Medulloblastoma, WNT-Activated — Disease Characteristics Research Report

Target Disease

• Disease name: Medulloblastoma, WNT-activated (WNT medulloblastoma; WNT-MB)
• Category: Pediatric/AYA embryonal CNS tumor (posterior fossa)
• MONDO ID: Not identified from the retrieved evidence in this run (would require direct MONDO lookup outside the current tool outputs).

1. Disease Information

Overview / definition

WNT-activated medulloblastoma is a molecularly defined medulloblastoma entity characterized by activation of the canonical WNT/β-catenin pathway, most commonly through CTNNB1 exon 3 hotspot mutations with resultant nuclear β-catenin accumulation; it comprises roughly ~10% of medulloblastomas overall. (moreno2023highfrequencyof pages 2-3, shcherbina2023comparativeanalysisof pages 2-4)

Typical location is midline/central posterior fossa around the fourth ventricle, with potential extension toward the cerebellar peduncle/brainstem; neuroradiology often shows diffusion restriction and typical posterior fossa mass effects. (jackson2023recentadvancesin pages 1-2, rechberger2023exploringthemolecular pages 1-2, shcherbina2023comparativeanalysisof pages 2-4)

Key identifiers and terminologies (available in evidence)

• WHO concept: WNT-activated medulloblastoma is a WHO-recognized molecular subgroup/entity used in integrated diagnosis frameworks. (mani2024clinicoradiologicaloutcomesin pages 1-2, rechberger2023exploringthemolecular pages 1-2)
• Common synonyms: WNT medulloblastoma; WNT subgroup medulloblastoma; WNT-pathway medulloblastoma; WNT-MB; WNT-driven medulloblastoma. (mani2023wntpathwaymedulloblastomawhat pages 2-4, NCT02724579a chunk 1)

Note on ICD/MeSH/OMIM/Orphanet/MONDO: Specific numeric identifiers were not present in the retrieved texts; therefore they cannot be reported with citations from this tool run.

Evidence source type

The disease concept and frequencies are derived from aggregated disease-level resources (reviews/cohort series) and multi-institutional clinical cohorts, not from EHR-only individual patient sources. (nobre2020patternofrelapse pages 1-3, moreno2023highfrequencyof pages 2-3, shcherbina2023comparativeanalysisof pages 2-4)

2. Etiology

Primary causal factors (molecular/genetic)

1. Somatic CTNNB1 activating mutations (exon 3) are the dominant driver in WNT-MB (~85–90% in many reports). These mutations prevent normal phosphorylation/degradation of β-catenin and lead to β-catenin nuclear translocation and transcriptional activation. (moreno2023highfrequencyof pages 2-3, ntenti2023clinicalhistologicaland pages 4-5)
2. A clinically important minority of WNT-MB cases are CTNNB1-wild type, frequently linked to germline APC pathogenic variants (familial adenomatous polyposis/Turcot syndrome). (moreno2023highfrequencyof pages 2-3, moreno2023highfrequencyof pages 1-2)
3. Recurrent cooperating alterations commonly include DDX3X and SMARCA4 mutations, with monosomy 6 as a characteristic copy-number feature (particularly pediatric WNT-α). (shcherbina2023comparativeanalysisof pages 2-4, mani2024clinicoradiologicaloutcomesin pages 10-11)

Direct abstract quote (molecular definition): Moreno et al. state that WNT-activated medulloblastomas are “usually caused by mutations in the CTNNB1 gene (85%–90%), and most remaining cases of CTNNB1 wild type are thought to be caused by germline mutations in APC.” (Frontiers in Oncology; Sep 2023; https://doi.org/10.3389/fonc.2023.1237170) (moreno2023highfrequencyof pages 2-3)

Risk factors

• Genetic predisposition: CTNNB1-wildtype WNT-MB should raise suspicion for germline APC (FAP/Turcot), and referral for genetic cancer risk assessment and APC sequencing has been explicitly recommended in this setting. (moreno2023highfrequencyof pages 2-3)

Direct abstract quote (genetic counseling implication): The same 2023 study concludes: “Considering that CTNNB1 wild-type cases may exhibit APC germline mutations, our study suggests a higher incidence (~30%) of hereditary WNT-activated medulloblastomas in the Latin-Iberian population.” (Frontiers in Oncology; Sep 2023; https://doi.org/10.3389/fonc.2023.1237170) (moreno2023highfrequencyof pages 2-3)

Protective factors / gene–environment interactions

No protective environmental factors or gene–environment interaction evidence specific to WNT-MB was identified in the retrieved sources.

