. Die Mehrheit sind gutartige oder niedriggradige langsam wachsende Neoplasien mit entsprechend langsam progredienter Klinik, die sich oft zuerst als ein unspezifisches Schmerzsyndrom und später als eine zunehmende Myelopathie zeigt. Die Ausnahme sind infiltrativ wachsende höhergradige Gliome, die eine rasch progrediente Verschlechterung bis hin zum akuten Querschnitt verursachen. Die Therapie intramedullärer Ependymome, pilozytischer WHO I Astrozytome und Hämangioblastome fokussiert sich in erster Linie auf die Komplettresektion des Tumors. Bei den beiden letztgenannten Entitäten ist damit meistens ein kuratives Ergebnis erreicht. Auch WHO I und II Ependymome zeigen nach einer chirurgischen Komplettresektion eine ausgesprochen benigne Prognose mit einem progressionsfreien 5-Jahres-Überleben von > 70 % und einem 5-Jahres-Gesamtüberleben von fast 90 %. Diffus wachsende astrozytäre Tumore können dagegen i. d. R. nicht komplett reseziert werden: hier ist das Ziel die Sicherung der Histologie und allenfalls Tumordebulking mit dem Ziel einer Syrinxdekompression und einer Stabilisierung der neurologischen Situation vor der geplanten adjuvanten Radiochemotherapie. Auch die Prognose dieser Entitäten ist deutlich schlechter: das mediane Gesamtüberleben der Patienten mit höhergradigen spinalen Gliomen beträgt lediglich 13 Monate.

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Lozano, Fernando, Renata Ursu, Anna Luisa Di Stefano, François Ducray, Nadia Younan, Mehdi Touat, Antoine Carpentier, and Ahmed Idbaih. "Manifestations cliniques et facteurs pronostiques de la COVID-19 chez les patients souffrant de gliome diffus." Revue Neurologique 177 (April 2021): S37. http://dx.doi.org/10.1016/j.neurol.2021.02.161.

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Muller, Catherine. "Peut-on observer l’épigenèse (J-P Changeux) d’un Gliome Diffus de Bas Grade (GDBG), tumeur cérébrale à évolution lente, et comprendre son cadre d’occurence ?" Revue Neurologique 173 (March 2017): S52. http://dx.doi.org/10.1016/j.neurol.2017.01.041.

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Fauvet, Cordélia, Marie Villain, and Peggy Gatignol. "Effets d’une réopération en condition éveillée sur la qualité de vie de patients porteurs d’un gliome diffus de l’adulte : revue systématique de la littérature et méta-analyse." Revue Neurologique 180 (April 2024): S66. http://dx.doi.org/10.1016/j.neurol.2024.02.127.

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Fauvet, Cordélia, Marie Villain, and Peggy Gatignol. "Effets d’une réopération en condition éveillée sur la survenue de crises comitiales chez des patients porteurs d’un gliome diffus de l’adulte : revue systématique de la littérature et méta-analyse." Revue Neurologique 180 (April 2024): S5. http://dx.doi.org/10.1016/j.neurol.2024.02.008.

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Weller, Michael, Christiane B. Knobbe-Thomsen, Emilie Le Rhun, and Guido Reifenberger. "Die WHO-Klassifikation der Tumoren des zentralen Nervensystems 2021." Der Onkologe 28, no. 2 (January 17, 2022): 155–63. http://dx.doi.org/10.1007/s00761-021-01083-7.

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Zusammenfassung Hintergrund Die von der Weltgesundheitsorganisation (WHO) herausgegebene Klassifikation der Tumoren des zentralen Nervensystems (ZNS) wurde 2016 überarbeitet, um molekulare Biomarker aufzunehmen, die für die Diagnosestellung und klinische Entscheidungsfindung wichtig sind. Danach verfeinerte ein internationales Konsortium die ZNS-Tumor-Klassifikation durch einige Empfehlungen, die aktuell in die neue WHO-Klassifikation 2021 eingeflossen sind. Fragestellung Welche Neuerungen in der WHO-Klassifikation 2021 haben direkte Auswirkungen auf die Diagnostik und Behandlung von erwachsenen Patienten mit diffusen Gliomen? Material und Methoden Die diagnostischen Kriterien der WHO-Klassifikation 2021 für diffuse Gliome wurden bezüglich dieser Fragestellung untersucht. Ergebnisse Mutationen in den Isocitratdehydrogenase(IDH)-Genen 1 oder 2 spielen eine entscheidende Rolle bei der Klassifikation von Gliomen. Unter den IDH-mutierten Gliomen identifiziert der Verlust der nukleären ATRX-Expression IDH-mutierte Astrozytome, während der Nachweis einer 1p/19q-Kodeletion für Oligodendrogliome diagnostisch ist. Die Nomenklatur für das IDH-mutierte Glioblastom wurde in Astrozytom, IDH-mutiert, ZNS-WHO-Grad 4 geändert. Die homozygote Deletion des CDKN2A/B-Genlocus ist ein molekularer Marker für diese Tumoren. Die Bezeichnungen „anaplastisches Astrozytom“ bzw. „anaplastisches Oligodendrogliom“ für IDH-mutierte Gliome des ZNS-WHO-Grads 3 entfallen. Diffuse astrozytäre Gliome ohne IDH-Mutation, die eine Mutation im Promotor des Telomerase-Reverse-Transkriptase(TERT)-Gens, eine Amplifikation des epidermalen Wachstumsfaktorrezeptorgens (EGFR), einen kombinierten Gewinn von Chromosom 7 und Verlust von Chromosom 10 (+7/−10) oder mehrere dieser Veränderungen aufweisen, werden jetzt als Glioblastom, IDH-Wildtyp, ZNS-WHO-Grad 4 klassifiziert, auch wenn histologisch weder pathologische Gefäßproliferate noch Nekrosen nachweisbar sind. Zudem wurden neue Gliome vom pädiatrischen Typ eingeführt, die vornehmlich bei Kindern, Jugendlichen und jungen Erwachsenen auftreten und von den o. g. häufigen Gliomen vom adulten Typ differenziert werden. Diskussion Die WHO-Klassifikation 2021 hat neben neuen Tumortypen auch grundlegende Veränderungen auf dem Boden neuer molekularpathologischer Erkenntnisse berücksichtigt, welche die diagnostische Präzision erhöhen und die klinische Versorgung durch modifizierte Behandlungsempfehlungen verbessern. Die neue Klassifikation hat zudem große Auswirkungen auf das Design zukünftiger klinischer Studien in der Neuroonkologie.

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Faraji-Rad, Mohammad. "Epidemiological Study of Molecular and Genetic Classification in Adult Diffuse Glioma." International Journal of Surgery & Surgical Techniques 6, no. 2 (2022): 1–5. http://dx.doi.org/10.23880/ijsst-16000171.

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Background: Mutations in isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2) are frequent in lowgrade and high-grade gliomas. However, the diagnostic criteria, in particular for gliomas, are highly various. The aim of our study was to establish genetic profiles for mutation and calcification of diffuse gliomas and to evaluate their predictive factors. Methods: We estimate the different clinical and molecular characterization between IDH1, IDH2 mutant gliomas, p53, ATRX and 1p19q. In addition, whole-transcriptome sequencing and DNA extraction data were used to evaluate the distribution of genetic changes in IDH1 and IDH2 mutant gliomas in a Iranian high grade glioma. Results: Between 2016-2019, among 53 gliomas in our study, 29 cases (54.7% %) harbored an IDH1,2 mutation, 21 cases (39.6 %) harbored an p53 mutation and 19 cases (35.8 %) harbored an ATRX. In addition, 1p19q co-deletion mutation was found in 7 cases (12.2%). We found that IDH1 and IDH2 are mutually entirely in gliomas. There was no significant relation between histopathology, tumor location and clinical finding with diagnosed mutations. Conclusion: Our study discloses an associated distinction between IDH1 and IDH2 mutant gliomas nearly in half of patients, followed by p53. These mutations should be reviewed separately because their differences could have indication for the diagnosis and treatment of IDH1/2 mutant gliomas.

