Analysis of Angiographic Findings and Clinical Impact of Anterior Clinoidectomy in Internal Carotid-Posterior Communicating Artery Aneurysm Surgery - Clinical Research - / 대한뇌혈관외과학회지

OBJECTIVE: In the case of internal carotid-posterior communicating (ICPCom) artery aneurysm it is possible to successfully clip the aneurysmal neck without any difficulty. However, if the aneurysmal neck is wide, the aneurysmal sac is giant, the aneurysmal sac is hidden by the anterior clinoid process (ACP), or its dome is located in ventral portion or low-lying ICPCom aneurysm, it is difficult to open the proximal aneurysmal neck and we encounter a barrier in controlling bleeding in case of premature rupture of the aneurysm. They need to be resected the ACP for successful aneurysmal clipping. We propose angiographic criteria for predicting necessity of resection of the ACP before clipping of the ICPCom artery aneurysm. METHODS: Between 1999 and 2003, 16 patients with ICPCom artery aneurysm were treated with the resection of the ACP prior to applying the clip on the neck of the aneurysm. We retrospectively analyzed the preoperative cerebral angiographies, and the clinical and operative findings. We measured various radiometric parameters to reveal the angiographic characteristics. RESULTS: The mean value of the radiographic measurement in case of the cerebral angiography in 16 patients is as follows: angle A (the angle between the midline of the skull and the axis of the C1 segment on A-P view) ranged from 15 to 80 degrees (mean+/-SD, 42+/-5 degrees), angle B (the angle between the axes of the C1 and C2 segments on A-P view) ranged from 70 to 150 degrees (mean+/-SD, 110+/-15 degrees), and distance C (the distance between the tip of the ACP and the most proximal portion of the aneurysmal neck on the lateral view) ranged from 2 to 9 mm (mean+/-SD, 4.5+/-1 mm). CONCLUSION: We have resected the ACP in 16 of the 40 ICPCom aneurysms. The mean values of angle A, angle B, and distance C is 42+/-5 degrees, 110+/-15 degrees, and 4.5+/-1 mm, respectively. We did not encounter any difficulty in clipping in all the cases in which there was no premature rupture of the aneurysm. Most of cases had a good outcome.

Potentials and limitations of adenovirus-p53 gene therapy for brain tumors

We investigated the antineoplastic potentials of recombinant adenovirus containing wild-type p53 cDNA (Ad5CMV-p53) for malignant gliomas. In four human glioma cell lines (U-251 and LG expressing endogenous mutant p53, and U-87 and EFC-2 expressing wild-type p53) and two rat glioma cell lines (9L and C6, each expressing mutant and wild-type p53), gene transfer efficiency determined by X-gal staining and Western blotting was varied (10-99% at 10-500 multiplicity of infection, MOI). Growth inhibitory effect was drastic (>90% at 100 MOI) in U-251 cells and only moderate or minimal in other cell lines harboring wild-type p53 or low gene transfer efficiency. Ex vivo transduction of U-251 cells with Ad5CMV-p53 suppressed the in vivo tumorigenicity of the cells. Histopathologic examination for Ad5CMV-p53 toxicity to rat brains showed inflammatory reactions in half of the tested brains at 10(8) MOI. U-251 cells were inoculated intracerebrally in nude mice and injected Ad5CMV-p53 into the tumor, in which neither the tumor suppression nor the survival benefit was observed. In conclusion, heterogeneity of the cellular subpopulations of malignant glioma in p53 status, variable and insufficient gene delivery to tumor, and adenoviral toxicity to brain at higher doses may be limiting factors to be solved in developing adenovirus-p53 gene therapy for malignant gliomas.

Potentials and limitations of adenovirus-p53 gene therapy for brain tumors

We investigated the antineoplastic potentials of recombinant adenovirus containing wild-type p53 cDNA (Ad5CMV-p53) for malignant gliomas. In four human glioma cell lines (U-251 and LG expressing endogenous mutant p53, and U-87 and EFC-2 expressing wild-type p53) and two rat glioma cell lines (9L and C6, each expressing mutant and wild-type p53), gene transfer efficiency determined by X-gal staining and Western blotting was varied (10-99% at 10-500 multiplicity of infection, MOI). Growth inhibitory effect was drastic (>90% at 100 MOI) in U-251 cells and only moderate or minimal in other cell lines harboring wild-type p53 or low gene transfer efficiency. Ex vivo transduction of U-251 cells with Ad5CMV-p53 suppressed the in vivo tumorigenicity of the cells. Histopathologic examination for Ad5CMV-p53 toxicity to rat brains showed inflammatory reactions in half of the tested brains at 10(8) MOI. U-251 cells were inoculated intracerebrally in nude mice and injected Ad5CMV-p53 into the tumor, in which neither the tumor suppression nor the survival benefit was observed. In conclusion, heterogeneity of the cellular subpopulations of malignant glioma in p53 status, variable and insufficient gene delivery to tumor, and adenoviral toxicity to brain at higher doses may be limiting factors to be solved in developing adenovirus-p53 gene therapy for malignant gliomas.