Delivery systems and molecular targets of mechanism-based therapies for GBM

References

• CBTRUS. Statistical Report: Primary Brain Tumors in the United States, 1995–1999. Central Brain Tumor Registry of the United States. Chicago, IL, USA (2002).
   Google Scholar
• •Good report on the incidence of primary benign and malignant brain tumor.
   Google Scholar
• Levin VA, Uhm JH, Jaeclde KA et al. Phase III randomized study of postradiotherapy chemotherapy with a-difluoromethylornithine-procarbazine, N-(2-chloroethyl)-N'-cyclohexyl-N-(2-chloroethyl)-N'-cyclohexyl-N-nitrosurea, vincristine (DFMO-PCV) versus PCV for glioblastoma multiforme. Gun. Cancer Res. 6,3878-3884 (2000).
   Google Scholar
• Levin VA, Leibel SA, Gutin PH. Neoplasms of the central nervous system. In: Cancer' Principles and Practice of Oncology Sixth Edition. DeVita VTJ, Hellman S, Rosenberg SA (Eds). Lippincott-Raven, PA, USA, 2100–2160 (2001).
   Google Scholar
• DeAngelis LM, Burger PC, Green SB et al. Malignant glioma: who benefits from adjuvant chemotherapy? Ann. Neural 44, 691–695 (1998).
   Google Scholar
• Bailey P, Cushing HA. Classification of Tumors of the Glioma Group. Lippincott, PA, USA (1926).
   Google Scholar
• Burger P, Scheitauer BW. TUMOIN of the Central Nervous System. Forces Institute of Pathology, Washington DC, USA (1994).
   Google Scholar
• Kleihues P, Cavenee W World Health Organization Classification of Tumors: Pathology and Genetics of Tumors of the Nervous System. International Agency for Research on Cancer. IARC Press, Lyon, France (2000).
   Google Scholar
• Cavenee WK, Furnari FB, Nagane M et al Infiltrating astrocytomas. In: Pathology and Genetics of Tumours of the Nervous System. Second Edition. Kleihues P, Cavenee WK (Eds). International Agency for Research on Cancer. International Agency for Research, Lyon, France, 10–21 (2000).
   Google Scholar
• Reifenberger G, Kros JM, Burger PC et al Oligodendroglioma. In: Pathology and Genetics of MIMI'S of the Nervous System. Second Edition. Kleihues P, Cavenee WK, (Eds). International Agency for Research on Cancer. IARC Press, Lyon, France, 56–61 (2000).
   Google Scholar
• Reifenberger G, Kros JM, Burger PC et al. Anaplastic oligodendroglioma. In: Pathology and Genetics of TUMOIN of the Nervous System. Second Edition Kleihues P, Cavenee WK, (Eds). International Agency for Research on Cancer. IARC Press, Lyon, France, 62–64 (2000).
   Google Scholar
• Reifenberger G, Kros JM, Burger PC et al. Anaplastic oligodendroglioma. In: Pathology and Genetics of TUMOIN of the Nervous System. Second Edition Kleihues P, Cavenee WK, (Eds). International Agency for Research on Cancer. IARC Press, Lyon, France, 65–67 (2000).
   Google Scholar
• Reifenberger G, Kros JM, Burger PC et al Anaplastic oligodendroglioma. In: Pathology and Genetics of TUMOIN of the Nervous System. Second Edition Kleihues P, Cavenee WK, (Eds). International Agency for Research on Cancer. IARC Press, Lyon, France, 68–69 (2000).
   Google Scholar
• Coons SW Johnson PC, Scheithauer BW et al Improving diagnostic accuracy and interobserver concordance in the classification and grading of primary gliomas. Cancer 79,1381–1393 (1997).
   Google Scholar
• •Demonstrates the high degree of inter-observer variability in diagnostic neuropathology indicating a need for improved molecular methods for classification.
   Google Scholar
• Fuki G, Ishii N, Van Meir EG et al p53 and brain tumors: from gene mutations to gene therapy, Brain Pathol 8,599–613 (1998).
   Google Scholar
• Hunter SB, Brat DJ, Olson JJ et al. Alterations in molecular pathways of diffusely infiltrating astrocytomas: application to tumor classification and antitumor therapy. Int. j Oncol 23, 857–869 (2003).
   PubMed Web of Science ®Google Scholar
• Reifenberger G, Liu L, Ichimura K et al Amplification and over expression of the MDM2 gene in a subset of human malignant gliomas without p53 mutations, Cancer Res. 53,2736–2739 (1993).