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Rousseau, Audrey. "Diagnostic moléculaire des gliomes diffus." Revue Francophone des Laboratoires 2018, no. 506 (November 2018): 61–67. http://dx.doi.org/10.1016/s1773-035x(18)30324-1.

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Hennika, Tammy, and Oren J. Becher. "Diffuse Intrinsic Pontine Glioma." Journal of Child Neurology 31, no. 12 (July 20, 2016): 1377–85. http://dx.doi.org/10.1177/0883073815601495.

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Aziz-Bose, Razina, and Michelle Monje. "Diffuse intrinsic pontine glioma." Current Opinion in Oncology 31, no. 6 (November 2019): 522–30. http://dx.doi.org/10.1097/cco.0000000000000577.

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Esparragosa, Inés, Ricardo Díez-Valle, Sonia Tejada, and Jaime Gállego Pérez-Larraya. "Management of diffuse glioma." La Presse Médicale 47, no. 11-12 (November 2018): e199-e212. http://dx.doi.org/10.1016/j.lpm.2018.04.014.

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Punt, J., and M. Cartmill. "Diffuse brain stem glioma." Child's Nervous System 15, no. 5 (May 20, 1999): 235–37. http://dx.doi.org/10.1007/s003810050379.

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Norris, Gregory, Andrew Donson, Sarah Milgrom, Alisa Gaskell, Nicholas Willard, Nicholas Foreman, Ahmed Gilani, and Nathan Dahl. "HGG-17. Novel Fusion in Congenital Brainstem Diffuse High-Grade Glioma." Neuro-Oncology 24, Supplement_1 (June 1, 2022): i64. http://dx.doi.org/10.1093/neuonc/noac079.232.

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Abstract BACKGROUND: Infant-type hemispheric glioma, previously termed infantile glioblastoma multiforme, is a rare infantile neoplasm with improved survival and distinct molecular features when compared to other pediatric and adult-type high-grade glioma. Infant-type high-grade gliomas are typically located in the cerebral hemispheres and are characterized by ALK, ROS1, MET, and NTRK fusions. Typical brainstem gliomas (diffuse midline glioma, H3 K27-altered or diffuse intrinsic pontine glioma) are comparatively rare in this age group. As a result, the biology of brainstem congenital high-grade gliomas is poorly described. RESULTS: A 3 month old female who initially presented with failure to thrive had an apneic event and was found to have an infiltrative mass in the medulla with expansion into the pons and cervical spine on magnetic resonance imaging. She underwent surgical biopsy with pathology revealing diffuse high-grade glioma, WHO grade 4. Next generation sequencing showed no alterations to H3F3A, IDH, or fusions involving BRAF, ALK, ROS1, MET, or NTRK. Whole-transcriptome sequencing revealed a novel fusion of PDGFRB:APOBEC3C. She received chemotherapy with 2 cycles of carboplatin/etoposide and 2 cycles of carboplatin/etoposide/imatinib before having disease progression. She then underwent palliative radiation (35 Gy in 10 fractions) with near complete regression of her disease. Surprisingly, our patient has not had any progression of disease or new lesions now two years from her last therapy. CONCLUSION: Congenital high-grade glioma is a rare, unique entity that greatly differs from its adult and childhood counterparts. Here, we discuss a previously-unreported fusion of PDGFB:APOBEC3C in a patient with congenital brainstem diffuse high-grade glioma with a favorable clinical course. This highlights the importance of routine molecular characterization, both to better understand the complex biology of this rare disease and to guide prognosis and clinical decision making for individual patients and families.

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Onishi, Shumpei, Fumiyuki Yamasaki, Motoki Takano, Ushio Yonezawa, Kazuhiko Sugiyama, and Kaoru Kurisu. "NI-17 T2-FLAIR MISMATCH SIGN IN DIFFUSE GLIOMA AND DYSEMBRYOPLASTIC NEUROEPITHELIAL TUMOR." Neuro-Oncology Advances 1, Supplement_2 (December 2019): ii28. http://dx.doi.org/10.1093/noajnl/vdz039.128.

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Abstract BACKGROUND T2-FLAIR mismatch sign was reported as a specific imaging marker for diffuse astrocytoma with IDH-mutant and 1p/19q non-codeletion. However, most of the previous studies for T2-FLAIR mismatch were confirmed only among low grade glioma. The purpose of this study is to assess the T2-FLAIR mismatch sign in supratentorial diffuse glioma, diffuse midline glioma and dysembryoplastic neuroepithelial tumor (DNT) to unveil the exception rules of the sign. METHODS In total, 51 patients were included in this study; 33 supratentorial diffuse glioma (18 diffuse astrocytoma with IDH mutant (IDHmut-Noncodel), 12 oligodendroglioma with IDH-mutant and 1p19q codeletion (IDHmut-Codel), 3 diffuse astrocytoma with IDH wildtype (IDHwt)), 18 diffuse midline glioma and 11 DNT. The tumors were evaluated by 2 independent reviewers to assess presence or absence of T2-FLAIR mismatch sign. RESULT Ten out of 18 cases of IDHmut-Noncodel presented T2-FLAIR mismatch sign. None of the other supratentorial diffuse glioma (IDHmut-Codel and IDHwt) presented T2-FLAIR mismatch. The T2-FLAIR mismatch sign for IDHmut-Noncodel presented 100% positive predictive values among supratentorial diffuse glioma. However, 8 out of 18 cases of diffuse midline glioma and 8 out of 11 cases of DNT also presented the T2-FLAIR mismatch. CONCLUSION The T2-FLAIR mismatch sign was specific marker for IDHmut-NonCodel among supratentorial diffuse glioma. Physicians need to be aware that diffuse midline glioma and DNT could present the T2-FLAIR mismatch sign.

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Dellaretti, Marcos, Gustavo Touzet, Nicolas Reyns, François Dubois, Sebastião Gusmão, Júlio Leonardo Barbosa Pereira, and Serge Blond. "Correlation among magnetic resonance imaging findings, prognostic factors for survival, and histological diagnosis of intrinsic brainstem lesions in children." Journal of Neurosurgery: Pediatrics 8, no. 6 (December 2011): 539–43. http://dx.doi.org/10.3171/2011.9.peds1167.

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Object The aim of this study was to compare MR imaging characteristics with histopathological findings of intrinsic brainstem lesions and also to show the prognostic factors in patients with diffuse brainstem glioma. Methods Between February 1988 and August 2007, 44 brainstem biopsies were performed at the Roger Salengro Hospital in Lille, France, in children with intrinsic brainstem lesions not amenable to excision. Twenty-six were female and 18 male, and the mean age was 6 years. Results Histological evaluation revealed diffuse brainstem glioma in all patients with diffuse nonenhancing brainstem lesions. Diffuse brainstem glioma was found in 18 patients (90%) with diffuse enhancing brainstem lesions. Pathological entities different from diffuse glioma were verified in 2 patients (10%)—1 with ependymoma and 1 with ganglioglioma. In 4 of 5 patients with a focal nonenhancing brainstem lesion, the histopathological diagnosis was diffuse low-grade glioma. In 6 of 10 patients with focal enhancing brainstem lesion, the diagnosis was diffuse brainstem glioma, and pathological entities different from diffuse brainstem glioma were verified in 2 (20%), both with pilocytic astrocytoma. The mean 1-year actuarial survival rates for patients classified with low-grade and high-grade glioma were 80.4% ± 0.08% and 48.6% ± 0.14%, respectively. Conclusions The impact of stereotactic biopsy on intrinsic brainstem lesions was greater in patients with MR imaging–documented enhancing lesions in whom the diagnosis of diffuse glioma was less frequent. Patients with low-grade glioma seem to have longer survival than those with high-grade glioma.

