Nonanastomotic Indirect Bypass Surgery In The Surgical Treatment Of Malignant Glial Tumors

Year 2010, Volume: 27 Issue: 1, 31 - 34, 25.01.2012

Ersoy Kocabıçak Cengiz Çokluk Kerameddin Aydın

Abstract

The primary treatment of malignant glial tumors is surgical intervention for maximally reducing and/or total removing of tumors. The purpose of this report was to describe pial sinangiosis or indirect nonanastomotic bypass surgery for diversion of blood brain barrier for enhancing of systemic blood-brain tissue penetration in the enhancing of the effect of chemotherapy. The other purposes are the increasing of oxygen and metabolic product providing, enhancing of radiation sensitivity, and stabilization of brain tissue around the tumor bed for reducing of malignant transformation. We used the technique of indirect non anastamotic by-pass surgery technique during the surgical treatment of malignant glial tumors. Preoperative and postoperative magnetic resonance images were obtained to evaluate peri-lesional edema and residual complications. This technique was used in three cases of malignant glial tumors. There were no operative mortality and morbidity related to this technique. This technique may be used during the surgical treatment of malignant glial tumors to enhance penetration of chemotherapeutic agents, increasing of radiation sensitivity and providing of tissue stability.

Key Words: Pial synangiosis, indirect bypass surgery, malignant glial tumors, surgical treatment.

Keywords

Pial Synangiosis, Indirect Bypass Surgery, Malignant Glial Tumors, Surgical Treatment, Cerebral Reperfasyon, Chemotheraph

References

• Baldwin, A.S., 2001.Control of oncogenesis and cancer therapy resistance by the transcription factor NF-κB. J. Clin. Invest. 107, 241–246.
• Barnholtz-Sloan, J.S., Sloan, A.E., Davis, F.G., Vigneau, F.D., Lai, P., Sawaya, R.E., 2004. Incidence proportions of brain metastases in patients diagnosed (1973 to 2001) in the Metropolitan Detroit Cancer Surveillance System. J. Clin. Oncol. 22, 2865-2872.
• Bellavance, M.A., Blanchette, M., Fortin, D., 2008. Recent advances in blood-brain barrier disruption as a CNS delivery strategy. AAPS J. 10, 166-177.
• Caro, J., 2001. Hypoxia regulation of gene transcription. High Alt. Med. Biol. 2,145–154.
• Deeken, J.F., Löscher, W. 2007. The blood-brain barrier and cancer: transporters, treatment, and Trojan horses. Clin. Cancer Res. 13, 1663-1674.
• Graeber, T.G., Osmanian, C., Jacks, T., 1996. Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours. Nature. 379, 88–91.
• Hockel, M., Schlenger, K., Aral, B., 1996. Association between tumor hypoxia and malignant progression in advanced cancer of the uterine cervix. Cancer Res. 56, 4509–4515.
• Hockel, M., Vaupel, P., 2001. Biological consequences of tumor hypoxia. Semin Oncol. 28, 36–41
• Lassman, A.B., DeAngelis, L.M. 2003.Brain metastases. Neurol. Clin. 21, 1-23.
• Motl, S., Zhuang, Y., Waters, C.M., Stewart, C.F. 2006. Pharmacokinetic considerations in the treatment of CNS tumours. Clin. Pharmacokinet. 45, 871-903.
• Rofstad, E.K., 2000. Microenvironment-induced cancer metastasis. Int. J. Radiat Biol. 76, 589–605.