   Google Scholar
• Fuki G, Labuhn M, Maier D et al. EG. p53 gene mutation and ink4a-arf deletion appear to be two mutually exclusive events in human glioblastoma. Oncogene 19, 3816–3822 (2000).
   Google Scholar
• Nakamura M, Watanabe T, Klangby U et al. p14ARF deletion and methylation in genetic pathways to glioblastomas. Brain Pathol 11, 159–168 (2001).
   PubMed Web of Science ®Google Scholar
• Schmidt MC, Antweiler S, Urban N et al. Impact of genotype and morphology on the prognosis of glioblastoma. I Neuropathol Exp. Neural. 61,321–328 (2002).
   PubMed Web of Science ®Google Scholar
• Smith JS, Tachibana I, Passe SM et al PTEN mutation, EGFR amplification and outcome in patients with anaplastic astrocytoma and glioblastoma multiforme. J.NatlCancerinst. 93,1246–1256 (2001).
   Google Scholar
• •Excellent multivariate analysis of genetic alterations in malignant astrocytomas as they relate to patient outcome.
   Google Scholar
• Leenstra S, Oskam NT, Bijleveld EH et al Genetic subtypes of human malignant astrocytoma correlate with survival. Int. J. Cancer79, 159–165 (1998).
   PubMed Web of Science ®Google Scholar
• Simmons ML, Lamborn KR, Takahashi M et al Analysis of complex relationships between age, p53, epidermal growth factor receptor and survival in glioblastoma patients. Cancer Res. 61,1122–1128 (2001).
   PubMed Web of Science ®Google Scholar
• Newcomb EW, Cohen H, Lee SR et al Survival of patients with glioblastoma multiforme is not influenced by altered expression of p16, p53, EGFR, MDM2 or Bc1-2 genes. Brain Pathol 8,655–667 (1998).
   PubMed Web of Science ®Google Scholar
• Shiraishi S, Tada K, Nakamura H et al. Influence of p53 mutations on prognosis of patients with glioblastoma. Cancer 95, 249–257 (2002).
   PubMed Web of Science ®Google Scholar
• Rasheed A, Herndon JE, Stenzel TT et al Molecular markers of prognosis in astrocytic tumors. Cancer 94,2688–2697 (2002).
   PubMed Web of Science ®Google Scholar
• Schmidt EE, Ichimura K, Reifenberger G et al CDKN2 (p16/MTS1) gene deletion or CDK4 amplification occurs in the majority of glioblastomas. Cancer Res. 54, 6321–6324 (1994).
   PubMed Web of Science ®Google Scholar
• Nishikawa R, Fumari FB, Lin H et al Loss of P16INK4 expression is frequent in high-grade gliomas. Cancer Res. 55,1941–1945 (1995).
   PubMed Web of Science ®Google Scholar
• Costello JF, Plass C, Arap W et al Cyclin- dependent kinase 6 (CDK6) amplification in human gliomas identified using two- dimensional separation of genomic DNA. Cancer Res. 57,1250–1254 (1997).
   PubMed Web of Science ®Google Scholar
• Biernat W, Tohma Y, Yonekawa Y et al Alterations of cell cycle regulatory genes in primary (de nova) and secondary glioblastomas. Acta Neuropathol Oer1). 94, 303–309 (1997).
   Google Scholar
• Maruno M, Yoshimine T, Muhammad AK et al Loss of heterozygosity of microsatellite loci on chromosome 9p in astrocytic tumors and its prognostic implications. Neuro-oncol 30,19–24 (1996).
   Google Scholar
• Perry A, Anderl K, Borell TJ et al Detection of p16, RB, CDK4 and p53 gene deletion and amplification by fluorescence in situ hybridization in 96 gliomas. Am. Clin. Pathol 112,801–809 (1999).
   Google Scholar
• Burton EC, Lamborn KR, Feuerstein BG et al Genetic aberrations defined by comparative genomic hybridization distinguish long-term from typical survivors of glioblastoma. Cancer Res. 62, 6205–6210 (2002).
   PubMed Web of Science ®Google Scholar
• Kraus JA, Glesmann N, Beck M et al Molecular analysis of the PTEN, TP53 and CDKN2A tumor suppressor genes in long-term survivors of glioblastoma multiforme. Neum-oncol 48,89–94 (2000).