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Duffau, H. "Gliomes diffus de bas grade et neuroplasticité." Journal de Radiologie Diagnostique et Interventionnelle 95, no. 10 (October 2014): 935–45. http://dx.doi.org/10.1016/j.jradio.2014.07.002.

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Roux, A., and J. Pallud. "Grossesse et gliomes diffus de bas grade." EMC - Neurologie 40, no. 4 (October 2017): 1–8. https://doi.org/10.1016/s0246-0378(17)62868-9.

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Dellaretti, Marcos, Nicolas Reyns, Gustavo Touzet, François Dubois, Sebastião Gusmão, Júlio Leonardo Barbosa Pereira, and Serge Blond. "Diffuse brainstem glioma: prognostic factors." Journal of Neurosurgery 117, no. 5 (November 2012): 810–14. http://dx.doi.org/10.3171/2012.7.jns111992.

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Object Brainstem gliomas were regarded as a single entity prior to the advent of MRI; however, several studies investigating MRI have recognized that these lesions are a heterogeneous group, and certain subgroups have a better prognosis for long-term survival. The aim of this study was to conduct a retrospective analysis of prognostic factors of patients with brainstem gliomas confirmed by histopathological diagnosis, particularly regarding assessment of whether histological grade, age, and MRI findings are prognostic factors for patient survival. Methods The study evaluated 100 patients diagnosed with brainstem glioma. There were 63 adults (40 men and 23 women; age range 18–75 years, mean 41 years) and 37 children (19 boys and 18 girls; age range 2–12 years, mean 6.9 years). Results The mean overall survival of this population, measured from the date of biopsy, was 57 months for diffuse low-grade glioma and 13.8 months for diffuse high-grade glioma (p < 0.001). The mean survival among patients with nonenhancing contrast lesions on MRI was 54.2 months, whereas for patients with enhancing lesions, it was 21.7 months (p < 0.001). Comparisons between the Kaplan-Meier survival curves of adults and children revealed similar median survival periods of 25 and 16 months, respectively (p > 0.05). The multivariate analysis (Cox proportional hazards regression) revealed that only histological grade was a significant prognostic factor (p < 0.001). Conclusions The study revealed that histological grade and MRI features were significant prognostic factors for survival in these patients, but in multivariate analysis, only histological grade remained a significant factor.

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Zaghloul, M., S. Ahmed, E. Eldebaway, A. Mousa, A. Amin, N. Elkhateeb, M. Sabry, et al. "DIFFUSE INTRINSIC PONTINE GLIOMA (DIPG)." Neuro-Oncology 14, suppl 1 (June 1, 2012): i26—i32. http://dx.doi.org/10.1093/neuonc/nos098.

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Minagar, A. "Diffuse brainstem glioma: prognostic factors." Yearbook of Neurology and Neurosurgery 2013 (2013): 119–20. https://doi.org/10.1016/j.yneu.2013.04.003.

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Joshi, Sabendra, Yuan-Kui Wu, Yi-Kai Xu, Xiao-Min Liu, and Hao Zhang. "Comparative study of diffuse midline glioma and glioblastoma: Magnetic Resonance Imaging (MRI) in the characteristics and demography." Nepal Journal of Neuroscience 19, no. 2 (July 7, 2022): 32–36. http://dx.doi.org/10.3126/njn.v19i2.43724.

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Introduction: Diffuse midline glioma and glioblastoma are classified as grade IV CNS tumors (WHO). The entity ‘diffuse midline glioma, H3 K27 mutant’ was introduced in the 4th revised edition of the 2016 WHO classification of brain tumors; however, there are only a few reports on Magnetic Resonance Imaging of these tumors. Thus, we conducted a retrospective study focused on Magnetic Resonance Imaging features of diffuse midline glioma compared to glioblastoma. This study aims to evaluate and compare the demographic characteristics, anatomic location of lesions, and MRI characteristics of diffuse midline glioma and glioblastoma. Methods: We histologically confirmed 30 patients with diffuse midline glioma and 70 patients with glioblastoma were enrolled in this retrospective study. Pretreatment MRI of each patient was reviewed by a neuroradiology issuing physician and neuroradiology reporting physician for MRI characteristics of tumors. Comparative analysis was performed of the imaging pattern to show differences between diffuse midline glioma and glioblastoma with the p-value. Results: The age of patients with diffuse midline glioma (mean age =24.7 ±10.4) was significantly lower than in those with glioblastoma (mean age =48.2 ±1). The majority of patients with diffuse midline glioma (56.7%) and glioblastoma (51.4%) were ≤ 25 and ≥ 50 years age group respectively. The most common location of diffuse midline glioma and glioblastoma were the thalamus (73.3%) and frontal lobe (37.1%) respectively. The presence of hydrocephalus, edema, and invasion were statistically significantly differences in patients with diffuse midline glioma (hydrocephalus = 46.7%, edema = 53.3%, and invasion =30%) than in those with glioblastoma (hydrocephalus = 12.9%, edema = 88.6%, and invasion =5.7%) (P < 0.05 each). Conclusions: Despite having similar imaging features, diffuse midline glioma exhibited marked differences in age, edema, invasion, and hydrocephalus in MRI compared to Glioblastoma.

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Barron, Tara, Belgin Yalçın, Aaron Mochizuki, Evan Cantor, Kiarash Shamardani, Dana Tlais, Andrea Franson, et al. "CNSC-01. GABAERGIC NEURON-TO-GLIOMA SYNAPSES IN DIFFUSE MIDLINE GLIOMAS." Neuro-Oncology 25, Supplement_1 (June 1, 2023): i11. http://dx.doi.org/10.1093/neuonc/noad073.044.

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Abstract High-grade gliomas include clinically and molecularly distinct subtypes that stratify by anatomical location into diffuse midline gliomas (DMG) such as diffuse intrinsic pontine glioma (DIPG) and hemispheric high-grade gliomas. Neuronal activity drives high-grade glioma progression both through paracrine signaling and direct neuron-to-glioma synapses. Glutamatergic, AMPA receptor-dependent synapses between neurons and malignant glioma cells have been demonstrated in both pediatric and adult high-grade gliomas, but neuron-to-glioma synapses mediated by other neurotransmitters remain largely unexplored. Using whole-cell patch clamp electrophysiology, in vivo optogenetics and patient-derived glioma xenograft models, we have now identified functional, tumor-promoting GABAergic neuron-to-glioma synapses mediated by GABAA receptors in DMGs. GABAergic input has a depolarizing effect on DMG cells due to NKCC1 expression and consequently elevated intracellular chloride concentration in DMG tumor cells. As membrane depolarization increases glioma proliferation, we find that the activity of GABAergic interneurons promotes DMG proliferation in vivo. Increasing GABA signaling with the benzodiazepine lorazepam – a positive allosteric modulator of GABAA receptors commonly administered to children with DMG for nausea or anxiety - increases GABAA receptor conductance and increases glioma proliferation in orthotopic xenograft models of DMG. Conversely, levetiracetam, an anti-epileptic drug that attenuates GABAergic neuron-to-glioma synaptic currents, reduces glioma proliferation in patient-derived DMG xenografts and extends survival of mice bearing DMG xenografts. Concordant with gene expression patterns of GABAA receptor subunit genes across subtypes of glioma, depolarizing GABAergic currents were not found in hemispheric high-grade gliomas. Accordingly, neither lorazepam nor levetiracetam influenced the growth rate of hemispheric high-grade glioma patient-derived xenograft models. Retrospective real-world clinical data are consistent with these conclusions and should be replicated in future prospective clinical studies. Taken together, these findings uncover GABAergic synaptic communication between GABAergic interneurons and DMG cells, underscoring a tumor subtype-specific mechanism of brain cancer neurophysiology with important potential implications for commonly used drugs in this disease context.