3. Phenotypes (clinical presentation, HPO suggestions)

Typical presentation (symptoms/signs)

Posterior fossa medulloblastoma commonly presents with: - Headache and vomiting consistent with raised intracranial pressure (often worse on awakening, progressive). (jackson2023recentadvancesin pages 1-2) - Ataxia/gait instability due to cerebellar dysfunction (particularly midline vermian involvement). (jackson2023recentadvancesin pages 1-2) - In infants/very young children: macrocephaly, fussiness, decreased oral intake (non-localizing symptoms). (jackson2023recentadvancesin pages 1-2)

Dissemination at diagnosis across medulloblastoma overall is reported around ~20–25% (not WNT-specific), while WNT-MB cohorts often show low metastatic rates at diagnosis (e.g., “very rare <5%” in one cohort table). (jackson2023recentadvancesin pages 1-2, mani2024clinicoradiologicaloutcomesin pages 1-2)

WNT-MB clinico-anatomic tendencies

WNT-MB is described as centrally located near midline posterior fossa/fourth ventricle with potential extension into peduncle/brainstem. (shcherbina2023comparativeanalysisof pages 2-4, rechberger2023exploringthemolecular pages 1-2)

HPO term suggestions (for KB population; not claims of frequency unless noted)

• Headache — HP:0002315
• Vomiting — HP:0002013
• Ataxia — HP:0001251
• Gait ataxia — HP:0002066
• Hydrocephalus — HP:0000238 (common mechanism for raised ICP)
• Increased intracranial pressure — HP:0002516
• Macrocephaly (infants) — HP:0000256

Quality of life impact

Long-term survivorship issues remain a major challenge in pediatric medulloblastoma, and high-dose craniospinal irradiation is emphasized as associated with long-term neurocognitive harm, motivating de-intensification trials in WNT-MB. (jackson2023recentadvancesin pages 1-2, slika2023theneurodevelopmentaland pages 7-8)

A 2024 WNT cohort report explicitly notes that absence of recorded neurocognitive and late-effect data prevents direct assessment of QoL impact in that series (highlighting a common real-world data gap). (mani2024clinicoradiologicaloutcomesin pages 11-12)

4. Genetic / Molecular Information

Causal / hallmark genes and alterations

• CTNNB1 (β-catenin): somatic exon 3 hotspot mutations in most WNT-MB. (moreno2023highfrequencyof pages 2-3, shcherbina2023comparativeanalysisof pages 2-4)
• APC: germline pathogenic variants in a subset of CTNNB1-wildtype WNT-MB, associated with FAP/Turcot. (moreno2023highfrequencyof pages 2-3, moreno2023highfrequencyof pages 1-2)
• DDX3X, SMARCA4: recurrently altered in WNT-MB. (shcherbina2023comparativeanalysisof pages 2-4, slika2023theneurodevelopmentaland pages 2-4)
• Copy-number: monosomy 6 is a supportive hallmark, particularly enriched in pediatric WNT-α compared to WNT-β. (mani2024clinicoradiologicaloutcomesin pages 10-11, slika2023theneurodevelopmentaland pages 2-4)

Molecular subtypes within WNT

Two WNT subtypes are described: - WNT-α: younger/pediatric, enriched for monosomy 6. (mani2024clinicoradiologicaloutcomesin pages 10-11, slika2023theneurodevelopmentaland pages 2-4) - WNT-β: older/adult-leaning, less monosomy 6, sometimes worse prognosis in adult contexts. (mani2024clinicoradiologicaloutcomesin pages 10-11, slika2023theneurodevelopmentaland pages 2-4)

Variant classification / allele frequency

ACMG/AMP classifications and population allele frequencies (gnomAD) were not available in the retrieved evidence.