   PubMedGoogle Scholar
• Brat DJ, Seiferheld W, Perry A et al Analysis of lp, 19q, 9p and 10q as prognostic markers for high-grade astrocytomas using fluorescence in situ hybridization on tissue microarrays from RTOG trials. Neuro-oncology6, 96–103 (2004).
   PubMedGoogle Scholar
• Ekstrand AJ, James CD, Cavenee WK et al Genes for epidermal growth factor receptor, transforming growth factor alpha and epidermal growth factor and their expression in human gliomas in vivo. Cancer Res. 51,2164–7212 (1991).
   PubMed Web of Science ®Google Scholar
• Shinojima N, Tada K, Shiraishi S et al Prognostic value of epidermal growth factor receptor in patients with glioblastoma multiforme. Cancer Res. 63,6962–6970 (2003).
   PubMed Web of Science ®Google Scholar
• Huncharek M, Kupelnick B. Epidermal growth factor receptor gene amplification as a prognostic marker in glioblastoma multiforme: results of a meta-analysis. Oncol Res. 12,107–112 (2000).
   PubMedGoogle Scholar
• Fujisawa H, Kurrer M, Reis RM et al Acquisition of the glioblastoma phenotype during astrocytoma progression is associated with loss of heterozygosity on 10q25-qter. Am. I Pathol 155,387–394 (1999).
   Google Scholar
• Zhou XP, Li YJ, Hoang-Xuan K et al Mutational analysis of the PTEN gene in gliomas: molecular and pathological correlations. hit.j Cancer 84,150–154 (1999).
   PubMed Web of Science ®Google Scholar
• Li J, Yen C, Liaw D et al PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast and prostate cancer. Science 275,1943–1947 (1997).
   PubMed Web of Science ®Google Scholar
• Kunwar S, Mohapatra G, Bollen A et al Genetic subgroups of anaplastic astrocytomas correlate with patient age and survival. Cancer Res. 61,7683–7688 (2001).
   PubMedGoogle Scholar
• Tada K, Shiraishi S, Kamiryo T et al Analysis of loss of heterozygosity on chromosome 10 in patients with malignant astrocytic tumors: correlation with patient age and survival. Neurosurg. 95,651–659 (2001).
   Google Scholar
• Balesaria S, Brock C, Bower M et al Loss of chromosome 10 is an independent prognostic factor in high-grade gliomas. BE Cancer81, 1371–1377 (1999).
   Google Scholar
• Ganju V, Jenkins RB, OFallon JR et al Prognostic factors in gliomas. A multivariate analysis of clinical, pathologic, flow cytometric, cytogenetic and molecular markers. Cancer 74,920–927 (1994).
   Google Scholar
• Caimcross JG, Ueki K, Zlatescu MC et al Specific genetic predictors of chemotherapeutic response and survival in patients with anaplastic oligodendrogliomas. I Natl Cancer Inst. 90, 1473–1479 (1998).
   PubMedGoogle Scholar
• •Demonstrates that lp/19q codeletion in oligodendroglioma is predictive of a therapeutic response. A conceptual break through in neuro-oncology.
   Google Scholar
• Glass J, Hochberg H, Gruber ML et al The treatment of oligodendrogliomas and mixed oligodendroglioma- astrocytomas with PCV chemotherapy. I Neumsurg. 76, 741–745 (1992).
   PubMed Web of Science ®Google Scholar
• Jenkins RB, Curran W, Scott CB et al Pilot evaluation of lp and 19q deletions in anaplastic oligodendrogliomas collected by a national cooperative cancer treatment group. ArnI Clin. 017C01. 24,506-508 (2001).
   Google Scholar
• Hussein MR, Baidas S et al Advances in diagnosis and management of oligodendroglioma. Expert Rev AntiCancer Ther. 2,520–528 (2002).
   PubMedGoogle Scholar
• Smith JS, Perry A, Borell TJ, Lee HK et al Alterations of chromosome arms lp and 19q as predictors of survival in oligodendrogliomas, astrocytomas and mixed oligoastrocytomas. I Clin. Oncol 18,636–645 (2000).
   Google Scholar
• •Addresses the important issue of whether lip 19 loss in astrocytic neoplasms was predictive of therapeutic response. No survival differences were noted.
   Google Scholar
• Perry A, Fuller CE, Banerjee R et al Ancillary FISH analysis for lp and 19q status: preliminary observations in 287 gliomas and oligodendroglioma mimics. Front Biosci. 8,1–9 (2003).
