Volume 112, Issue 6 pp. 948-950
Article

Proliferation Potential in Recurrent Acoustic Schwannoma Following Gamma Knife Radiosurgery versus Microsurgery

Frank Lee MD

Frank Lee MD

Department of Otolaryngology–Head & Neck Surgery, University of California, Irvine Medical Center, Orange, California, U.S.A.

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Fred Linthicum Jr., MD

Fred Linthicum Jr., MD

House Ear Institute, Section on Histopathology, Los Angeles, California, U.S.A.

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Gene Hung MD

Corresponding Author

Gene Hung MD

House Ear Institute, Section on Histopathology, Los Angeles, California, U.S.A.

Gene Hung, MD, House Ear Institute, Section on Gene-Based Therapy, 2100 W. Third St., Los Angeles, CA 90057, U.S.A.Search for more papers by this author
First published: 02 January 2009
Citations: 26

Presented at the Western Section Meeting of the Triological Society, Pasadena, CA, February 3, 2002.

Abstract

Objective To evaluate the proliferation potential of recurrent acoustic schwannoma following gamma knife radiosurgery (GKR) versus microsurgery.

Study Design Retrospective study.

Methods A review of surgical records of the House Ear Clinic revealed 8 patients who had undergone GKR and 15 patients who had undergone microsurgery who had unilateral acoustic schwannoma recurrences. Immunohistochemical studies were performed to evaluate the expression of proliferating cell nuclear antigen (PCNA) on archival paraffin-embedded blocks.

Results All 8 GKR and 15 microsurgical tumors had positive staining for PCNA. The recurrent GKR tumors had significantly lower proliferation levels than in the microsurgical group (P = .03). Two GKR tumors had high proliferation levels.

Conclusions Our study indicates that recurrent vestibular schwannomas treated with GKR have lower proliferation potential as assessed by PCNA compared with recurrences following microsurgery. Radiation-induced apoptosis is thought to contribute to the lower tumor cell proliferation in GKR tumor. The two GKR tumors with high proliferation potential could be a result of radiation-induced sporadic mutation, resulting in high tumor cell proliferation.

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