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Twenty-two patients undergoing CT-guided stereotaxic biopsies had intraoperative monopolar and bipolar impedance monitoring along the trajectory of the biopsy. Patterns of tissue impedance were retrospectively correlated with CT scans demonstrating decreased impedance generally corresponding to low density regions and increased impedance to the enhancing lesions. [ABSTRACT FROM AUTHOR]

Eighteen patients underwent CT guided stereotactic biopsies using either a Riechert-Mundinger stereotactic frame modified for use in the CT scanner or the CT-based intracranial landmark technique of Gildenberg and a Todd-Wells frame. In seven patients undergoing biopsy with the modified frame technique, representative tissue samples were obtained in all cases. Eleven patients had biopsies using the Gildenberg technique and representative tissue samples were obtained in 10 of the 11. No major postoperative complications occurred in either group. Both techniques allowed samples of intracranial tissue to be obtained safely and efficiently. The modified frame technique provided a higher degree of accuracy while the Gildenberg technique required significantly less CT time and provided a satisfactory degree of accuracy. In seven patients with ring enhancing lesions, biopsies of the enhancing rim provided diagnostic tissue while biopsy of the central low density center of the lesion in three patients provided necrotic material which was useful in histologically grading the tumour. [ABSTRACT FROM AUTHOR]

Objective: To determine the facial nerve outcomes at a tertiary neurotological referral center specializing in acoustic neuroma and skull base surgery., Study Design: Retrospective review of 100 consecutive patients in whom acoustic neuromas were removed using all of the standard surgical approaches., Methods: Functional facial nerve outcomes were independently assessed using the House-Brackmann facial nerve grading system., Results: The tumors were categorized as small, medium, large, and giant. If one excludes the three patients with preoperative facial palsies, 100% of the small tumors, 98.6% of the medium tumors, 100% of the large tumors, and 71% of the giant tumors had facial nerve function grade I-II/VI after surgery., Conclusion: Facial nerve results from alternative nonsurgical treatments must be compared with facial nerve outcomes from experienced surgical centers. Based on the facial nerve outcomes from our 100 consecutive patients, microsurgical resection remains the preferred treatment modality for acoustic tumors.

During a 3-year period, 25 caudalis dorsal root entry zone (DREZ) operations were done for severe, facial pain. Intraoperative brainstem recordings were done before and after DREZ in all patients. Primary diagnosis included refractory trigeminal neuralgia, atypical headaches or facial pain, posttraumatic closed head injuries, postsurgical anesthesia dolorosa, multiple sclerosis, brainstem infarction, postherpetic neuralgia and cancer-related pain. At the time of discharge, good to excellent pain relief was present in 24/25 patients and fair relief in 1. At 1 month, 19/25 (76%) patients had good to excellent results and at 3 months following surgery, 17/25 (68%) continued to have good to excellent pain relief. One year following surgery, 18 patients could be evaluated, 12/18 (67%) still considered their relief as good to excellent, 2 fair and 4 poor. Transient postoperative ataxia was present in 15/25 patients (60%), but was largely resolved at 1 months. In 3/18 (17%) patients, a degree of ataxia was still present at 1 year although in none was it disabling. Two patients had transient diplopia, and 3 had increased corneal anesthesia with 1 later developing a keratitis. No surgical or postsurgical mortality was noted. This procedure has proven to be a satisfactory treatment for many patients with debilitating facial pain syndromes with acceptable morbidity.

Stereotactic neurosurgery is the arena in which the past meets the present on many levels. Preserved skulls from South America, Africa, and Europe testify to man's early attempts at cranial surgery. Stereotactic approaches and systems, as well as the new innovative interactive image-guided devices, are efforts to explore and treat the afflictions of the human brain in both its literal and figurative aspects.

The development of monoclonal antibodies has resulted in marked expansion in understanding the central nervous system (CNS). This has been especially true in the study of human neuroectodermal tumors where monoclonal antibodies have been used as physiological probes to define and characterize human neuroectodermal tumor-associated antigens. Utilizing monoclonal antibodies, neuroectodermal tumor-associated antigens have been described in four broad categories; biochemically defined markers, shared nervous system-lymphoid cell markers, shared neuroectodermal-oncofetal markers, and putative restricted tumor markers. Preliminary data have demonstrated the ability to localize animal and human tumors in vitro, ex vivo, and in vivo. Early application of monoclonal antibody technology to neuroimmunology and neuro-oncology has resulted in a new awareness of the complex relationships that exist within the CNS. Their specificity and reproducibility may provide the means to qualitatively and quantitatively define the phenotypic heterogeneity of human neuroectodermal tumors. Potentially, monoclonal antibodies, alone or as carriers of radionuclides, drugs, or toxins, may allow successful diagnosis and treatment of human neuroectodermal tumors.

