Transforming growth factor-beta1 expression in human acoustic neuroma

The differing clinical behavior of acoustic neuroma (AN) may be explained by the presence of specific biological features involved in tumorigenesis and growth.

Transforming growth factor (TGF) beta1 is known to participate in the regulation of peripheral nerve tumors, modulating cell proliferation and differentiation with mechanisms different from those of glial growth factors (GGF) and fibroblastic growth factors (FGF), which are responsible for Schwann cells' mitogen activity.

Surgically removed human AN specimens were fixed in formalin and embedded in paraffin for immunohistochemistry studies. Expression and localization of TGF-beta1 in different tumor regions were assessed after incubation of paraffin sections with a mouse monoclonal anti-TGF beta1 antibody (DBA, Milan, Italy). Clinically, the time elapsed between the beginning of symptomatology and AN size as shown by preoperative computed tomography, magnetic resonance imaging, or both was calculated as rough value of growth rate, which enabled slow-growing and fast-growing ANs to be distinguished.

Eighty-four percent of AN specimens expressed TGF-beta1 positivity at the level of the cytoplasm of the Schwann cells. TGF-beta1 reactivity was also shown in the blood vessel walls (96.15%) and the tumor capsule (80.86%). TGF-beta1 reaction appeared higher in Antoni A regions than in Antoni B regions. No significant relationship was found between TGF-beta1 positivity and AN growth rate in the two groups.

TGF-beta1 could participate in the biological behavior of AN, particularly as an important factor of tumor growth prediction by allowing rapidly progressive or potentially recurrent tumors to be differentiated from slow-growing tumors that are unlikely to recur. The clinical course of patients with AN is currently still of little help in predicting the rate of AN growth.