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Decoding craniopharyngioma: From mechanisms to therapy.

Jose Mario Gonzalez-Meljem¹, Lei Cao², John Richard Apps³

¹Tecnologico de Monterrey, School of Engineering and Sciences, Mexico City, Mexico.

Best Practice & Research. Clinical Endocrinology & Metabolism

|October 12, 2025

Summary

Recent craniopharyngioma research decodes subtypes, revealing senescence-driven pathogenesis in adamantinomatous craniopharyngioma (ACP) and BRAF mutations in papillary craniopharyngioma (PCP). This advances targeted therapies for improved patient outcomes.

Keywords:

MAPK inhibitors cellular senescence craniopharyngioma senolytics

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Area of Science:

Neuro-oncology
Molecular biology
Tumor microenvironment research

Background:

Craniopharyngioma is a complex sellar tumor with distinct subtypes.
Recent research has elucidated the genetic drivers and pathogenesis of these subtypes.

Purpose of the Study:

To summarize recent advancements in understanding craniopharyngioma subtypes.
To highlight the translation of these findings into novel therapeutic strategies.

Main Methods:

Genetic and histological subtyping (adamantinomatous craniopharyngioma [ACP] and papillary craniopharyngioma [PCP]).
Development of ACP mouse models and human studies.
Single-cell RNA sequencing to analyze tumor ecosystems.

Main Results:

ACP is linked to CTNNB1 mutations and WNT pathway activation.
PCP is characterized by BRAF-V600E mutations.
Senescence-driven pathogenesis in ACP involves paracrine signaling, creating a tumor-promoting microenvironment.

Conclusions:

Foundational insights into craniopharyngioma biology are paving the way for targeted therapies.
BRAF/MEK inhibitors for PCP and senescence-associated secretory phenotype (SASP) inhibitors for ACP show therapeutic promise.