Memory and language dysfunction has been sporadically reported following stereotaxic thalamotomies. In order to determine which patients are at greatest risk and to better define the nature of this dysfunction, we have prospectively evaluated 18 patients undergoing stereotaxic thalamotomies for movement disorders (MDs). Patients were evaluated clinically, with computed tomography (CT) and with memory and language protocols (MLPs) pre- and postoperatively. Patients exhibiting postoperative deficits were again evaluated with the MLP on follow-up visits to the clinic. Significant changes in memory and language function occurred in 7 out of 18 patients. These 7 patients had diverse etiologies for their MDs. Five of the 18 patients had undergone previous thalamotomies on the contralateral side. Three of these 5 patients with bilateral thalamotomies experienced postoperative functional impairments in memory and language while only 4 of 13 patients with a unilateral thalamotomy experienced these problems. The postoperative functional impairments noted were primarily those requiring orientation and speech. All patients with postoperative memory and language impairments were again evaluated with MLPs months after the operation. In 3 of 7 patients, no improvement was noted, while the remaining 4 did recover to baseline. More severe deficits tended to occur in those patients with ventriculomegaly or evidence of other major cerebral tissue loss by preoperative CT scan and in those patients with lower MLP scores preoperatively. Postoperative memory and language dysfunction was not correlated with the number or size of the lesions made, the postoperative general neurologic examination or CT scans, or the clinical response of the MDs. From our data, it appears that patients with more profound neurologic compromise and/or bilateral involvement as evidenced by poor performance on the MLP, tissue loss on CT scanning, or previous thalamic lesion, are most at risk for memory and language dysfunction postoperatively. However, this dysfunction is not necessarily permanent. Preoperative evaluation with MLPs and CT scanning appear to be of value in predicting those patients at greatest risk for postoperative and language dysfunction.

Fifteen permanent cell lines derived from human gliomas which are individually distinct by immunologic and biochemical criteria were evaluated to determine if morphologic or cell biologic parameters distinguished the 4 lines which were tumorigenic in athymic nude mice. By subjective morphologic appraisal, the 4 tumorigenic lines were considered "malignant" or "borderline," but 4 of the non-tumorigenic lines were also classified in this way. By objective criteria, these 15 lines varied markedly in percentage of piled-up cells, chromatin pattern, pleomorphism, nuclear to cytoplasmic ratio, number of bizarre multinucleate giant cells, presence of abnormal mitotic figures, percentage of colony formation in soft agar, saturation density, population doubling time, and absolute plating efficiency. Among these criteria, percentage of colony formation in soft agar had the highest correlation coefficiency with tumorigenicity, and when this parameter was held constant the only additional characteristic which correlated significantly (p less than .05) was the number of bizarre multinucleate giant cells. When the 11 non-tumorigenic lines were ranked by these 2 criteria, 1 non-tumorigenic line (U-251 MGsp) had greater than .95 predicted probability of tumorigenicity. Although further tumorigenicity testing may increase the number of tumorigenic lines, the lines with few "malignant" characteristics may correspond to the population resembling cells of low grade astrocytomas seen within glioblastomas. The histologic pleomorphism of human gliomas is reflected in their morphologic and cell biologic diversity in culture.

