Choroid plexus tumors (CPTs) are rare neuroepithelial tumors primarily affecting the pediatric population. CPTs usually occur in the ventricles of the brain. At Alfa Cytology, we are committed to pioneering new therapeutic approaches for choroid plexus tumors therapy for our clients.
Introduction to Choroid Plexus Tumors
The cerebrospinal fluid produced by choroid plexus tissue surrounds the brain and spinal cord, so as choroid plexus tumors grow, they block the flow of cerebrospinal fluid. CPT can be classified as benign or malignant.
Choroid Plexus Papillomas (CPP)
CPP is the most common. Approximately 80% of choroid plexus tumors are CPP. These tumors are slow growing and have a low likelihood of spreading.
Choroid Plexus Carcinoma (CPC)
CPC is a cancerous form of choroid plexus tumor. About 10-20% of choroid plexus tumors are CPCs, which grow more rapidly and are more likely to spread to other tissues through the cerebrospinal fluid.
CPTs are particularly significant due to their association with genetic syndromes, such as Li-Fraumeni syndrome (LFS), characterized by germline mutations in the TP53 gene. Epidemiological studies indicate that approximately 40% of children diagnosed with CPC may have underlying LFS, highlighting the importance of genetic predisposition in tumor development.
Therapeutic Development for Choroid Plexus Tumors
The therapeutic landscape for CPTs has improved with advances in chemotherapy and surgery. High-dose chemotherapy (HDCx) followed by autologous hematopoietic progenitor cell rescue (AuHPCR) has shown promising survival rates, with about 58% of children remaining CPC-free at ten years. Additionally, targeted therapies are emerging as vital advancements in CPT treatment. Preclinical studies have identified key molecular targets, such as mTOR, ATR, and CDK, involved in tumor growth and survival.
|
NCT |
Target |
Therapeutics |
Phase |
| NCT03173950 |
PD-1 |
Nivolumab |
|
| NCT03638167 |
Epidermal Growth Factor Receptor |
EGFR806-specific Chimeric Antigen Receptor (CAR) T Cell |
|
| NCT03500991 |
HER2 |
HER2-specific Chimeric Antigen Receptor (CAR) T Cell cell |
|
| NCT01975116 |
Non-HDM2 Mediated Peptide Inhibitor of p53 Ubiquitination |
Azurin-Derived Cell-Penetrating Peptide p28 |
|
| NCT04185038 |
B7H3 |
B7H3-specific Chimeric Antigen Receptor (CAR) T Cell |
|
| NCT04541082 |
Agonist of the Mitochondrial Protease ClpP and G Protein-Coupled Receptor |
ONC206 |
|
| NCT00006247 |
VEGFR Inhibitor |
Semaxanib |
|
Our Services
Alfa Cytology specializes in providing preclinical services that support the development of innovative therapies for choroid plexus tumors. Our expertise includes molecular profiling, in vivo and in vitro studies, biomarker discovery, and strategic consultation.
Therapeutics Development
Case Study - Choroid Plexus Carcinoma Mouse Model
Model Introduction
The choroid plexus carcinoma (CPC) mouse model provides a clinically relevant preclinical platform for evaluating novel therapeutic strategies for this rare and aggressive pediatric brain tumor. This genetically engineered mouse model, generated by crossing StopFLMYC mice with Nestin-Cre mice to drive c-Myc overexpression in the choroid plexus, recapitulates key features of human CPC.
Model Information
- Model: Choroid Plexus Carcinoma (CPC) Mouse Model
- Animal: C57BL/6J
- Weight: 20-22 g
Model Construction
The CPC genetic mouse model was established by breeding StopFLMYC mice with Nestin-Cre mice to generate c-Myc overexpressing (MYC-OE) mice. These mice develop CPC predominantly in the choroid plexus of the lateral and fourth ventricles, with tumors detectable by 4 weeks of age and complete penetrance by 8 weeks. Tumor growth was monitored using magnetic resonance imaging (MRI) throughout model development.
Fig. 1 Workflow of CPC genetic mouse model establishment and treatment regimen. (Source: Alfa Cytology)
In Vivo Efficacy Evaluation
This study employed the established CPC genetic mouse model to evaluate the therapeutic efficacy of combination chemotherapy delivered via intra-arterial administration.
- Drug A + Drug B Combination Therapy: A single intra-arterial injection of drug A combined with drug B significantly extended median survival compared to vehicle-treated controls.
- Drug C + Drug B Combination Therapy: The same dose of drug C combined with drug B administered via intra-arterial injection did not significantly improve survival.
- Single Agent Controls: Drug A alone and drug B alone each failed to improve survival, demonstrating the synergistic benefit of combination therapy.
Fig. 2 Drug A + drug B combination therapy significantly improves survival in the CPC genetic mouse model. Data are presented as mean ± SEM. (Source: Alfa Cytology)
Contact Us
Alfa Cytology focuses on choroid plexus tumorigenesis and progression, and we seek to provide you with deeper insights and accelerate your research in this area through a variety of solutions. Please feel free to contact us to submit your research needs.
Reference
- Fang, F.Y.; Rosenblum, J.S.; Ho, W.S.; Heiss, J.D. New Developments in the Pathogenesis, Therapeutic Targeting, and Treatment of Pediatric Medulloblastoma. Cancers 2022, 14, 2285. Lombardi, G.; et al. (2022). Diagnosis and Treatment of Pineal Region Tumors in Adults: A EURACAN Overview[J]. Cancers. 14, 3646.
All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.
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