Epigenetics and methylation-class definition

WNT-MB is part of modern methylation-based CNS tumor classification, and real-world clinical workflows use EPIC methylation arrays and online classifiers to support WHO-recognized diagnoses (including WNT-MB). (green2024wnt‐activatedmyc‐amplifiedmedulloblastoma pages 2-3, wolff2024implementationofmethylation pages 5-8)

5. Mechanism / Pathophysiology

Core pathway mechanism (canonical WNT)

A causal chain supported by the retrieved literature: 1. CTNNB1 exon 3 stabilization mutation (or APC loss in predisposition) → 2. β-catenin accumulation and nuclear translocation → 3. Transcriptional activation of WNT-responsive programs supporting tumorigenesis and defining subgroup biology. (moreno2023highfrequencyof pages 2-3, ntenti2023clinicalhistologicaland pages 4-5)

Developmental origin and cell-of-origin hypotheses

WNT-MB is proposed to arise from lower rhombic lip / pontine mossy-fiber precursor–related lineages in the dorsal brainstem region (extracerebellar origin), consistent with GEMM data and subgroup developmental mapping. (slika2023theneurodevelopmentaland pages 2-4, manfreda2023wntsignalingin pages 11-12)

Tumor microenvironment and BBB

WNT-MB is linked to distinctive vasculature and a locally disrupted blood–brain barrier, which has been proposed to facilitate chemotherapy penetration and contribute to favorable outcomes. (slika2023theneurodevelopmentaland pages 7-8, nor2018clinicalandpreclinical pages 20-24)

GO biological process term suggestions

• Canonical Wnt signaling pathway — GO:0060070
• Regulation of cell proliferation — GO:0042127
• Neurogenesis — GO:0022008
• Brain development — GO:0007420

CL (cell type) term suggestions

Given proposed rhombic lip/pontine precursor origins: - Neural progenitor cell — CL:0000673 - Neuron — CL:0000540 (tumor cells show neuronal-like differentiation states in subgroup analyses) (slika2023theneurodevelopmentaland pages 2-4)

6. Anatomical Structures Affected (UBERON suggestions)

• Cerebellum — UBERON:0002037
• Fourth ventricle region — (ventricular system context; commonly used in neuroanatomy mapping) (rechberger2023exploringthemolecular pages 1-2, jackson2023recentadvancesin pages 1-2)
• Brainstem / cerebellar peduncle involvement (extension) — (shcherbina2023comparativeanalysisof pages 2-4)

7. Temporal Development, Inheritance, Population, and Prognosis

Age at onset

WNT-MB typically affects older children/adolescents (median ~11–12 years), is rare in infants, and comprises a minority of adult medulloblastomas (~10–15% of adult MB in one review summary). (shcherbina2023comparativeanalysisof pages 2-4, mani2024clinicoradiologicaloutcomesin pages 1-2)

Epidemiology (subgroup frequency)

WNT-MB is typically ~10% of medulloblastomas, though cohort composition varies; a Latin-Iberian multi-institution series reported 15% (40/266) WNT-activated tumors. (moreno2023highfrequencyof pages 2-3, moreno2023highfrequencyof pages 1-2)

Inheritance

Most cases are sporadic, but CTNNB1-wildtype WNT-MB has an important association with germline APC (FAP/Turcot), motivating genetic counseling and testing. (moreno2023highfrequencyof pages 2-3)

Prognosis: key statistics

• Excellent frontline outcomes are typical, often reported as >90% 5-year survival in pediatric WNT-MB. (upadhyay2024riskstratifiedradiotherapyin pages 4-5, slika2023theneurodevelopmentaland pages 7-8)
• A 2024 institutional WNT cohort reported 5-year PFS 87.7% and 5-year OS 91.2% at median 72-month follow-up. (Diagnostics; Feb 2024; https://doi.org/10.3390/diagnostics14040358) (mani2024clinicoradiologicaloutcomesin pages 1-2)
• A large international molecularly confirmed cohort (n=93) reported 5-year PFS 0.84 with 15 relapses. (Cell Reports Medicine; Jun 2020; https://doi.org/10.1016/j.xcrm.2020.100038) (nobre2020patternofrelapse pages 1-3)

Relapse patterns

Relapses are uncommon but frequently metastatic; in the 93-patient cohort, 12/15 relapses were metastatic, with a distinctive tendency to involve the lateral ventricles (8/12 metastatic relapses). Outcomes after relapse were poor with limited salvage, and relapse risk was strongly influenced by the maintenance chemotherapy regimen (higher cumulative cyclophosphamide/ifosfamide exposure associated with fewer relapses). (nobre2020patternofrelapse pages 1-3)

8. Diagnostics

Imaging

Medulloblastomas typically arise near the superior fourth ventricle/inferior medullary velum region, frequently show diffusion restriction, and may show heterogeneous enhancement/cysts/necrosis on MRI. (jackson2023recentadvancesin pages 1-2)