The addition of exogenous cyclic nucleotides to cultured neoplastic cells has been reported by others to cause changes in growth properties and cellular morphology. We have studied the in vitro morphologic response to exogeneous dibutyryl adenosine 3':5'-cyclic monophosphate (DBcAMP) of twelve permanent cell lines derived from human gliomas, thirteen sublines and clonal lines derived from human gliomas, and nine cell lines derived from neoplastic and non-neoplastic human tissue from sources other than gliomas. Replicate samples from each cell line were evaluated during log phase growth by counting cells with cytoplasmic extensions greater than two times the diameter of the cell body and at saturation density for the percentage of cells morphologically responding to DBcAMP. The mean percentage of glioma-derived cells responding ranged from 5.0 to 97.3 percent during log phase growth and from 0 to 100 percent at saturation density; from 0 to 95.0 percent of non-glioma derived cells responded. The percentages of responding cells from gliomas and controls for any given line was reproducible within and between triplicate observations. Further evaluation of the twelve permanent human glioma-derived cell lines during log phase growth and at confluence delineated two clearly separate groups of cell lines. During log phase growth, eight of twelve lines had between 19.7 and 88.0 percent responding cells. At confluence, these same cell lines had between 25 and 100 percent responding cells. The other four cell lines had, respectively, 5.7 to 7.7 percent and 0 to 10 percent responding cells. The spectrum of percentage of responding cells and the variable nature of the response elicited provide evidence for the heterogeneity of the cell populations present within human glioma-derived cultured cell lines. The in vitro morphologic response to DBcAMP was reproducible and could be quantitated, but the nature and mechanism of the response to DBcAMP, whether "toxic," "differentiating," or otherwise, could not be determined from these studies.

Sixteen of 17 anaplastic human gliomas (AHGs) transplanted into athymic mice produced progressively growing subcutaneous nodules at the site of implantation. Thirty-four of 68 animals (50%) receiving transplanted tissue developed 500 m3 tumors in 24 to 364 days. Fourteen AHG were passed to a second animal generation, and 11 showed continued growth. Eight of these were serially passed, with one reaching a sixth animal generation, four reaching a fifth, and a three third. Once growth occurred in a second animal generation, no AHGs were lost in subsequent passages because of failure to grow. Of 234 animals receiving tumors beyond the first animal generation, 189 (80.8%) developed tumors. Average doubling times of the exponentially growing tumors in serial passage ranged from 3.0 to 19.1 days. This growth rate tended to increase and stabilize in early animal passages. The tumors growing in animals contained cell types which were present in the original human tumors, including fibrillary and protoplasmic astrocytes, small anaplastic cells, gemistocytes, anaplastic spindle cells, and multinucleate giant cells. Glial fibrillary acidic protein (GFAP) was detected in 15 of 17 biopsy specimens and in 12 of 14 AHGs in animals. These data illustrate the value of the athymic mouse system for the investigation of human brain tumors by demonstrating a high rate of successful transplantation, quantitative growth data on serially passed tumors, and morphological and immunochemical resemblance of the tumors in mice to the original human tumors.

Lack of tumor specificity renders current modalities for treating malignant glioma ineffective. The administration of 131I-labeled monoclonal antibody (Mab) 81C6, which reacts with the glioma-associated extracellular matrix antigen, tenascin, to nude mice carrying s.c. human glioma xenografts has resulted in significant tumor growth delay and tumor regression. In this study, we evaluated the therapeutic efficacy of 131I-labeled 81C6 in athymic rats bearing intracranial human glioma xenografts, a more appropriate model for human gliomas. Mab 81C6, an IgG2b immunoglobulin, and an isotype-matched control Mab, 45.6, were labeled at 12.5-23.6 mCi/mg with chloramine-T. The Mabs were given i.v. at 1.25 and 2.5 mCi/animal for 131I-labeled 81C6, and 1.25 mCi for 131I-labeled 45.6 control. Therapeutic response was evaluated by survival prolongation using Wilcoxon rank sum analysis. Three experiments were done. No significant survival prolongation was found in the trial in which the average tumor size at the time of Mab administration was 60 +/- 14 mm3, two-thirds the size which causes animal death. In experiment 2, Mab was given at 16 +/- 14 mm3 average intracranial tumor volume. Statistically significant (P less than or equal to 0.005) survival prolongation was found for animals treated with 2.5 mCi 131I-labeled 81C6. In that experiment, male animals with intracranial xenografts had significantly shorter survival than females (P less than or equal to 0.005). When only female animals were used in the analysis, the 1.25-mCi 81C6 group also was found to have longer survival benefit (P less than or equal to 0.01). In the third experiment, only female animals were used and the tumor size at the initiation of treatment was 20 +/- 9 mm3. Highly significant survival prolongation again was found in both 1.25 (P = 0.001) and 2.5 mCi (P less than 0.001) 131I-labeled 81C6 groups. The estimated dose to intracranial tumors from 1.25 mCi of 131I-labeled Mab was 1585 rads for 81C6 and 168 rads for 45.6. Dose to other organs from 81C6 and 45.6 was similar, ranging between 31 rads to the brain and 734 rads to the bone marrow. However, normocellularity was observed in most marrow tissue examined microscopically. Three animals receiving the low dose (1.25 mCi 81C6) survived for more than 71 days with apparent cures. In conclusion, intracranial human glioma xenografts were treated successfully with 131I-labeled 81C6 but not control Mab.