   Google Scholar
• Ino Y, Zlatescu MC, Sasaki H et al. Long survival and therapeutic responses in patients with histologically disparate high-grade gliomas demonstrating chromosome lp loss. .1. Neurosurg. 92,983-990 (2002).
   Google Scholar
• Pomeroy SL, Tamayo P, Gaasenbeek M et al Prediction of central nervous system embryonal tumour outcome based on gene expression. Nature 415,436–442 (2002).
   PubMed Web of Science ®Google Scholar
• •First article to show that gene expression profiles and computational algorithms can be used to successfully classify medulloblastomas and predict outcomes.
   Google Scholar
• Nutt CL, Mani DR, Betensky RA et al Gene expression-based classification of malignant gliomas correlates better with survival than histological classification. Cancer Res. 63,1602–1607 (2003).
   PubMed Web of Science ®Google Scholar
• •First article to show that gene expression profilesand computational algorithms can be used to successfully classify glial neoplasms and predict outcome.
   Google Scholar
• Tremont-Lukas I, Gilbert M. Advances in molecular therapies in patients with brain tumors. Cancer Contro110, 125–137 (2003).
   Google Scholar
• •Reviews early results of clinical trials of targeted therapy agents.
   Google Scholar
• Grossman SA, Fisher JD, Pdiantadosi S et al The New Approaches to Brain Tumor Therapy (NAB1-1) CNS Consortium:organization, objectives and activities. Cancer ControI5, 107–114 (1998).
   PubMedGoogle Scholar
• •Reviews the organization structure of National Cancer Institute sponsored NABTT CNS Consortium in the USA.
   Google Scholar
• Ciardiello F, Tortora G. Antiepidermal growth factor receptor drugs in cancer therapy. Expert Opin. Investig. Drugsll, 755–768 (2002).
   Google Scholar
• Eller JL, Longo SL, Hicklin DJ et al Activity of antiepidermal growth factor receptor monoclonal antibody C225 against glioblastoma multiforme, Neurosurgety51,1005–1014 (2002).
   Google Scholar
• Moasser MM, Basso A, Averbuch SD et al The tyrosine kinase inhibitor ZD1839 ('Iressa) inhibits HER2-driven signaling and suppresses the growth of HER2-overexpressing tumor cells. Cancer Res. 61, 7184–7188 (2001).
   PubMed Web of Science ®Google Scholar
• Arteaga, CL, Johnson DH. Tyrosine kinase inhibitors-ZD1839 (Iressa), Cun: Opin. Oncol 13,491–498 (2001).
   Google Scholar
• Hirata A, Ogawa S, Kometani T et al ZD1839 (Iressa) induces antiangiogenic effects through inhibition of epidermal growth factor receptor tyrosine kinase, Cancer Res. 62,2554–2560 (2002).
   Google Scholar
• Lieberman FS, Cloughesy T, Malkin M et al Phase I—II study of ZD-1839 for recurrent malignant gliomas and meningiomas progressing after radiation therapy. Proc. Am. Soc. Clin. Oncol 22,105 (2003).
   Google Scholar
• Rich JN, Reardon DA, Peery T et al Phase II trial of gefitinib in recurrent glioblastoma.j Clin. Oncol 22 (1), 133–142 (2004).
   Google Scholar
• Prados M, Chang S, Burton E etal. Phase I study of OSI-774 alone or with temozolomide in patient with malignant glioma. Pnx. Am Soc. Clin Oncol 22,99 (2003).
   Google Scholar
• Hayahi Y, Ueki K, Waha A, Wiestler OD, Louis DN, von Deimling A. Association of EGFR gene amplification and CDKN2 (p12/MTS1) gene deletion in glioblastoma multiforme. Brain Pathol 7, 871–875 (1997).
   Google Scholar
• Murthy YK, Thiemann JE, Coronelli C et al Alanosine, a new antiviral and antitumour agent isolated from a Streptomyces. Nature 211,1098–1199 (1966).
   Google Scholar
• Gale GR, Schmidt GB. Mode of action of alanosine. Biochem. Pharmacol 17, 363–368 (1968).
   PubMedGoogle Scholar
• Graff JC, Plagermann PG. Alanosine toxicity in Novikoff rat hepatoma cells due to inhibition of the conversion of inosine monophosphate to adenosine mmonophosphae. Cancer Res. 36, 1428–1440 (1968).
   Google Scholar
• University of California, San Diego (USCD) IND 52, 312 Annual Report to FDA, October, (2000).