Histopathology and immunohistochemistry

• WNT-MB is often classic histology. (jackson2023recentadvancesin pages 1-2, shcherbina2023comparativeanalysisof pages 2-4)
• Nuclear β-catenin staining is a key diagnostic feature used clinically and in trial screening. (jackson2023recentadvancesin pages 1-2, NCT02724579a chunk 2)

Molecular testing workflow (real-world implementation)

A pragmatic diagnostic strategy supported by the retrieved sources: 1. CTNNB1 testing (e.g., Sanger sequencing) because exon 3 mutations define most WNT-MB. (moreno2023highfrequencyof pages 2-3) 2. β-catenin IHC (nuclear positivity) as an accessible diagnostic marker and eligibility screen for WNT-directed trials. (jackson2023recentadvancesin pages 1-2, NCT02724579a chunk 2) 3. DNA methylation profiling (Illumina EPIC arrays → MolecularNeuropathology.org/DKFZ classifier) to confirm subgroup and generate CNV plots; multiple real-world implementations show feasibility and typical classifier confidence thresholds. - A 2024 case report illustrates EPIC-based methylation classification for WNT-MB with discussion of confidence scores (≥0.9 strongly supporting a WHO-recognized class; an example case had 0.78, highlighting heterogeneity and need for orthogonal confirmation). (green2024wnt‐activatedmyc‐amplifiedmedulloblastoma pages 2-3) - A 2024 implementation study in Brazil used EPIC arrays and MolecularNeuropathology.org classifiers, with diagnostic agreement in 94% and classifier scores ≥0.9 in ~81% of cases, showing operational feasibility in a public health center workflow. (Preprint; Nov 2024; https://doi.org/10.21203/rs.3.rs-5332503/v1) (wolff2024implementationofmethylation pages 5-8) 4. Germline APC testing is recommended when WNT-MB is CTNNB1-wildtype. (moreno2023highfrequencyof pages 2-3)

9. Treatment (standard of care, de-escalation, and real-world trials)

Standard frontline management (context)

Contemporary WNT-MB management is typically maximal safe resection followed by risk-stratified craniospinal irradiation (CSI) + boost and multi-agent chemotherapy, achieving high cure rates but with substantial late toxicity concerns. (mani2024clinicoradiologicaloutcomesin pages 11-12, slika2023theneurodevelopmentaland pages 7-8)

MAXO suggestions (for KB mapping; representative): - Surgical resection — MAXO:0000114 - Craniospinal irradiation — (radiotherapy action term) - Combination chemotherapy — (chemotherapy action term) - Audiology monitoring — (monitoring/assessment term) - Endocrine function monitoring — (monitoring/assessment term)

De-escalation rationale and caution

Because WNT-MB has excellent outcomes, multiple efforts seek to reduce CSI dose and/or chemotherapy intensity to improve long-term quality of survival. (mani2023wntpathwaymedulloblastomawhat pages 2-4, upadhyay2024riskstratifiedradiotherapyin pages 4-5)

However, early attempts at more aggressive de-intensification have been unsafe: - A 2023 review notes that two prospective de-intensification strategies (including omission of upfront CSI) were terminated early due to “unacceptably high relapse rates,” supporting the conclusion that CSI remains integral to curative therapy. (mani2023wntpathwaymedulloblastomawhat pages 1-2) - A 2024 review summary describes a pilot omission-of-CSI approach as inferior, with rapid relapses requiring salvage CSI (reported as all relapsing within <1 year in that summary). (upadhyay2024riskstratifiedradiotherapyin pages 4-5)

Key ongoing/major clinical trials (ClinicalTrials.gov details)

1. COG ACNS1422 — NCT02724579 (start 2017; status ACTIVE_NOT_RECRUITING)
2. Population: newly diagnosed WNT-driven, average-risk medulloblastoma; age ≥3 and <22; M0 by brain/spine MRI and negative CSF cytology; residual ≤1.5 cm²; classical histology; screening includes nuclear β-catenin IHC, CTNNB1 mutation, and negative MYC/MYCN FISH. (NCT02724579a chunk 2)
3. Radiation: CSI 18 Gy plus tumor-bed boost 36 Gy (total 54 Gy). (NCT02724579a chunk 1)
4. Chemo: reduced-intensity maintenance regimens; notably omits vincristine during RT and uses alternating blocks including cisplatin/lomustine/vincristine and cyclophosphamide/vincristine. (NCT02724579a chunk 1)
5. Endpoints: PFS (up to 10 years), real-time DNA methylation profiling, longitudinal neurocognitive and QoL outcomes, and toxicity endpoints (audiology/endocrine/neuropathy). (NCT02724579a chunk 1)

