Spontaneous Regression of Germinomas After Salvage Surgery and Possible Mechanism of Induced Apoptosis.

Abstract

BACKGROUND:

A few cases of spontaneous regression of germ cell tumors have been reported. Possible mechanisms include steroid medication, surgical intervention, diagnostic radiation exposure, and immune response. None of these hypotheses has been supported by sufficient data.

CASE DESCRIPTION:

Two cases of germinoma demonstrated spontaneous regression before antitumor therapy. In the first case, a 19-year-old man presented with acute hydrocephalus due to a pineal mass and underwent emergent endoscopic third ventriculostomy. The pineal tumor started to regress on the 4th postoperative day after endoscopic third ventriculostomy. In the second case, a 22-year-old man presented with acute hydrocephalus and panhypopituitarism due to a suprasellar mass and underwent emergent external ventricular drainage, biopsy, and septostomy on the day of admission. Apparent regression of the tumor was discovered on the 5th day after initial surgery. Pathologic diagnosis was pure germinoma in both cases. Remarkable accumulations of CD4-positive lymphocytes and some apoptotic cells positive for terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling staining were detected in both cases. Diagnostic radiation exposure is the only common condition in all reported cases.

CONCLUSIONS:

This unusual phenomenon of spontaneous regression of germinoma may be caused by a combination of pathognomonic characteristics of anatomic location with paraventricular development and stress induction as a trigger, such as salvage surgery or diagnostic radiation, including at extremely low dosage.

• Authors: Kazuma Doi, Terushige Toyooka, Kojiro Wada, Naoki Otani, Satoru Takeuchi, Arata Tomiyama, Hirokazu Nakatogawa, Tokutaro Tanaka, Hideyuki Shimazaki, Katsumi Hayashi, Kentaro Mori
• Journal: World neurosurgery (World Neurosurg) Vol. 124 Pg. 178-183 (Apr 2019) ISSN: 1878-8769 [Electronic] United States
• PMID: 30659974 (Publication Type: Journal Article)
• Copyright: Copyright © 2019 Elsevier Inc. All rights reserved.