Nine patients with autonomic dysfunction syndrome (ADS) characterised by sympathetic discharge and extensor posturing are presented. Morphine was given to three patients and in all cases consistently stopped the episodes. Dantrolene was given to one patient and reduced the severity of the extensor posturing without affecting the other components of the ADS. Bromocriptine was given to three patients and appeared to have both short- and long-term effects. Acutely, the drug partially corrected the hyperthermia and diaphoresis associated with these episodes. Two patients were given bromocriptine long-term. In one patient, the ADS was completely controlled and in the other, the frequency of the episodes decreased. The autonomic dysfunction syndrome appears to be related to both severe closed head injury and acute hydrocephalus. The clinical similarity of the two diverse etiologic groups and the absence of precipitating increased ICP in the former suggests the common theme is a release of the brain stem from higher control. The responses to morphine and bromocriptine suggest that the opiate and dopaminergic pathways play roles in the entity.

The brain has long been considered an immunologically privileged site. Tissue transplanted to the central nervous system (CNS) is immunologically better tolerated than grafts to other regions of the body. With improved graft survival, tissue transplantation may provide new treatment options for previously incurable CNS disorders. The normal immune response is reviewed, followed by a discussion of the factors responsible for graft rejection. The modification of these factors to allow successful CNS transplantation is discussed.

Our previous karyotypic studies of malignant human gliomas have demonstrated that their most consistent early or primary gross changes include gains of #7, losses of #10, #22, and the gonosomes, and the presence of double minutes. Karyotypes of 15 additional malignant human gliomas reported here have confirmed these observations and, by enlarging our series, we can now show that in addition to double minutes, certain other gross structural abnormalities also are clearly associated with the early evolution of this type of tumor. The most prevalent deviations are deletions and translocations involving 9p. Other chromosomes commonly involved in rearrangements are #1, #6, and #13, and less frequently #7, #11, and #16.

Two patients with posttraumatic diencephalic seizures, characterized by autonomic dysfunction and extensor posturing, had partial responses to bromocriptine and complete responses to morphine. Probable synergism between the two agents was noted. These 2 cases suggest the potential effectiveness of this regimen for the treatment of diencephalic seizures, raise questions regarding the role of the dopaminergic and opioid systems in this disease entity, and support the hypothesis that diencephalic seizures represent a release phenomenon in the brain.

A case of peroneal nerve entrapment is reported in a patient with scleroderma. Compression was due to a lipoma in the popliteal fossa and resulted in increasingly severe foot-drop. Complete recovery occurred after the lipoma was resected. A brief review of peroneal nerve palsies and lipomatosis is presented.

The development of Mabs, particularly those reactive with primary brain tumors but not with normal brain, provides a potential means of delivering therapeutic agents selectively to human malignant gliomas. Mab 81C6, an IgG2b immunoglobulin, which defines an epitope of the glioma-associated extracellular matrix protein tenascin, has been shown to bind to human glioma cell lines, glioma xenografts in nude mice, and primary human gliomas, but not to normal adult or fetal brain. To test the therapeutic potential of this Mab for targeted delivery of isotopes, nude mice bearing progressively growing s.c. xenografts of D-54 MG, a human glioma cell line, were given injections via the tail vein of either buffer, unlabeled 81C6, 131I-labeled 81C6, or 131I-labeled 45.6, a nonspecific control Mab of the same isotype. Specific activities of the Mab range from 6.0 to 15.5 mCi/mg with protein doses from 7.6 to 167 micrograms. The doses given by injection per animal for labeled 81C6 were 50, 250, 500, and 1000 mu Ci and 500 and 1000 mu Ci for 45.6. Tumor response was measured by growth delay in reaching 1000 or 5000 mm3 tumor volumes using the Wilcoxon rank sum test, and by comparing the proportion of tumors that had regression in volume after treatment using the Fisher exact test. Statistically significant growth delays at 1000 mm3 were noted in 1 of 3 experiments with 500 mu Ci 81C6 (P less than 0.001) and 2 of 3 for 1000 mu Ci 81C6 (P = 0.001 and less than 0.001). At 5000 mm3, statistically significant growth delays were seen with radiolabeled 81C6 in 2 of 2 experiments at 250 mu Ci (P = 0.01 and 0.02), 4 of 4 at 500 mu Ci (P = 0.03-less than 0.001), and 2 of 2 at 1000 mu Ci (P = less than or equal to 0.001) and with radiolabeled 45.6 in 1 of 1 at 1000 mu Ci (P = 0.01). The percentage of animals with tumor regression progressively increased with increasing doses of isotope. For radiolabeled 45.6, there were 0 of 10 regressors at 500 and 1 of 10 at 1000 mu Ci. For radiolabeled 81C6, there were 0 of 6 regressors at 50 mu Ci, 1 of 16 (6%) at 250 mu Ci, 7 of 38 (18%) at 500, and 15 of 28 (54%) at 1000 mu Ci. Statistically significant tumor regression was seen only at doses of 500 and 1000 mu Ci of 131I-81C6.(ABSTRACT TRUNCATED AT 400 WORDS)