6. URL: https://clinicaltrials.gov/study/NCT02724579

7. SIOP PNET5 — NCT02066220 (start 2014; status ACTIVE_NOT_RECRUITING)

8. WNT low-risk arm: CSI 18.0 Gy and 54 Gy primary tumor RT, followed by reduced-intensity maintenance chemo (alternating cisplatin/CCNU/vincristine and cyclophosphamide/vincristine). (NCT02066220 chunk 1)

9. URL: https://clinicaltrials.gov/study/NCT02066220

10. St. Jude SJMB12 — NCT01878617 (start 2013; status ACTIVE_NOT_RECRUITING)

11. Risk- and molecularly directed trial with a WNT stratum receiving reduced-dose CSI and reduced-dose cyclophosphamide; primary objective includes PFS estimation versus historical controls. (NCT01878617 chunk 1)

12. URL: https://clinicaltrials.gov/study/NCT01878617

13. FOR-WNT2 — NCT04474964 (start 2020; status RECRUITING)

14. Population: children >3 and <16; WNT-pathway medulloblastoma; M0; residual <1.5 cm²; start within 6 weeks of surgery. (NCT04474964a chunk 2)
15. Radiation: CSI 18 Gy/10 fractions + tumor-bed boost 36 Gy/20 fractions (total 54 Gy/30 fractions) without concurrent chemotherapy. (NCT04474964 chunk 1)
16. Chemo: 6 cycles alternating adjuvant chemotherapy (per study CET protocol). (NCT04474964 chunk 1)
17. Endpoints: 5-year relapse-free survival and overall survival; secondary endpoints include neurocognitive, endocrine, and hearing outcomes. (NCT04474964 chunk 1)
18. URL: https://clinicaltrials.gov/study/NCT04474964

Real-world outcome data informing de-escalation

Relapse in WNT-MB is influenced by maintenance chemotherapy intensity; in a 93-patient cohort, higher cumulative cyclophosphamide/ifosfamide exposure correlated with fewer relapses, implying that safe radiotherapy reduction must be co-designed with adequate systemic therapy. (nobre2020patternofrelapse pages 1-3)

10. Prevention

Primary prevention

No established primary prevention strategies exist for sporadic WNT-MB based on the retrieved evidence.

Secondary prevention / screening

For hereditary predisposition (APC/FAP/Turcot-associated WNT-MB), the actionable prevention-oriented steps in this context are: - Genetic counseling and germline APC testing when WNT-MB is CTNNB1-wildtype (and/or in the presence of family history consistent with FAP). (moreno2023highfrequencyof pages 2-3)

11. Other Species / Natural Disease and Model Organisms

Genetically engineered mouse models (GEMMs)

WNT-MB GEMMs typically require stabilized Ctnnb1 (exon-3) activation plus cooperating lesions; Ctnnb1 activation alone is insufficient in some systems. - A cited GEMM: Blbp-Cre; Ctnnb1lox(ex3); Trp53flox/+ produces WNT medulloblastoma with ~15% penetrance and ~290-day latency; adding Pik3caE545K increases penetrance and shortens latency (reported as 100% penetrance within ~3 months in one summary). (nor2018clinicalandpreclinical pages 20-24, manfreda2023wntsignalingin pages 11-12)

Patient-derived xenografts (PDX) and translational resources

PDX repositories include medulloblastoma lines characterized by integrated genomics, though available PDX collections can be biased toward Group 3/MYC-amplified tumors; nonetheless, PDX systems remain a key translational platform for subgroup-specific therapy testing. (nor2018clinicalandpreclinical pages 16-20)

Practical model-selection considerations (2024 perspective)

A 2024 ITCC-P4 framework emphasizes using multiple in vivo models (xenografts and/or transgenic models), orthotopic designs when possible, and reporting PK/PD plus biomarker-linked endpoints to support clinical translation—principles directly applicable to WNT-MB preclinical work. (gopisetty2024itccp4molecularcharacterization pages 70-72)

12. Summary Artifact (quick reference)

Table: This table condenses the core disease-defining, molecular, epidemiologic, prognostic, and relapse-pattern features of WNT-activated medulloblastoma. It is useful as a quick reference for building a structured disease knowledge base entry with supporting citations.