   Google Scholar
• Harland SP, Kuc RE, Pickard JD et al Expression of endothelin (A) receptors in human gliomas and ameningiomas, with high affinity for the selective antagonist PD 156707. Aiwasurgery43 (4), 890–899 (1998).
   Google Scholar
• Pagotto U, Arzberger T, Hopfine U et al Cellular localization of endothelin receptor mRNAa (ETA and ETB) in brain tumors and normal human brain. J. Canliovasc. Pharmacol 26\(Suppl. 3), 104–106 (1995).
   Google Scholar
• Tsutsumi K, Niwa M, Kitagawa N et al Enhanced expression of an endothelin ETA receptor in capillaries from human glioblastoma: a quantative receptor autoradiographic analysis using a radioluminographic imaging plate system. Neurochem. 63(6), 2240–2247 (1994).
   Google Scholar
• Stiles JD, Ostrow PT, Balos LL et al Correlation of endolthelin-1 and transforming growth factor-betal with malignancy and vascularity in human gliomas. I Neuropath. Exp. Nemo'. Exp. Neural 56 (4) 435–439 (1997).
   Google Scholar
• Carducci MA, Nelson JB, Bowling MK et al Atrasentran, an endothelin-receptor antagonist for refractory adenocarcinomas; safety and pharmacokinetics. j Clin. Oncol 20,2171–2180 (2002).
   PubMed Web of Science ®Google Scholar
• Phuphanich S, Grossman SA, Lesser G et a/. A phase I evaluation of the safety and pharmacokinetic (PK) of atransentan in adults with recurent malignant glioma; preliminary report. Proceedings of the 9th Annual Meeting of the Society for Neuro-Oncology 18–21 (2004).
   Google Scholar
• Rowinsky E, Windle J, Hoff Von DD et al Ras protein famesyltranferase: a strategic target for anticancer therapeutic development.j Clin. Oncol, 17, 3631–3652 (1999).
   PubMed Web of Science ®Google Scholar
• Sklar M. The ras oncognes increase the intrinsic resistance of NIH 3R3 cells to ionizing radiation. Science 239,645–647 (1988).
   PubMed Web of Science ®Google Scholar
• Pirollo KF, Tong YA, Villegas Z et al Oncogene-transformed NIH 3T3 cells display radiation resistance levels indicative of a signal transduction pathway leading to the radiation-resistant phenotype. Radial Res. 135(2), 234–243 (1993).
   Google Scholar
• McKenna WG, Weiss MC, Endlich B et al Synergistic effect of of the v-myc oncogene with H-ras on radioresistance. Cancer Res. 50(1) 97–102 (1990).
   Google Scholar
• McKenna WG, Maids G, Weiss MC et al Increased G2 delay in radiation-resistant cells obtained by transformation of primary rat embryo cells with the oncogenes H-ras and vmyc. Radial Res. 125(3), 283–287 (1991).
   Google Scholar
• Miller AC, Kariko K, Myers CE et al Increased radioresistance of EJras-transformed human osteosarcoma cells and its modulation by lovastatin, an inhibitor of p21 ras isoprenylatiob. Int. J. Cancer 53(2), 302–307 (1993).
   Google Scholar
• Jackson J, Cochrane CG, Bourne JR et al Farnesol modification of Kirsten-ras exon 4B protein is essential for transformation. Proc. Natl Acad. Sci USA 87,3042–3046 (1990).
   Google Scholar
• Zhang F, Casey P. Protein prenylation: molecular mechanisms and functional consequences. Ann. Rev. Biochem. 65, 241–261 (1996).
   PubMed Web of Science ®Google Scholar
• Willumsen BM, Christensen A, Hubbert NL et al The p21 ras C-terminus is required for transformation and membrane association. Nature 310 (5978), 583–586 (1984).
   Google Scholar
• Kato K, Cox AD, Hisaka MM et al Isoprenoid addition to ras protein is the critical modification for its membrane association and transforming activity. Proc. Natl. Acad. Sc]. USA 89,6403–6407 (1992).
   PubMed Web of Science ®Google Scholar
• Kohn N, Omer CA, Conner MW et al Inhibition of farnesyltransferase induces regression of mammary and salivary carcinomas in ras transgenic mice. Nature Med. 1,792–797 (1995).
   PubMedGoogle Scholar
• James GL, Brown MS, Cobb MH, Goldstein JL. Benzodiazepine peptidomimetic BZA-5B interrupts the MAPK activation pathway in H-Ras-transformed Rat-1 cells but not in untransformed cells. J. Biol. Chem. 269(4), 9141–9251 (1994).