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Dobler, Gabriele. "Diffuse Gliome: Zirkulierende Tumorzellen als Diagnose- und Prognosemarker." Onkologische Welt 15, no. 08 (December 2024): 531. https://doi.org/10.1055/a-2463-7440.

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ZusammenfassungZirkulierende Tumorzellen (CTCs – circulating tumor cells) können als nicht invasive Technik bei Krebserkrankungen zur Diagnose, zum Progressions-Monitoring und zur Prognose dienen. Im Gegensatz zu anderen soliden Tumoren liefern CTC-Konzentrationen bei Gliomen wegen unbekannter Korrelationen mit Malignität, Histopathologie und Überlebenszeiten wenig Informationen für klinische Entscheidungen. Die Studie evaluiert ihren klinischen Nutzen.

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Idbaih, Ahmed. "Carte d'identité génétique des gliomes diffus de l'adulte." Neurologie.com 2, no. 1 (January 2010): 20–21. http://dx.doi.org/10.1684/nro.2010.0188.

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Reguli, Štefan, Jakub Cvek, and Radim Lipina. "Diffuse low grade gliomas - how it is to diagnose and treat effectively?" Onkologie 13, no. 3 (May 24, 2019): 129–32. http://dx.doi.org/10.36290/xon.2019.025.

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Barthel, Floris, Kevin C. Johnson, Frederick Varn, Anzhela Moskalik, Georgette Tanner, Emre Kocakavuk, Kevin Anderson, et al. "GENE-28. LONGITUDINAL MOLECULAR TRAJECTORIES OF DIFFUSE GLIOMA IN ADULTS." Neuro-Oncology 21, Supplement_6 (November 2019): vi103. http://dx.doi.org/10.1093/neuonc/noz175.430.

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Abstract Treatment options for adult patients with glioma has remained largely unchanged over the past three decades. Targeted inhibitors and immunotherapies have improved outcomes for many cancer types but their relevance in glioma is unclear. The inevitability of glioma disease recurrence demands an understanding of mechanisms driving therapy resistance. The Glioma Longitudinal Analysis (GLASS) Consortium was initiated to establish a definitive portrait of the recurrence process and to discover vulnerabilities that render the tumor sensitive to therapeutic intervention. GLASS is a community-driven effort that seeks to overcome the logistical challenges in constructing adequately powered longitudinal genomic glioma datasets by pooling data from patients treated at institutions worldwide. Currently, the GLASS Data Resource comprises DNA sequencing data (exome and/or whole-genome) from 288 patients of whom high-quality data in at least two time points are present from 222 patients (n = 134 IDHwt, n = 63 IDHmutant-noncodel, n = 25 IDHmutant-codel). We inferred longitudinal mutation, copy number, clonal frequency, and neoantigen profiles and demonstrated that driver genes found at initial disease persisted into recurrence. Treatment with alkylating-agents resulted in a hypermutator phenotype at different rates across glioma subtypes, most frequently among IDHmutant-noncodels, and hypermutation was not associated with differences in overall survival. Acquired aneuploidy was frequently detected in recurrent IDHmutant-noncodel gliomas and further converged with acquired cell cycle pathway alterations and poor outcomes. We showed that the clonal architecture of each tumor remains largely intact over time and that genetic drift was associated with increased survival. Finally, we found that neoantigens were exposed to stable selective pressures throughout a tumor’s progression. Our results collectively suggest that the strongest selective pressures occur early during glioma development and that current therapies shape this evolution in a largely stochastic manner. The GLASS Data Resource provides a genomic reference to study the patterns of glioma evolution.

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Luhovskyi, Serhii P., and Tetiana Y. Kvitnytska-Ryzhova. "Age-related aspects of glioma: current understanding. Literature review." Ukrainian Neurosurgical Journal 30, no. 4 (December 30, 2024): 11–22. https://doi.org/10.25305/unj.310442.

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The updated 2021 WHO Classification of Central Nervous System (CNS) Tumors introduces, for the first time, an age-based approach to glioma classification, leveraging advances in molecular biology and epigenetics of CNS tumors. This classification groups gliomas within the category "Gliomas, glioneuronal tumors, and neuronal tumors," distinguishing between adult-type and pediatric-type diffuse gliomas, corresponding to low-grade and high-grade malignancies (LGG and HGG), highlighting the fundamental role of age in gliomagenesis. A review of current literature deepens the understanding of age-related characteristics, differences, and patterns in gliomagenesis across age groups, which is essential for effective diagnosis and treatment. Pediatric-type and adult-type low-grade gliomas (pLGG and aLGG) differ in location, biological behavior, and molecular-genetic profiles. Inherited syndromes (e.g., NF-1, TSC) associated with glioma development are linked to specific LGG subtypes occurring in childhood, adolescence, and adulthood. Moreover, pLGG differs from aLGG in its potential for malignant transformation and spontaneous regression, as well as in mutations affecting the MAPK (mitogen-activated protein kinase) pathway. While pediatric-type and adult-type high-grade gliomas (pHGG and aHGG) share histological features, they differ in location, biological behavior, molecular-genetic profiles, and prognosis. A major distinction between aHGG and pHGG lies in mutations such as IDH 1/2, EGFR gene expression, TERT mutations, chromosome alterations (+7/-10), and TP53 mutations, all contributing to a poorer prognosis in HGG gliomas. Additionally, changes in histone proteins H3.3 or 3.1 (H3.3 K27 and H3 G34) in pHGG, as opposed to aHGG, carry diagnostic and prognostic significance. An analysis of data on glioma epidemiology, risk factors, and characteristic molecular-genetic features considering age is provided. The next publication will cover certain clinical aspects of this issue.

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Marlow, Christine, Joshua A. Cuoco, Austin R. Hoggarth, Michael S. Stump, Lisa S. Apfel, and Cara M. Rogers. "Pediatric diffuse hemispheric glioma H3 G34-mutant with gains of the BRAF locus: An illustrative case." Rare Tumors 15 (January 2023): 203636132311687. http://dx.doi.org/10.1177/20363613231168704.

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Diffuse hemispheric glioma, H3 G34-mutant, is a recently recognized distinct high-grade glioma with a dismal prognosis. In addition to the H3 G34 missense mutation, numerous genetic events have been identified in these malignant tumors, including ATRX, TP53, and, rarely, BRAF genes. There are only a few reports to date that have identified BRAF mutations in diffuse hemispheric glioma, H3 G34-mutant. Moreover, to our knowledge, gains of the BRAF locus have yet to be described. Here, we present a case of an 11-year-old male with a diffuse hemispheric glioma, H3 G34-mutant, found to have novel gains of the BRAF locus. Furthermore, we emphasize the current genetic landscape of diffuse hemispheric glioma, H3 G34-mutant, and implications of an aberrant BRAF signaling pathway.

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Kobyakov, G. L., A. Belyashova, Y. Trunin, O. Absalyamova, K. Lodygina, and N. Kobiakov. "P14.103 Patterns of diffuse glioma progression." Neuro-Oncology 21, Supplement_3 (August 2019): iii92. http://dx.doi.org/10.1093/neuonc/noz126.338.

