Previous work has demonstrated the importance of protein kinase C in regulating 
glioma cell proliferation in vitro. Tamoxifen, a protein kinase C inhibitor when 
administered in high dosages, is currently being used as an adjuvant in the 
treatment of patients with malignant gliomas. The patient in the present study 
harbored a left frontal anaplastic astrocytoma adjacent to Broca's area and the 
paracentral region, which limited gross resection. After a subtotal resection of 
the tumor and after radiation, the patient was administered high-dose tamoxifen 
therapy for gross residual gadolinium-enhancing regions that were revealed by 
magnetic resonance imaging and by high glucose uptake as demonstrated by 
positron emission tomography. After treatment, a decrease in gadolinium 
enhancement on magnetic resonance images and a decrease in glucose uptake 
revealed by positron emission tomography were noted. A laboratory examination of 
the tissue obtained from the original surgical resection revealed resistance to 
radiation therapy but sensitivity to tamoxifen as measured by 
3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide assay. The 
subsequent in vitro testing of the tumor that was removed after the recurrence 
of tumor (22 months after the initiation of tamoxifen) revealed loss of 
sensitivity to tamoxifen. However, the recurrent tumor remained sensitive to 
growth inhibition by the potent protein kinase C inhibitor, hypericin, despite 
loss of sensitivity to tamoxifen in vitro, suggesting the potential clinical 
application of this agent. This close in vitro correlation with the clinical 
course of the patient in the present study suggests a potential role for such in 
vitro radiation and chemosensitivity testing in designing a rational 
individualized clinical course of treatment.