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Background <p>For over a century, the dominant hypothesis has maintained that meningiomas arise exclusively from arachnoid cap cells. However, emerging evidence from single-cell transcriptomics, spatial sequencing, developmental biology, and transgenic animal models suggests a significantly more complex and heterogeneous cellular origin.</p> Methods <p>This mini-review revisits historical perspectives and critically evaluates the limitations of the traditional arachnoid-based paradigm. By synthesizing classical histological insights with contemporary molecular and proteomic data, the study explores alternative hypotheses, particularly those implicating fibroblast-like or regionally distinct meningeal progenitors.</p> Results <p>The synthesis of multi-omic and developmental data indicates that a singular cellular source is insufficient to account for the clinical and biological diversity of meningiomas. Findings suggest that meningioma ontogeny is likely driven by a broader spectrum of progenitors whose characteristics vary according to anatomical location and embryological lineage.</p> Conclusions <p>A redefinition of meningioma ontogeny is necessary. Future classification and therapeutic strategies should reflect the inherent diversity of their cellular sources and anatomical environments, moving beyond the classical arachnoid-cap-cell model.</p>

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Current evidence on the cell of origin of meningiomas disputes the arachnoid cap cell dogma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月21日

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  • M. Necmettin Pamir,
  • Ayça Erşen-Danyeli,
  • Koray Özduman

摘要

Background

For over a century, the dominant hypothesis has maintained that meningiomas arise exclusively from arachnoid cap cells. However, emerging evidence from single-cell transcriptomics, spatial sequencing, developmental biology, and transgenic animal models suggests a significantly more complex and heterogeneous cellular origin.

Methods

This mini-review revisits historical perspectives and critically evaluates the limitations of the traditional arachnoid-based paradigm. By synthesizing classical histological insights with contemporary molecular and proteomic data, the study explores alternative hypotheses, particularly those implicating fibroblast-like or regionally distinct meningeal progenitors.

Results

The synthesis of multi-omic and developmental data indicates that a singular cellular source is insufficient to account for the clinical and biological diversity of meningiomas. Findings suggest that meningioma ontogeny is likely driven by a broader spectrum of progenitors whose characteristics vary according to anatomical location and embryological lineage.

Conclusions

A redefinition of meningioma ontogeny is necessary. Future classification and therapeutic strategies should reflect the inherent diversity of their cellular sources and anatomical environments, moving beyond the classical arachnoid-cap-cell model.