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Abstract BACKGROUND According to WHO 2016 Classification, all gliomas are considered potentially malignant. Earlier it was thought that the ultimate goal for treatment is local control of tumor growth: maximal surgical resection with subsequent local radiotherapy +/- chemotherapy. Disease progression was primarily linked only to local relapse. In the recent years, different progression patterns of diffuse glioma were identified: from distant growth into an anatomically unrelated area far from primary lesion, to bone metastases and even to visceral organ metastases. MATERIAL AND METHODS In this study we analyzed glioblastoma progression patterns in a cohort of 170 patients, who received radiation therapy as one of the treatment options for local relapse in Burdenko Neurosuregry Institute. All patients had a first relapse of glioblastoma at the age of 16 to 74 years old, 72 patients were female and 98 male. All patients initially underwent surgery and local radiotherapy (in combination with temozolomide) for a solitary supratentorial lesion of glioblastoma. Various methods of radiotherapy (including radiosurgery and hypofractionated radiation therapy) were used as one of the treatment options for recurrent tumor. One of our aims was to evaluate glioblastoma progression patterns in this cohort. RESULTS Comparing neuroimaging data at the time of tumor progression with initial MRI we found that in 127 of 170 patients disease progression was identified anatomically close to the primary tumor site, i.e. disease progressed as a local relapse. Recurrent lesions without obvious anatomical relation to primary site were identified in 33 patients (19.4%); in particular, 7 patients had a lesion in contralateral hemisphere, one patient had spinal subarachnoid dissemination. A combination of local and distant tumor progression was identified in 10 of these 33 patients. CONCLUSION We identified the following progression patterns for diffuse glioma based to these data and previous clinical experience: (a) local brain relapse - anatomically close to the primary lesion; (b) brain and spinal subarachnoid spread; (c) distant relapse - anatomically unrelated to primary tumor (can be both in ipsilateral or contralateral brain hemisphere); (d) local tumor progression as infiltration of soft tissues of the head and cranial bones; (e) regional lymph node metastases; (f) distant metastases - skeletal bone metastases and/or visceral organ metastases. Naturally, different combinations of these diffuse malignant glioma progression patterns are possible. A quite high incidence and differences between diffuse glioma progression patterns require a more thorough evaluation both because of treatment strategies as well as to understand the origins of glial tumors (e.g. Why in some cases of complete remission at the primary tumor site there is tumor progression in contralateral hemisphere?)

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Pallud, Johan, and Guy M. McKhann. "Diffuse Low-Grade Glioma-Related Epilepsy." Neurosurgery Clinics of North America 30, no. 1 (January 2019): 43–54. http://dx.doi.org/10.1016/j.nec.2018.09.001.

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Robison, Nathan J., and Mark W. Kieran. "Diffuse intrinsic pontine glioma: a reassessment." Journal of Neuro-Oncology 119, no. 1 (May 3, 2014): 7–15. http://dx.doi.org/10.1007/s11060-014-1448-8.

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Cooney, Tabitha M., Evan Lubanszky, Rachna Prasad, Cynthia Hawkins, and Sabine Mueller. "Diffuse midline glioma: review of epigenetics." Journal of Neuro-Oncology 150, no. 1 (August 17, 2020): 27–34. http://dx.doi.org/10.1007/s11060-020-03553-1.

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Claes, An, Albert J. Idema, and Pieter Wesseling. "Diffuse glioma growth: a guerilla war." Acta Neuropathologica 114, no. 5 (September 6, 2007): 443–58. http://dx.doi.org/10.1007/s00401-007-0293-7.

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Van Gool, Stefaan, Jennifer Kosmal, Peter Van de Vliet, Linde Kampers, and Wilfried Stücker. "CTIM-17. INDIVIDUALIZED MULTIMODAL IMMUNOTHERAPY (IMI) FOR ADULTS WITH DIFFUSE MIDLINE GLIOMA OR DIFFUSE HEMISPHERIC GLIOMA." Neuro-Oncology 26, Supplement_8 (November 1, 2024): viii89. http://dx.doi.org/10.1093/neuonc/noae165.0350.

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Abstract Diffuse Midline Glioma (DMG, H3K27 mutant) and Diffuse Hemispheric Glioma (DHG, H3G34 mutant) are rare malignant CNS tumors with dismal prognosis. We retrospectively searched in our database for adults (>18y) with molecularly define DMG/DHG, treated between May 2015 and 2024 with IMI as part of first-line treatment. Amongst 157 IMI-treated malignant glioma patients, four patients fit these restrictions, pointing to scarce experience of IMI for DMG/DHG adult patients. HM (M, 29y) was diagnosed with a DMG in the pons. He received radiochemotherapy, and continued after 2x TMZm with BRAF-MEK-inhibition therapy. He received one IO-Vac® dendritic cell vaccine but showed fast progression thereafter. He died 9 months after diagnosis. GJE (F, 28y) had a DMG at the corpus callosum. She received radiochemotherapy and 6x TMZm, followed by 2x IO-Vac® and 3x maintenance immunogenic cell death (ICD) immunotherapy (NDV injections, sessions of modulated electrohyperthermia), combined with WT1 and H3K27M long-peptide vaccines. She progressed after 20 months, for which a new IO-Vac® and an H3K27M short- and long-peptide vaccine were given. She died 5 months later. Overall Survival (OS) was 26 months after initial diagnosis. JD (F, 27y) was diagnosed with a DMG in C2-C6. She received radiochemotherapy followed by IMI alone, including 2x IO-Vac®, one ICD immunotherapy, and four doses of anti-PD1. She died 17 months later, making OS 27 months after diagnosis. VJ (F, 21y) had a DHG in the left cerebrum. She received radiochemotherapy and 12 cycles of maintenance TMZ (TMZm), between which ICD immunotherapy was inserted each time. Afterwards, she received two IO-Vac®. Finally, she received ICD immunotherapy (6x) combined with checkpoint inhibitors (4x anti-CTLA4, 10x anti-PD1). Thirty months after diagnosis, she is in remission with a stable Health Utility Index of 0.72. IMI might have contributed to a better OS in three out of four DMG/DHG patients, and should be explored further as part of the treatment for these patients.

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Harat, M., I. Miechowicz, J. Rakowska, I. Zarębska, and B. Małkowski. "P15.15.B DIFFUSE ADULT-TYPE GLIOMA INFILTRATION DEFINED ON FET-PET." Neuro-Oncology 25, Supplement_2 (September 1, 2023): ii113. http://dx.doi.org/10.1093/neuonc/noad137.379.

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Abstract BACKGROUND O-(2-[18F]fluoroethyl)-L-tyrosine (FET)-PET is a valuable tool in glioma imaging used to the definition of biopsy site, monitoring of treatment response and differentiation of treatment-related changes from glioma progression The physiological uptake within reactive astrogliosis may limits FET-PET ability to precisely define glioma extent. For the implementation of FET-PET into clinical trials, a methodological PET standardization is urgently needed to enable more precise and reproducible FET PET quantification. The primary aim of our study was to define a glioma infiltration using threshold based method between astrogliosis and tumoral tissue in FET-PET. RESULTS Astrogliosis presented similar uptake to grade 2 glioma samples. Standard threshold method (1,6x uptake in contralateral brain) in PET aquisiton 40-60 minutes post injection is effective but the accuracy decrease outside contrast enhancement within FLAIR to 56% sensitivity and 41% specificity. Adding second aquisition increased sensitivity within FLAIR to 71%. Finally, using tumor-to-plexus ratio, it is possible to differentiate astrogliosis and grade 2, and achieve sensitivity of 73% and specificty of 84% within FLAIR or 90% sensitivity with 61% specificity. ROC curves are significantly different related to method used with best results specific to new strategy. CONCLUSION Determining glioma extent using standard threshold method in PET or FLAIR is limited. Improving is possible with dual aquisition and/or different tumor to background ratio. This may largely improve delineation of glioma for surgery or radiotherapy.