Multiple fusions following immunization of athymic mice with the extensively characterized human glioma cell line D-54 MG resulted in the selection of several antibodies (Mabs) highly reactive with tumors of neuroectodermal origin and unreactive with normal nervous system tissue. Two Mabs, C12 and D12, which localized specifically to tumors in athymic mouse-human glioma xenograft paired label localization assays, are IgG3 antibodies; both bind readily to staphylococcal protein A in column purification and radioimmunoprecipitation procedures. Both iodinate via the chloramine-T method yielding 125I-immunoreactive product by direct cell surface radioimmunoassay and absorption assay. By indirect cell surface radioimmunoassay, a cultured cell line panel consisting of 17 gliomas, 3 medulloblastomas, 2 neuroblastomas, 2 melanomas, and 2 fetal and 2 adult brain-derived cell lines was examined; the two Mabs were highly similar but distinct in their reactivity profiles. Each was positive with greater than 47% of the gliomas tested (C12, 9 of 17; D12, 8 of 17); and with 1 of 3 medulloblastomas, 1 of 2 melanomas, and cell lines derived from 12- and 16-week-gestation human fetal brain. No reactivity was observed with neuroblastoma or adult brain-derived cell lines or with neutral glycolipids and gangliosides extracted from D-54 MG xenografts or human glioma cell lines. Notable extraneuroectodermal reactivity included that of Mab D12 for splenic trabeculae and the spermatids and Sertoli cells in the testes. Following immunoprecipitation of [3H]leucine labeled cell membrane preparations, Mabs C12 and D12 have consistently yielded unique bands in the Mr 180,000 and Mr 88,000 regions respectively. When used in paired label localization experiments in s.c. D-54 MG xenograft-bearing athymic mice, Mabs C12 and D12 demonstrate similar localization patterns, attaining peak localization indices at day 3 (D12) or 4 (C12); the maximum percentage of injected Mab bound to tumor ranged from 5% (D12) to 8% (C12). The peak tumor/normal brain localization ratios (167-181) attained by these Mabs at days 1-2 followed by their rapid clearance suggest that these Mabs are potentially useful imaging and therapeutic agents for further investigation.

