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CANCER:

Oligodendroglioma

Related cancers:
5d
Expanding the molecular grading criteria in IDH-mutant astrocytoma. (PubMed, Neuro Oncol)
The presence of CDK4, CCND2, PDGFRA, PIK3R1, MYCN, and EGFR alterations result in an intermediate patient survival in IDH-mutant astrocytoma. Adding these molecular alterations should be considered in future diagnostic classification systems to improve stratification of high-risk patients.
Journal
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • TERT (Telomerase Reverse Transcriptase) • MYCN (MYCN Proto-Oncogene BHLH Transcription Factor) • CDK4 (Cyclin-dependent kinase 4) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • PIK3R1 (Phosphoinositide-3-Kinase Regulatory Subunit 1) • CCND2 (Cyclin D2)
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EGFR mutation • PIK3CA mutation • EGFR amplification • CDKN2A deletion • MYCN amplification • PDGFRA mutation
6d
Trial suspension
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BIRC5 (Baculoviral IAP repeat containing 5)
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CLD-101
6d
From a Polymorphous Low-Grade Neuroepithelial Tumor to a Glioblastoma in an Adult Patient with FGFR3-TACC3 Fusion: A Case Report and Literature Review of the Molecular Profile. (PubMed, Curr Oncol)
During follow-up, the patient underwent a second neurosurgery, where histological evaluation indicated a GMB. This article presents clinical and radiological data, morphology, immunohistochemistry, molecular features, and treatment to enhance the clinical and pathological understanding of PLNTY with FGFR3-TACC3 fusion for all professionals involved in medical decisions.
Review • Journal
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BRAF (B-raf proto-oncogene) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • FGFR3 (Fibroblast growth factor receptor 3) • TACC3 (Transforming acidic coiled-coil containing protein 3) • ATRX (ATRX Chromatin Remodeler) • GFAP (Glial Fibrillary Acidic Protein) • OLIG2 (Oligodendrocyte Transcription Factor 2)
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BRAF V600E • BRAF V600 • FGFR3-TACC3 fusion • FGFR fusion
7d
Delta-like ligand 3 expression in isocitrate dehydrogenase-mutant and isocitrate dehydrogenase-wildtype glioma is largely retained at recurrence, supporting its potential as a therapeutic target. (PubMed, Neurooncol Adv)
DLL3 expression level is retained or increased in the majority of recurrent gliomas. Inclusion in trials with DLL3-targeting agents in recurrent glioma based on primary tumor material is justified, depending on the required level of DLL3 positivity for inclusion.
Journal
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DLL3 (Delta Like Canonical Notch Ligand 3)
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DLL3 expression • DLL3 positive • IDH wild-type
9d
The 1p/19q co-deletion induces targetable and imageable vulnerabilities in glucose metabolism in oligodendrogliomas. (PubMed, Neuro Oncol)
We have identified ENO2 and PHGDH as metabolic vulnerabilities induced by the 1p/19q co-deletion in oligodendrogliomas and [6,6'-2H]-glucose as a non-invasive tracer of early response to therapy.
Journal
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ENO1 (Enolase 1) • PHGDH (Phosphoglycerate Dehydrogenase)
17d
Temporally-modulated Pulsed Radiation Therapy (TMPRT) After Prior EBRT for Recurrent IDH-mutant Gliomas (clinicaltrials.gov)
P=N/A, N=13, Completed, Washington University School of Medicine | Active, not recruiting --> Completed
Trial completion
18d
Detection of Copy-Number Variations in CNS Tumours From Off-Target Reads of Hybrid-Capture Sequencing. (PubMed, Neuropathol Appl Neurobiol)
Focal copy-number variations on Chr7q suggestive of BRAF fusions were observed in 5/6 fusion-positive pilocytic astrocytomas. These findings demonstrate that off-target reads from minimal targeted NGS panels can generate genome-wide CNV profiles, comparable to methylation array data, without the need for additional assays or specialised probe designs.
Journal
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EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • MYCN (MYCN Proto-Oncogene BHLH Transcription Factor) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • MDM4 (The mouse double minute 4)
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CDKN2A deletion • BRAF fusion
22d
CL1-95032-005: Study of Vorasidenib and Pembrolizumab Combination in Recurrent or Progressive IDH-1 Mutant Glioma (clinicaltrials.gov)
P1, N=60, Active, not recruiting, Institut de Recherches Internationales Servier | Recruiting --> Active, not recruiting
Enrollment closed
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • ATRX (ATRX Chromatin Remodeler)
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IDH1 R132
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Keytruda (pembrolizumab) • Voranigo (vorasidenib)
22d
New P1/2 trial
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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IDH wild-type
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Zynyz (retifanlimab-dlwr)
23d
Prognostic Impact of Calcification, Corpus Callosum Invasion, and CDKN2A/B Hemizygous Deletion in Oligodendroglioma: A Single-center Retrospective Study. (PubMed, Neurol Med Chir (Tokyo))
On univariable Cox analysis for overall survival, corpus callosum invasion, calcification, and CDKN2A/B hemizygous deletion were significant adverse prognostic factors. In simple multivariable Cox models, CDKN2A/B hemizygous deletion remained associated with shorter overall survival.Calcification, corpus callosum invasion, and CDKN2A/B hemizygous deletion may be prognostic markers in oligodendroglioma.
Retrospective data • Journal
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CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B)
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CDKN2A deletion
25d
Association of CDKN2A/B and MTAP deletions in adult-type diffuse gliomas. (PubMed, J Neuropathol Exp Neurol)
Discordant CDKN2A/B and MTAP tumors affect the association between MTAP IHC and copy number status of MTAP and CDKN2A/B. These findings suggest that adult-type diffuse gliomas, regardless of IDH status, follow a stereotypic pathway involving concurrent CDKN2A/B and MTAP heterozygous deletion but may diverge for CDKN2A/B and MTAP homozygous deletion.
Journal
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CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • MTAP (Methylthioadenosine Phosphorylase) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B)
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CDKN2A deletion • MTAP deletion
25d
BRAF-mutant high-grade glioma with pleomorphic and pseudopapillary features (HPAP): A PLNTY mimic demonstrating tumor progression during longitudinal follow-up. (PubMed, Neurooncol Adv)
This case represents a rare example of BRAF p.V600E-mutant HPAP with PLNTY-like features in which a subclonal pTERT mutation likely emerged during tumor evolution, contributing to rapid tumor progression. The combination of a prolonged indolent phase followed by rapid growth, along with the intratumoral genetic heterogeneity observed, provides novel insights into the biological diversity and evolutionary dynamics of HPAP.
Journal
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BRAF (B-raf proto-oncogene) • TERT (Telomerase Reverse Transcriptase) • CD34 (CD34 molecule)
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BRAF V600E • BRAF mutation • BRAF V600