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Omura, Takaki, Masamichi Takahashi, Makoto Ohno, Yasuji Miyakita, Shunsuke Yanagisawa, Yukie Tamura, Miyu Kikuchi, et al. "Clinical Application of Comprehensive Genomic Profiling Tests for Diffuse Gliomas." Cancers 14, no. 10 (May 16, 2022): 2454. http://dx.doi.org/10.3390/cancers14102454.

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Next-generation sequencing-based comprehensive genomic profiling test (CGPT) enables clinicians and patients to access promising molecularly targeted therapeutic agents. Approximately 10% of patients who undergo CGPT receive an appropriate agent. However, its coverage of glioma patients is seldom reported. The aim of this study was to reveal the comprehensive results of CGPT in glioma patients in our institution, especially the clinical actionability. We analyzed the genomic aberrations, tumor mutation burden scores, and microsatellite instability status. The Molecular Tumor Board (MTB) individually recommended a therapeutic agent and suggested further confirmation of germline mutations after considering the results. The results of 65/104 patients with glioma who underwent CGPTs were reviewed by MTB. Among them, 12 (18.5%) could access at least one therapeutic agent, and 5 (7.7%) were suspected of germline mutations. A total of 49 patients with IDH-wildtype glioblastoma showed frequent genomic aberrations in the following genes: TERT promoter (67%), CDKN2A (57%), CDKN2B (51%), MTAP (41%), TP53 (35%), EGFR (31%), PTEN (31%), NF1 (18%), BRAF (12%), PDGFRA (12%), CDK4 (10%), and PIK3CA (10%). Since glioma patients currently have very limited standard treatment options and a high recurrence rate, CGPT might be a facilitative tool for glioma patients in terms of clinical actionability and diagnostic value.

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Roux, Alexandre, Myriam Edjlali, Sayuri Porelli, Arnault Tauziede-Espariat, Marc Zanello, Edouard Dezamis, Gilles Zah-Bi, et al. "Developmental venous anomaly in adult patients with diffuse glioma." Neurology 92, no. 1 (November 30, 2018): e55-e62. http://dx.doi.org/10.1212/wnl.0000000000006690.

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ObjectiveTo determine the prevalence of developmental venous anomaly in adult patients with diffuse glioma.MethodsWe performed a retrospective cohort study (2010–2016) of consecutive adult patients harboring a supratentorial diffuse glioma in 2 centers: Sainte-Anne Hospital (experimental and control sets) and Pitié-Salpêtrière Hospital (external validation set). We included 219 patients with diffuse glioma (experimental set), 252 patients with brain metastasis (control set), and 200 patients with diffuse glioma (validation set). The inclusion criteria were age ≥18 years at diagnosis, histopathologic diagnosis of diffuse glioma according to the 2016 World Health Organization classification of tumors of the CNS, surgery as first-line treatment without previous oncologic treatment, available presurgical MRI performed with similar acquisition protocol, and absence of a nodular-like or a ring-like pattern of contrast enhancement on MRI that may preclude the identification of a possible developmental venous anomaly within the glioma.ResultsWe found more developmental venous anomaly in the experimental set (21.5%) than in the control set (5.2%, p < 0.001). Similarly, we found more developmental venous anomaly in the validation set (23.5%) than in the control set (5.2%, p < 0.001). There was no difference in the developmental venous anomaly prevalence between the experimental and validation sets. The developmental venous anomaly distribution was not significantly associated with histopathologic, molecular, or imaging findings of the diffuse gliomas.ConclusionsWe report and replicate in an external cohort a high prevalence of developmental venous anomaly in adult patients with diffuse glioma, which suggests a potential underlying common predisposition or a causal relationship that requires deeper investigations.

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Ohno, Makoto, Juntaro Matsuzaki, Junpei Kawauchi, Yoshiaki Aoki, Junichiro Miura, Satoko Takizawa, Ken Kato, et al. "ACTR-17. DIAGNOSTIC UTILITY OF SERUM microRNA CLASSIFICATION IN DIFFUSE GLIOMA." Neuro-Oncology 21, Supplement_6 (November 2019): vi16. http://dx.doi.org/10.1093/neuonc/noz175.060.

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Abstract To improve clinical outcomes, a less invasive screening test for detection of diffuse glioma is needed. The purpose of this study is to establish models using serum microRNAs (miRNAs) to distinguish between diffuse glioma patients from non-cancer controls (Glioma Index) and between glioblastoma (GBM), primary central nervous system lymphoma (PCNSL), and metastatic brain tumors (Meta) (3-Tumor Index). A total of 580 patients, including 266 with brain or spinal tumors and 314 non-cancer controls, were analyzed. Non-cancer control samples were collected from the National Cancer Center Biobank and members of the general population undergoing routine health examinations. Expression of serum 2565 miRNAs was assessed in each sample, and the expression profiles were compared between diffuse glioma patients and non-cancer controls, and between GBM, PCNSL, and Meta. Diagnostic models were established using a training set, and diagnostic performance was confirmed in validation and exploratory sets and area under the receiver operating curve (AUC), sensitivity, specificity, and accuracy were used to evaluate their diagnostic performances. The Glioma Index was constructed using three miRNAs. The AUC was 99%, with sensitivity of 95% and specificity of 97% in the validation set. The Glioma Index classified 93% of PCNSL, 89% of Meta, 91% of benign brain tumors, and 0% of spinal tumors as positive in the exploratory set. The 3-Tumor Index was constructed using 48 miRNAs and had an accuracy of 0.80 in the validation set, positively detecting 94.1% of GBM, 80% of Meta, and 50% of PCNSL. In conclusion, we developed novel serum miRNA discriminant models to detect diffuse glioma from non-cancer control and to discriminate tumor histology. These models could serve as less invasive screening tools or complementary diagnostic tools, thereby decreasing neurosurgical risks.

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Rehfeld, Marten, Jakob Matschke, Christian Hagel, Kerstin Willenborg, Markus Glatzel, and Christian Bernreuther. "Differential expression of stem cell markers in proliferating cells in glioma." Journal of Cancer Research and Clinical Oncology 147, no. 10 (June 25, 2021): 2969–82. http://dx.doi.org/10.1007/s00432-021-03704-5.

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Abstract Purpose The identification of prognostically and therapeutically relevant molecular markers is fundamental to the further development of personalised therapies in brain tumours. Current therapeutic options for the treatment of gliomas rely mainly on surgical resection and the inhibition of tumour cell proliferation by irradiation and chemotherapy. Glioma stem cells are a subpopulation of proliferating tumour cells that have self-renewal capacity and can give rise to heterogeneous cells that comprise the tumour and are thought to play a role in the resistance of gliomas to therapy. The aim of this study was to evaluate the expression of markers of glioma stem cells and differentiated glial cells in proliferating glioma cells in comparison to the overall expression of the respective markers in the tumour tissue. Methods Tissue microarrays were assembled from specimen of pilocytic astrocytoma, diffuse astrocytoma, anaplastic astrocytoma, glioblastoma, oligodendroglioma, anaplastic oligodendroglioma, ependymoma, and anaplastic ependymoma. These were immunohistochemically double stained with antibodies against the proliferation-associated antigen Ki67 and marker proteins for glioma stem cells (CD133, Nestin, Musashi, CD15, CD44), and differentiated glioma cells (GFAP, MAP2c). Results The expression of both glial and glioma stem cell markers differs between proliferating and non-proliferating glioma cells. Furthermore, the proliferating cells in the different glial tumour entities show a different expression profile. Conclusion Further analysis of marker expression in proliferating glioma cells and correlation with clinical outcome and susceptibility to irradiation and chemotherapy might help establish new biomarkers and therapies for glioma.

