Advanced Neuroimaging Approaches to Pediatric Brain Tumors
Abstract
:Simple Summary
Abstract
1. Introduction
2. Pediatric Brain Tumors
2.1. Overview of Pediatric Brain Tumors
2.2. Medulloblastoma
2.3. Glioma
2.4. Ependymoma
3. MRI Techniques
3.1. Introduction to MRI Modalities
3.2. Diffusion-Weighed Imaging (DWI)
3.3. Diffusion Tensor Imaging (DTI) and Tractography
3.4. Functional MRI (fMRI)
3.5. Arterial Spin Labeling (ASL) Perfusion Imaging
3.6. Magnetic Resonance Spectroscopy (MRS)
3.7. Magnetic Resonance Elastography (MRE)
3.8. Amide Proton Transfer (APT)-Weighted Imaging
3.9. Radiomics and Radiogenomics
3.10. Response Evaluation of Pediatric Brain Tumors
4. Positron Emission Tomography (PET) Imaging
4.1. Introduction to PET Imaging
4.2. Investigational Probes
5. Single-Photon Emission Computed Tomography (SPECT) Investigative Tracers
6. Multimodality Fusion Techniques and Treatment Planning
7. Conclusions
Author Contributions
Funding
Conflicts of Interest
References
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Family | Tumor Type | Additional Subtyping Based on Molecular Alterations | Frequent Molecular Alterations (*) |
---|---|---|---|
CNS embryonal tumors | |||
Medulloblastomas | WNT-activated | CTNNB1; often in conjunction with monosomy chromosome 6, DDX3X, SMARCA4, and TP53 mutations | |
SHH-activated (wildtype TP53) | SHH-1, SHH-2, SHH-4 | PTCH1, SUFU, SMO | |
SHH-activated with mutant TP53 | SHH-3 | TP53, MYCN amplification, GLI2 amplification | |
Non-WNT/non-SHH (Group 3 and Group 4) | Subtypes 1-8 | MYC or MYC/MYCN amplification, GFI/GFI1B alterations, OTX2, CDK6 or SNCAP1 amplifications; isochromosome 17; PRDM6, KBDBD4 mutations | |
Atypical teratoid/ rhabdoid tumors | ATRT-TYR, ATRT-SHH, ATRT-MYC | SMARCB1, SHH, NOTCH, loss of 22q, tyrosinase overexpression, MYC activation, HOXC | |
Gliomas, glioneuronal and neuronal tumors | |||
Diffuse high-grade gliomas | Diffuse midline glioma, H3 K27-altered | H3.3 K27-mutant; H3.1 or H3.2 K27-mutant; H3 wildtype with EZHIP overexpression; EGFR (and H3 K27) mutant | Histone 3 mutations, TP53, PPM1D, PDGFRA, PIK3CA, PIK3R1, PTEN mutations, EZHIP overexpression, EGFR mutations |
Diffuse hemispheric glioma, H3 G34-mutant | Histone 3 mutation, TP53, ATRX mutations | ||
Diffuse pediatric-type high-grade glioma, H3-wildtype and IDH-wildtype | RTK1; RTK2; MYCN | Enriched for PDGFRA, EGFR or MYCN amplification | |
Infant-type hemispheric glioma | NTRK-altered; ROS1-altered; ALK-altered; MET-altered | NTRK1/2/3 fusion; ROS1 fusion; ALK fusion; MET amplification/fusion | |
Diffuse low-grade gliomas | Diffuse astrocytoma | MYB-altered; MYBL1-altered | MYB fusion or MYBL fusion commonly with PCDHGA1, MMP16 and MAML2 |
Angiocentric glioma | MYB alterations, commonly fused with QKI | ||
Polymorphous low-grade neuroepithelial tumor | MAPK pathway–BRAF pV600E, fusions with FGFR2 or FGFR3 | ||
Diffuse low-grade glioma, MAPK pathway-altered | FGFR1 tyrosine kinase domain-duplicated; FGFR1 mutant; BRAF pV600E-mutant | MAPK pathway–FGFR1; BRAF pV600E | |
Astrocytic gliomas | Pilocytic astrocytoma | Pilomyxoid astrocytoma; pilocytic astrocytoma with histological features of anaplasia | KIA1549:BRAF fusion; NF1; BRAF p.V600E; FGFR1 mutation/fusion; KRAS; RAF1 or NTRK fusion |
High-grade astrocytoma with piloid features | NF1; FGFR; BRAF:KIAA1549 fusion; often with homozygous deletion of CDKN2A/B | ||
Pleomorphic xanthoastrocytoma | BRAF pV600E typically with homozygous deletion of CDKN2A/B | ||
Subependymal giant cell astrocytoma | |||
Astroblastoma | MN1 fusion with BEND2 or CXXC5 | ||
Glioneuronal/ neuronal tumors | Ganglioglioma | Most commonly BRAF p.V600E mutation, other MAPK pathway alterations | |
Desmoplastic infantile ganglioglioma/astrocytoma | BRAF or RAF1 fusions or mutations | ||
Dysembryoplastic neuroepithelial tumor | FGFR1 mutation, fusion or intragenic duplication | ||
Diffuse glioneuronal tumor with oligodendroglioma-like features and nuclear clusters | Monosomy of chromosome 14 | ||
Diffuse leptomeningeal glioneuronal tumor | With 1qgain; methylation class 1; methylation class 2 | KIAA1549:BRAF fusion or other MAPK alteration, combined with 1p deletion | |
Multinodular and vacuolating neuronal tumor | MAPK pathway | ||
Ependymomas | Supratentorial ependymomas | ZFTA fusion-positive; YAP fusion-positive; additional molecular subgroups awaiting to be defined | ZFTA fusion most commonly with RELA; YAP1 fusion most commonly with MAMLD1 |
Posterior fossa ependymomas | Group A (PFA); group B (PFB)-retained H3K27 trimethylation; additional molecular subgroups awaiting to be defined | Loss of H3K27 trimethylation, EZHIP overexpression |
Imaging Characteristics | Wnt | SHH | Group 3 | Group 4 |
---|---|---|---|---|
Location | Cerebellar peduncle/cerebellopontine angle | Cerebellar hemispheres | Midline/fourth ventricle | Midline/fourth ventricle |
Post-contrast enhancement | Variable | Present, intense | Present | Variable, can be non-enhancing |
Drop metastasis | Rare | Rare | Frequent | Frequent |
MRS | - | Prominent choline and lipids, low creatine, no or small taurine peak | Readily detectable taurine and creatine levels | Readily detectable taurine and creatine levels |
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Nikam, R.M.; Yue, X.; Kaur, G.; Kandula, V.; Khair, A.; Kecskemethy, H.H.; Averill, L.W.; Langhans, S.A. Advanced Neuroimaging Approaches to Pediatric Brain Tumors. Cancers 2022, 14, 3401. https://doi.org/10.3390/cancers14143401
Nikam RM, Yue X, Kaur G, Kandula V, Khair A, Kecskemethy HH, Averill LW, Langhans SA. Advanced Neuroimaging Approaches to Pediatric Brain Tumors. Cancers. 2022; 14(14):3401. https://doi.org/10.3390/cancers14143401
Chicago/Turabian StyleNikam, Rahul M., Xuyi Yue, Gurcharanjeet Kaur, Vinay Kandula, Abdulhafeez Khair, Heidi H. Kecskemethy, Lauren W. Averill, and Sigrid A. Langhans. 2022. "Advanced Neuroimaging Approaches to Pediatric Brain Tumors" Cancers 14, no. 14: 3401. https://doi.org/10.3390/cancers14143401