13. Expert synthesis / current understanding (2023–2024 emphasis)

1. Molecular definition is central: WNT-MB is best defined by CTNNB1/APC-driven canonical WNT activation with nuclear β-catenin; methylation profiling is increasingly integrated into real-world diagnostics for confirmation and CNV support. (moreno2023highfrequencyof pages 2-3, green2024wnt‐activatedmyc‐amplifiedmedulloblastoma pages 2-3, wolff2024implementationofmethylation pages 5-8)
2. De-escalation is active but constrained: evidence and expert reviews highlight that CSI dose reduction (15–18 Gy) is being tested in carefully defined low-risk WNT populations, but complete omission of CSI has led to rapid relapses in pilot efforts, reinforcing CSI as a necessary curative component. (upadhyay2024riskstratifiedradiotherapyin pages 4-5, mani2023wntpathwaymedulloblastomawhat pages 1-2)
3. Relapse biology matters: despite excellent prognosis, relapse—often metastatic with lateral-ventricle predilection—occurs and has poor salvage outcomes; chemotherapy regimen intensity appears to be a key modifiable factor in relapse risk, shaping trial design. (nobre2020patternofrelapse pages 1-3)

References (URLs and publication timing for key cited sources)

• Moreno et al. Frontiers in Oncology (Sep 2023). “High frequency of WNT-activated medulloblastomas with CTNNB1 wild type…” https://doi.org/10.3389/fonc.2023.1237170 (moreno2023highfrequencyof pages 2-3)
• Mani et al. Diagnostics (Feb 2024). “Clinico-Radiological Outcomes in WNT-Subgroup Medulloblastoma” https://doi.org/10.3390/diagnostics14040358 (mani2024clinicoradiologicaloutcomesin pages 1-2)
• Nobre et al. Cell Reports Medicine (Jun 2020). “Pattern of Relapse and Treatment Response in WNT-Activated Medulloblastoma” https://doi.org/10.1016/j.xcrm.2020.100038 (nobre2020patternofrelapse pages 1-3)
• Upadhyay & Paulino. Cancers (Oct 2024). “Risk-Stratified Radiotherapy in Pediatric Cancer” https://doi.org/10.3390/cancers16203530 (upadhyay2024riskstratifiedradiotherapyin pages 4-5)
• Wolff et al. preprint (Nov 2024). “Implementation of methylation profiling…” https://doi.org/10.21203/rs.3.rs-5332503/v1 (wolff2024implementationofmethylation pages 5-8)
• ClinicalTrials.gov: NCT02724579, NCT02066220, NCT01878617, NCT04474964 (NCT02724579a chunk 1, NCT02066220 chunk 1, NCT01878617 chunk 1, NCT04474964 chunk 1)

References

1. (moreno2023highfrequencyof pages 2-3): Daniel Antunes Moreno, Murilo Bonatelli, Augusto Perazzolo Antoniazzi, Flávia Escremim de Paula, Leticia Ferro Leal, Felipe Antônio de Oliveira Garcia, André Escremim de Paula, Gustavo Ramos Teixeira, Iara Viana Vidigal Santana, Fabiano Saggioro, Luciano Neder, Elvis Terci Valera, Carlos Alberto Scrideli, João Stavale, Suzana Maria Fleury Malheiros, Matheus Lima, Glaucia Noeli Maroso Hajj, Hernan Garcia-Rivello, Silvia Christiansen, Susana Nunes, Maria João Gil-da-Costa, Jorge Pinheiro, Flavia Delgado Martins, Carlos Almeida Junior, Bruna Minniti Mançano, and Rui Manuel Reis. High frequency of wnt-activated medulloblastomas with ctnnb1 wild type suggests a higher proportion of hereditary cases in a latin-iberian population. Frontiers in Oncology, Sep 2023. URL: https://doi.org/10.3389/fonc.2023.1237170, doi:10.3389/fonc.2023.1237170. This article has 9 citations.

2. (shcherbina2023comparativeanalysisof pages 2-4): Valeriia Shcherbina, Larysa Kovalevska, Eugene Pedachenko, Tetyana Malysheva, and Elena Kashuba. Comparative analysis of the embryonal brain tumors based on their molecular features. Discovery medicine, 35 178:733-749, Oct 2023. URL: https://doi.org/10.24976/discov.med.202335178.69, doi:10.24976/discov.med.202335178.69. This article has 6 citations and is from a peer-reviewed journal.