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Nitta, Naoki, Tadateru Fukami, and Kazumichi Yoshida. "10143-COT-16 DIFFUSE BONE MARROW METASTASIS OF HIGH GRADE GLIOMA." Neuro-Oncology Advances 5, Supplement_5 (December 1, 2023): v15. http://dx.doi.org/10.1093/noajnl/vdad141.058.

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Abstract BACKGROUND Extraneural metastasis of the high grade glioma has rarely been reported and its diffuse bone marrow metastasis is extremely rare. Case description: A 32-year-old man was referred and admitted to Shiga University of Medical Science Hospital for the treatment for three remote recurrent lesions in the brain after the treatment of the primary brain tumor in the right frontal lobe in the referring hospital. One of those lesions was subtotally resected, with histological and immunohistochemical analysis showing a grade 4 glioma, and stereotactic radiation therapy was performed at all three lesions. A lumbar spine MRI showed signal changes in the first and 4th vertebral bodies and the level of LDH was gradually increased during this hospitalization. Three months later, the patient was referred to our hospital again because of intractable lumbago with metastatic lesions in the lumbar vertebrae and the psoae major. Laboratory data showed pancytopenia and extremely elevated level of LDH-1 and LDH-2, suggesting aggressive hemolysis. Abdominopelvic CT also showed slight osteolytic changes in the ilia, sacra, and femurs. Biopsy of the psoas major and iliac bone marrow showed invasion of grade 4 glioma cells. The patient was diagnosed as having diffuse bone marrow metastasis of grade 4 glioma, and died 12 days after the second admission. CONCLUSIONS We have presented a rare case of diffuse bone marrow metastasis of high grade glioma. LDH elevation might mean hemolysis by bone marrow metastasis in patients with high grade glioma.

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Eckel-Passow, Jeanette E., Kristen L. Drucker, Thomas M. Kollmeyer, Matt L. Kosel, Paul A. Decker, Annette M. Molinaro, Terri Rice, et al. "Adult diffuse glioma GWAS by molecular subtype identifies variants in D2HGDH and FAM20C." Neuro-Oncology 22, no. 11 (May 9, 2020): 1602–13. http://dx.doi.org/10.1093/neuonc/noaa117.

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Abstract Background Twenty-five germline variants are associated with adult diffuse glioma, and some of these variants have been shown to be associated with particular subtypes of glioma. We hypothesized that additional germline variants could be identified if a genome-wide association study (GWAS) were performed by molecular subtype. Methods A total of 1320 glioma cases and 1889 controls were used in the discovery set and 799 glioma cases and 808 controls in the validation set. Glioma cases were classified into molecular subtypes based on combinations of isocitrate dehydrogenase (IDH) mutation, telomerase reverse transcriptase (TERT) promoter mutation, and 1p/19q codeletion. Logistic regression was applied to the discovery and validation sets to test for associations of variants with each of the subtypes. A meta-analysis was subsequently performed using a genome-wide P-value threshold of 5 × 10−8. Results Nine variants in or near D-2-hydroxyglutarate dehydrogenase (D2HGDH) on chromosome 2 were genome-wide significant in IDH-mutated glioma (most significant was rs5839764, meta P = 2.82 × 10−10). Further stratifying by 1p/19q codeletion status, one variant in D2HGDH was genome-wide significant in IDH-mutated non-codeleted glioma (rs1106639, meta P = 4.96 × 10−8). Further stratifying by TERT mutation, one variant near FAM20C (family with sequence similarity 20, member C) on chromosome 7 was genome-wide significant in gliomas that have IDH mutation, TERT mutation, and 1p/19q codeletion (rs111976262, meta P = 9.56 × 10−9). Thirty-six variants in or near GMEB2 on chromosome 20 near regulator of telomere elongation helicase 1 (RTEL1) were genome-wide significant in IDH wild-type glioma (most significant was rs4809313, meta P = 2.60 × 10−10). Conclusions Performing a GWAS by molecular subtype identified 2 new regions and a candidate independent region near RTEL1, which were associated with specific glioma molecular subtypes.

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Barron, Tara, Vilina Mehta, Pamelyn Woo, and Michelle Monje. "HGG-04. TARGETING GABAERGIC NEURON-GLIOMA SYNAPSES IN DIFFUSE INTRINSIC PONTINE GLIOMA (DIPG) THROUGH ANTI-EPILEPTIC DRUG REPURPOSING." Neuro-Oncology 23, Supplement_1 (June 1, 2021): i17—i18. http://dx.doi.org/10.1093/neuonc/noab090.070.

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Abstract Pediatric high-grade gliomas, including diffuse intrinsic pontine glioma (DIPG), are the leading cause of brain cancer-related death in children. While enormous progress has been made in recent years for many forms of cancer, high-grade gliomas remain seemingly intractable, indicating that fundamental aspects of glioma growth are not yet sufficiently understood. Neuronal activity drives glioma growth both through paracrine signaling and through direct neuron-to-glioma synapses. Recently glutamatergic, AMPA receptor-dependent synapses were discovered between microenvironmental neurons and malignant glioma cells. The depolarizing current that results from synaptic and other forms of electrical neuron-glioma signaling promotes pediatric high-grade glioma proliferation and regulates growth. Neuron-glioma cell synapses mediated by other neurotransmitters remain largely unexplored, though glioma cells express genes encoding neurotransmitter receptors such as GABAA receptor subunits. Using whole-cell patch clamp electrophysiology in patient-derived DIPG xenografts, we have identified functional GABAergic neuron-to-glioma synapses mediated by GABAA receptors. GABAergic input has a depolarizing effect on glioma cells, but the magnitude of depolarization is heterogeneous between high-grade glioma subtypes and between patient-derived DIPG xenograft models. As membrane depolarization increases glioma proliferation, depolarizing GABAergic inputs to glioma cells could promote DIPG progression. Drugs that stimulate GABA signaling, such as benzodiazepines, are often given to pediatric glioma patients to treat nausea, seizures or anxiety. In patient-derived DIPG xenograftn models, lorazepam, a benzodiazepine that increases GABAA receptor conductance, increases glioma growth. Conversely, levetiracetam, an anti-epileptic drug that reduces synaptic transmission including at GABAergic neuron-glioma synapses, reduces glioma proliferation in patient-derived DIPG xenografts. This emerging understanding of brain cancer neurophysiology reveals new therapeutic targets and highlights commonly used drugs about which more study is required in this disease context.

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Lu, Victor M., Erica A. Power, Liang Zhang, and David J. Daniels. "Liquid biopsy for diffuse intrinsic pontine glioma: an update." Journal of Neurosurgery: Pediatrics 24, no. 5 (November 2019): 593–600. http://dx.doi.org/10.3171/2019.6.peds19259.

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Diffuse intrinsic pontine glioma (DIPG), otherwise known as diffuse midline glioma with H3K27M mutation, is a devastating brainstem glioma without a cure. Efforts are currently underway to better optimize molecular diagnoses through biological sampling, which today remains largely limited to surgical biopsy sampling. Surgical intervention is not without its risks, and therefore a preference remains for a less invasive modality that can provide biological information about the tumor. There is emerging evidence to suggest that a liquid biopsy, targeting biofluids such as CSF and blood plasma, presents an attractive alternative for brain tumors in general. In this update, the authors provide a summary of the progress made to date regarding the use of liquid biopsy to diagnose and monitor DIPG, and they also propose future development and applications of this technique moving forward, given its unique histone biology.