Currently numerous clinical trials are in progress utilizing intracarotid (i.c.) 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) for the treatment of malignant gliomas based upon the proposed focal nature of these tumors and the assumption that the i.c. route delivers higher levels of drug to the tumor. To date, however, increased efficacy in an animal model has not been clearly demonstrated for the i.c. delivery of BCNU. We have evaluated the dose-response curve for the i.v. and i.c. administration of BCNU in a commonly utilized experimental brain tumor model, the 9L rat gliosarcoma. An initial toxicity trial utilizing the i.p. 10% lethal dose (LD10) of BCNU by the i.v. and i.c. routes failed to demonstrate any significance in toxicity between the two routes. Tumor-bearing animals were then treated on Day 15-16 after tumor inoculations with 1, 10, 25, 50, 75, and 100% of the LD10 dose by either the i.v. or the i.c. route. Both i.v. and i.c. BCNU gave maximum survival increases at 75-100% LD10 doses, and there was no therapeutic advantage seen from i.c. delivery. However, at 50% of the LD10 dose (6.65 mg/kg), triplicate experiments demonstrated that the i.c. but not the i.v. dose maintained maximum efficacy equivalent to 100% of the LD10 given either i.v. or i.c. When the dose was reduced to 25% of the LD10 dose (3.33 mg/kg), two of three experiments showed efficacy of the i.c. delivery of this lower drug dosage to be equivalent to 100% of the LD10 given i.v. or i.c. The i.v. dosage resulted in a significant reduction in survival in all three trials. At 10% of the LD10 dose (1.30 mg/kg), neither the i.v. nor the i.c. administration retained equivalent efficacy to 100% of the LD10. However, in one of two trials, the i.c. groups had statistically better survival than controls, while in neither experiment was any advantage over controls seen in the i.v. treated groups. At 1% of the LD10 dose, neither the i.v. nor the i.c. route demonstrated any therapeutic efficacy. From our data, the advantage of the i.c. delivery of BCNU in the intracranial 9L rat gliosarcoma appears to be in the fact that significantly lower dosages than those given i.v. may be utilized to achieve equivalent survival with potentially less systemic toxicity.

Current diagnostic and therapeutic modalities for malignant human gliomas are largely nonspecific. The development of monoclonal antibodies (MA's) with their high degree of specificity may allow precise tumor imaging and selective administration of therapeutic agents. However, the ability of these antibodies to specifically localize tumor tissue in vivo remains speculative. This study compares the localization and imaging properties of two MA's: a specific human glioma-associated extracellular matrix glycoprotein MA, 81C6, and a nonspecific control MA, 45.6, against a human glioma cell line, D-54 MG, intracranially inoculated into athymic rats. Forty-one animals received MA's labeled with iodine-131 (131I) or 125I and underwent imaging with a gamma camera. The images were independently evaluated and compared to tissue radioactivity levels. Radiolabeled antiglioma MA 81C6 specifically localized in intracranial xenografts. The percent of injected dose per gram of tissue for tumor was 1.707 +/- 0.405/gm for 81C6 and 0.118 +/- 0.056/gm for 45.6. All other organs had equivalent levels of specific and nonspecific MA's. For brain, these were 0.004 +/- 0.002/gm and 0.005 +/- 0.005/gm, respectively, and for the other organs, the range was from 0.053 to 0.284/gm. Statistically, 45.6 achieved levels in tumor that were significantly higher than normal brain (p less than 0.05) but significantly less than that achieved with 81C6 (p less than 0.005). With 81C6, the degree of localization was high enough to allow imaging of intracranial tumors at sizes as small as 20 mg. Intracranial tumors were imaged with 45.6 only when they achieved sizes greater than 300 mg. In this imaging study, radiolabeled 81C6, a specific antiglioma MA, proved to be significantly better for imaging small and intermediate-sized tumors than the control MA's. Large tumors were visualized by both MA's, although higher quality scans were obtained earlier and more frequently with specific MA's than with nonspecific immunoglobulin G. These data suggest that specific MA's have a role to play in both the diagnosis and treatment of primary intracranial human tumors.

Fifteen permanent cell lines derived from human gliomas were subcutaneously transplanted into athymic nude mice (nu/nu genotype, NIH Swiss and BALB/c backgrounds). Four were tumorigenic. Three of the four (D-54 MG, U-118 MG, and U-251 MG) produced progressively growing, solid, noncystic tumors. Subcutaneous volume measurement of these tumors, which correlated directly with tumor weight, was a reliable method for monitoring growth. All three cell lines which produced progressively growing subcutaneous tumors were also tumorigenic when cells were inoculated intracerebrally. These grew as well-circumscribed, intraparenchymal brain tumors. After initial implantation, each of the progressively growing, solid, subcutaneous tumors was histologically similar to the permanent cell lines from which it was derived. Tumors could be reliably passed, and stabilization of latency periods and growth rates developed. Tumors became morphologically less distinct in later passages, though some individual features remained. Mice bearing subcutaneous tumors from each of these cell lines were treated with a single ip dose of 25 mg/kg BCNU and compared to controls receiving only drug vehicle. A significant, but different, amount of reduction in tumor mass occurred among each of the three tumor lines. This model allows cell lines derived from human gliomas to be grown in animal hosts, thereby providing a potential means for evaluating growth parameters and chemotherapeutic responsiveness of tumors derived from individual human gliomas or cell lines.