# Primordial germ cell-like cells residing in the pituitary may serve as the origin of intracranial germ cell tumors

## TL;DR

This study suggests that cells resembling primordial germ cells in the pituitary gland may be the origin of rare brain tumors called intracranial germ cell tumors.

## Contribution

The study provides evidence for the presence of PGC-like cells in the pituitary gland and their potential role in intracranial germ cell tumor formation.

## Key findings

- PGC-like cells were found to express germ cell markers in normal pituitary tissues.
- The highest levels of germ cell markers were observed in pituitary germ cell tumors.
- The findings support a potential link between pituitary PGC-like cells and intracranial germ cell tumor development.

## Abstract

Intracranial germ cell tumors (iGCTs) are rare, histologically classified as extragonadal germ cell tumors, and predominantly affect children and adolescents. These tumors are commonly found in the midline of the brain, with a notable male predominance and varying geographic incidences. The origins of iGCTs have been debated, particularly whether they arise from abnormal migration of primordial germ cells (PGCs) or transformed embryonic stem cells (ESCs). In this study, we hypothesize the potential presence of PGC-like cells in the pituitary gland, and these cells may differentiate into iGCTs during the complex and frequent regulation of the hypothalamic-pituitary–gonadal axis (HPGA).We analyzed the expression of four germ cell markers—MVH, OCT4, C-kit, and PLZF—using immunohistochemistry, Western blotting, and real-time quantitative PCR in human pituitary tissues, pituitary tumors, and pituitary germ cell tumors. Our findings indicate significant expression of these markers in pituitary tissues, with the highest levels found in pituitary germ cell tumors. These results support the existence of PGC-like cells that within the normal pituitary gland. This study provides new insights into the cellular origins of iGCTs and suggests further investigation into the regulatory mechanisms that may lead to tumorigenesis.

The online version contains supplementary material available at 10.1038/s41598-026-38060-2.