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Satrom, Katie M., Rachel A. Phelan, Christopher L. Moertel, H. Brent Clark, Dana E. Johnson, and Thomas N. George. "Neonatal Respiratory Failure Caused by Congenital Diffuse Intrinsic Pontine Glioma." Journal of Child Neurology 32, no. 6 (January 24, 2017): 533–36. http://dx.doi.org/10.1177/0883073816689640.

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The authors present a case of diffuse intrinsic pontine glioma presenting in a newborn with stridor and respiratory distress that progressed to respiratory failure. Magnetic resonance imaging (MRI) of the brain revealed findings compatible with the diagnosis of diffuse intrinsic pontine glioma. The family pursued palliative care and postmortem examination confirmed WHO grade III astrocytoma.

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Campos Paiva, Aline, João Luiz Vitorino Araujo, Guilherme Brasileiro de Aguiar, Gabriel Rezende Batistella, Marcos Maldaum, and José Esteves veiga. "SURG-11. NEOADJUVANT CHEMOTHERAPY FOR DIFFUSE GLIOMAS: A FEASIBLE OPTION?" Neuro-Oncology 22, Supplement_2 (November 2020): ii205. http://dx.doi.org/10.1093/neuonc/noaa215.858.

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Abstract BACKGROUND Diffuse gliomas are slow-growing tumors with predilection for deep and eloquent structures such as supplementary motor area and insula. They can reach huge dimensions which is a surgical challenging. OBJECTIVE Describe indications and limitations of neoadjuvant chemotherapy for diffuse gliomas. METHODS Systematic review was performed in November/2019 using Pubmed, Bireme and Cochrane databases. The following combinations were used: “Chemotherapy” AND “neoadjuvant” AND “diffuse glioma”, “Chemotherapy” AND “neoadjuvant” AND “low grade glioma”, “Chemotherapy” AND “preoperative” AND “diffuse glioma”, “Neoadjuvant” AND “Chemotherapy” AND “temozolomide” AND “diffuse glioma”. RESULTS After carefully analysis, 7 papers were selected. They had mixed surgical interventions and used different drugs. In general, it was observed that neoadjuvant Temozolomide for Oligodendrogliomas 1p19q codeleted with MGMT methylation had better response than other molecular groups. Tumor reduction was significant. CONCLUSIONS Quality of life is a main goal in neurooncology. Tumor reduction using chemotherapy is a promising therapeutic. Surgery, especially in eloquent areas, could remove more tumors with less morbidity. Recent publications are using this approach with good outcomes, however further studies with more patients and uniformization are required to stablish this approach.

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IJpelaar, Suzanne, Emma Van Kessel, Martine Van Zandvoort, Filip De Vos, Joost Verhoeff, Pierre Robe, and Tom Snijders. "NCOG-08. COGNITIVE DEFICITS AS A PREDICTOR OF THE COURSE OF TREATMENT IN DIFFUSE GLIOMA." Neuro-Oncology 21, Supplement_6 (November 2019): vi160. http://dx.doi.org/10.1093/neuonc/noz175.669.

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Abstract INTRODUCTION Over half of patients with a diffuse glioma suffer from cognitive deficits in one or more domains. Cognitive functioning, especially for the domains executive functioning (EF) and memory, is an independent prognostic factor for overall survival. A possible explanation for this prognostic effect is that patients with cognitive deficits receive less intensive treatment, or do not tolerate treatment as well as other patients. METHODS Retrospective cohort study of patients with a diffuse glioma (WHO grade 2–4) who underwent an awake craniotomy, with pre-operative neuropsychological testing, followed by adjuvant radio- and/or chemotherapy. Outcome measures were (a) choice of adjuvant treatment, compared to appropriate treatment according to contemporary guidelines; (b) intensity and compliance: number of received treatment cycles, and adherence to prescribed medication; and (c) complications. Cognitive deficits (in one or more domains, Z-score < -2), as well as deficits in the domains EF and memory, were correlated to the outcome measures. RESULTS We included 187 consecutive patients. Cognitive deficits in one or more domains, EF or memory were neither associated to the choice of treatment (adherence to guidelines), nor to intensity or compliance of treatment. Having a cognitive deficit was associated with an increased risk of complications (P < .001), including severe complications (CTCAE grade 3–5, p < .05). A deficit in EF was also associated with more complications (p < .005). This risk of complications was increased for the categories of infectious, cerebral, gastro-intestinal and hematological complications. CONCLUSION Of all patients with a diffuse glioma, patients with cognitive deficits have an increased risk of complications of postoperative antineoplastic therapy. Choice of, intensity of, and compliance to treatment did not differ from cognitively intact patients. The increased risk of complications may form an explanation for the poor prognosis of glioma patients with cognitive deficits.

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Park, Jong-Whi. "Metabolic Rewiring in Adult-Type Diffuse Gliomas." International Journal of Molecular Sciences 24, no. 8 (April 16, 2023): 7348. http://dx.doi.org/10.3390/ijms24087348.

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Multiple metabolic pathways are utilized to maintain cellular homeostasis. Given the evidence that altered cell metabolism significantly contributes to glioma biology, the current research efforts aim to improve our understanding of metabolic rewiring between glioma’s complex genotype and tissue context. In addition, extensive molecular profiling has revealed activated oncogenes and inactivated tumor suppressors that directly or indirectly impact the cellular metabolism that is associated with the pathogenesis of gliomas. The mutation status of isocitrate dehydrogenases (IDHs) is one of the most important prognostic factors in adult-type diffuse gliomas. This review presents an overview of the metabolic alterations in IDH-mutant gliomas and IDH-wildtype glioblastoma (GBM). A particular focus is placed on targeting metabolic vulnerabilities to identify new therapeutic strategies for glioma.

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Tanahashi, Kuniaki, Atsushi Natsume, Fumiharu Ohka, Hiroyuki Momota, Akira Kato, Kazuya Motomura, Naoki Watabe, et al. "Assessment of Tumor Cells in a Mouse Model of Diffuse Infiltrative Glioma by Raman Spectroscopy." BioMed Research International 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/860241.

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Glioma of infiltrative nature is challenging for surgeons to achieve tumor-specific and maximal resection. Raman spectroscopy provides structural information on the targeted materials as vibrational shifts. We utilized Raman spectroscopy to distinguish invasive tumors from normal tissues. Spectra obtained from replication-competent avian sarcoma-(RCAS-) based infiltrative glioma cells and glioma tissues (resembling low-grade human glioma) were compared with those obtained from normal mouse astrocytes and normal tissues. In cell analysis, the spectra at 950–1000, 1030, 1050–1100, 1120–1130, 1120–1200, 1200–1300, 1300–1350, and 1450 cm−1were significantly higher in infiltrative glioma cells than in normal astrocytes. In brain tissue analysis, the spectra at 1030, 1050–1100, and 1200–1300 cm−1were significantly higher in infiltrative glioma tissues than in normal brain tissues. These spectra reflect the structures of proteins, lipids, and DNA content. The sensitivity and specificity to predict glioma cells by distinguishing normal cells were 98.3% and 75.0%, respectively. Principal component analysis elucidated the significance of spectral difference between tumor tissues and normal tissues. It is possible to distinguish invasive tumors from normal tissues by using Raman spectroscopy.

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Journal articles on the topic 'Gliome diffus'

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