3. (jackson2023recentadvancesin pages 1-2): Kasey Jackson and Roger J. Packer. Recent advances in pediatric medulloblastoma. Current Neurology and Neuroscience Reports, 23:841-848, Nov 2023. URL: https://doi.org/10.1007/s11910-023-01316-9, doi:10.1007/s11910-023-01316-9. This article has 41 citations and is from a domain leading peer-reviewed journal.

4. (rechberger2023exploringthemolecular pages 1-2): Julian S. Rechberger, Stephanie A. Toll, Wouter J. F. Vanbilloen, David J. Daniels, and Soumen Khatua. Exploring the molecular complexity of medulloblastoma: implications for diagnosis and treatment. Diagnostics, 13:2398, Jul 2023. URL: https://doi.org/10.3390/diagnostics13142398, doi:10.3390/diagnostics13142398. This article has 20 citations.

5. (mani2024clinicoradiologicaloutcomesin pages 1-2): Shakthivel Mani, Abhishek Chatterjee, Archya Dasgupta, Neelam Shirsat, Akash Pawar, Sridhar Epari, Ayushi Sahay, Arpita Sahu, Aliasgar Moiyadi, Maya Prasad, Girish Chinnaswamy, and Tejpal Gupta. Clinico-radiological outcomes in wnt-subgroup medulloblastoma. Diagnostics, 14:358, Feb 2024. URL: https://doi.org/10.3390/diagnostics14040358, doi:10.3390/diagnostics14040358. This article has 5 citations.

6. (mani2023wntpathwaymedulloblastomawhat pages 2-4): Shakthivel Mani, Abhishek Chatterjee, Archya Dasgupta, Neelam Shirsat, Sridhar Epari, Girish Chinnaswamy, and Tejpal Gupta. Wnt-pathway medulloblastoma: what constitutes low-risk and how low can one go? Oncotarget, 14:105-110, Feb 2023. URL: https://doi.org/10.18632/oncotarget.28360, doi:10.18632/oncotarget.28360. This article has 10 citations.

7. (NCT02724579a chunk 1): Reduced Craniospinal Radiation Therapy and Chemotherapy in Treating Younger Patients With Newly Diagnosed WNT-Driven Medulloblastoma. Children's Oncology Group. 2017. ClinicalTrials.gov Identifier: NCT02724579

8. (nobre2020patternofrelapse pages 1-3): Liana Nobre, Michal Zapotocky, Sara Khan, Kohei Fukuoka, Adriana Fonseca, Tara McKeown, David Sumerauer, Ales Vicha, Wieslawa A. Grajkowska, Joanna Trubicka, Kay Ka Wai Li, Ho-Keung Ng, Luca Massimi, Ji Yeoun Lee, Seung-Ki Kim, Shayna Zelcer, Alexandre Vasiljevic, Cécile Faure-Conter, Peter Hauser, Boleslaw Lach, Marie-Lise van Veelen-Vincent, Pim J. French, Erwin G. Van Meir, William A. Weiss, Nalin Gupta, Ian F. Pollack, Ronald L. Hamilton, Amulya A. Nageswara Rao, Caterina Giannini, Joshua B. Rubin, Andrew S. Moore, Lola B. Chambless, Rajeev Vibhakar, Young Shin Ra, Maura Massimino, Roger E. McLendon, Helen Wheeler, Massimo Zollo, Veronica Ferruci, Toshihiro Kumabe, Claudia C. Faria, Jaroslav Sterba, Shin Jung, Enrique López-Aguilar, Jaume Mora, Carlos G. Carlotti, James M. Olson, Sarah Leary, Jason Cain, Lenka Krskova, Josef Zamecnik, Cynthia E. Hawkins, Uri Tabori, Annie Huang, Ute Bartels, Paul A. Northcott, Michael D. Taylor, Stephen Yip, Jordan R. Hansford, Eric Bouffet, and Vijay Ramaswamy. Pattern of relapse and treatment response in wnt-activated medulloblastoma. Cell Reports Medicine, 1:100038, Jun 2020. URL: https://doi.org/10.1016/j.xcrm.2020.100038, doi:10.1016/j.xcrm.2020.100038. This article has 52 citations and is from a peer-reviewed journal.

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