Brain Cancer: The Glioma Proteome
Gliomas are the most common malignant brain tumors, accounting for roughly 80% of cases, and they display remarkable heterogeneity in age of onset, histological features, malignancy grade, and clinical progression. Historically, diagnosis relied on tissue histology, but advances in molecular biology and proteomics have shifted the focus toward understanding the full protein landscape that drives tumor identity, behavior, and therapy response. Profiling the glioma proteome captures complex protein networks that regulate metabolism, chromatin remodeling, cell-cycle progression, DNA repair, immune interactions, and extracellular matrix dynamics—factors that collectively shape tumor aggressiveness and treatment resistance.
Proteomic signatures have become central to defining the major glioma entities recognized in the WHO classification. IDH-mutant astrocytomas, oligodendrogliomas with 1p/19q codeletion, and IDH-wildtype glioblastomas each display distinct protein expression programs that refine diagnosis and highlight biological pathways underlying progression.
Proteins like ATRX, whose loss marks IDH-mutant astrocytomas and activates alternative lengthening of telomeres, together with IDH1 R132H, p53, EGFR, GFAP, and Ki-67, provide a multidimensional molecular framework for classification.
This integrative proteomic perspective not only sharpens diagnostic accuracy but also uncovers potential therapeutic targets, opening avenues for more precise and effective interventions against one of the most lethal brain tumors.
Atlas Antibodies Panel for Glioma Subtypes According to WHO CNS5
| Glioma Subtype | Marker | Product ID | Clonality |
|---|---|---|---|
| Astrocytoma, IDH‑mutant | ATRX | AMAb90784 | Monoclonal |
| Astrocytoma, IDH‑mutant | ATRX | HPA001906 | Polyclonal |
| Astrocytoma, IDH‑mutant | IDH1 (mutant) | AMAb90578 | Monoclonal |
| Astrocytoma, IDH‑mutant | IDH1 | HPA035248 | Polyclonal |
| Astrocytoma, IDH‑mutant | p53 (TP53) | AMAb90956 | Monoclonal |
| Astrocytoma, IDH‑mutant | Ki‑67 (MKI67) | AMAb90870 | Monoclonal |
| Astrocytoma, IDH‑mutant | GFAP | AMAb91033 | Monoclonal |
| Oligodendroglioma, IDH‑mutant, 1p/19q-codeleted | ATRX | AMAb90784 | Monoclonal |
| Oligodendroglioma, IDH‑mutant, 1p/19q-codeleted | IDH1 (mutant) | AMAb90578 | Monoclonal |
| Glioblastoma, IDH‑wildtype | EGFR | AMAb90816 | Monoclonal |
| Glioblastoma, IDH‑wildtype | EGFR | HPA018530 | Polyclonal |
| Glioblastoma, IDH‑wildtype | ATRX | HPA001906 | Polyclonal |
| Glioblastoma, IDH‑wildtype | Ki‑67 (MKI67) | AMAb90870 | Monoclonal |
| Diffuse midline glioma, H3 K27–altered | H3F3A (Histone H3.3) | HPA042570 | Polyclonal |
| Diffuse hemispheric glioma, H3 G34‑mutant | H3.3‑3B / H3‑3B | HPA064058 | Polyclonal |
| Pediatric Glioma Subtype | Key Markers / Alterations |
|---|---|
| Diffuse midline glioma, H3 K27-altered | H3 K27M, H3K27me3 loss, EZHIP/CXorf67, TP53, ACVR1, PDGFRA, EGFR |
| Diffuse hemispheric glioma, H3 G34-mutant | H3.3 G34R/V, TP53, ATRX |
| Diffuse pediatric-type high-grade glioma, H3-wildtype & IDH-wildtype | PDGFRA, MYCN, EGFR, RTK pathway alterations |
| Infant-type hemispheric glioma | NTRK1/2/3, ROS1, ALK, MET fusions |
| Diffuse low-grade glioma, pediatric (MAPK pathway-altered) | BRAF, FGFR1, MAPK-pathway alterations |
| Diffuse astrocytoma, MYB- or MYBL1-altered | MYB, MYBL1 alterations |
| Angiocentric glioma | MYB alterations |
| PLNTY (Polymorphous low-grade neuroepithelial tumor of the young) | BRAF V600E, FGFR fusions |