   Google Scholar
• Kohl N, Wilson FR, Mosser SD. Protein farneyl transferase inhibitors block the growth of ras-dependent tumors in nude mice. Proc. Natl Acad. Sc]. USA 91, 9141–9251 (1994).
   Google Scholar
• Nagusu T, Yoshimatsu K, Roswell C et al Inhibition of human tumor xenograft growth by treatment with the famesyl transferase inhibitor B956. Cancer Res. 55, 5310–5314 (1994).
   Google Scholar
• Sun J, Qian AD, Hamilton AD, Sebti SM. Ras CAAX peptiodomimetic FTI 276 selectively blocks tumor growth in nude mice of a human lung carcinoma with k-ras mutation and p53 deletion. Cancer Res. 55, 4243–4247 (1995).
   PubMed Web of Science ®Google Scholar
• Sun J, Qian Y, Hamilton AD et al Both farnesyltransfeease and geranlygeranyltransferase I inhibitors are required for inhibition of oncogenic K-ras prenylation but each alone is sufficient to suppress human tumor growth in nude mouse xenografts. Oncogene 16(11), 1467–1473 (1998).
   PubMed Web of Science ®Google Scholar
• Sun J, Blaskovich MA, Knowles D et al Antitumor efficacy of a novel class of nonthiol-containing peptidomimetic inhibitors of farnesyltransferase and geranlygeranyltranserase I: combination of therapy with the cytotoxic agents cisplatin, taxol and gemcitabine. Cancer Res. 59(19), 4919–4926 (1999).
   Google Scholar
• Barrington RE, Subler MA, Rands E et al A famesyltransferase inhibitor induces tumor regression in transgenic mice harboring multiple oncogenic mutations by mediating alterations in both cell cycle control and apoptosis. Mal Cell Biol. 18(1), 85–92 (1998).
   Google Scholar
• Sepp-Lorenzino L, Ma Z, Rands NE et al. A peptidomimetic inhibitorof farnesyl: protein transferase blocks the anchorage-dependent and -independent growth of human tumor cell lines. Cancer Res. 55, 5302–5309 (1995).
   PubMed Web of Science ®Google Scholar
• Cloughesy TF, Kuhn J, Wen P et al Phase II trial of R115777 (Zamestra) in patients with recurrent glioma not taking enzyme inducing antiepileptic drugs (EIAED): a North American Brain Tumor Consortium (NABTC) report. Proc. Am. Soc. Clin. 017COI 21,317 (2002).
   Google Scholar
• Kock H, Harris MP, Anderson SC et al Adenovirus-mediated p53 gene transfer suppresses growth of human glioblastoma cells in vitro and in viva Int. J. Cancer 67, 808–815 (1996).
   Google Scholar
• Cirielli C, Inyaku K, Capogrossi MC et al. Adenovirus-mediated wild type p53 expression induces apoptosis and suppresses tumorigenesis of experimental intracranial human malignant glioma. I Neurooncol 43,99–108 (1999).
   PubMed Web of Science ®Google Scholar
• Cheney IW, Johnson DE, Vaillancourt MT et al Suppression of tumorigenicity of glioblastoma cells by adenovirus-mediated MMAC1/PTEN gene transfer. Cancer Res. 58,2331–2334 (1998).
   PubMed Web of Science ®Google Scholar
• Bykov VJ, Issaeva N, Shilov A et al Restoration of the tumor suppressor function to mutant p53 by a low-molecular-weight compound. Nature Med. 8,282–288 (2002).
   PubMed Web of Science ®Google Scholar
• Vassilev LT, Vu BT, Graves B et al In vivo activation of the p53 pathway by small-molecule antagonists of MDM2. Science 303,844–848 (2004).
   PubMed Web of Science ®Google Scholar
• Sarkaria JN, Tibbetts RS, Busby EC et al Inhibition of phosphoinositide 3-kinase related kinases by the radiosensitizing agent wortmannin. Cancer Res. 58,4375–4382 (1998).
   PubMed Web of Science ®Google Scholar
• Shingu T, Yamada K, Ham N et al Growth inhibition of human malignant glioma cells induced by the P13-K-specific inhibitor. J. Neurosurg. 98,154-161 (2003).
   Google Scholar
• Zakhary R, Keles GE, Berger MS et al Intraoperative imaging techniques in the treatment of brain tumors. C1.117: Opin. aryl 11,152–156 (1999).
   Google Scholar
• Uhm JH, Dooley NP, Villemure JG et al Mechanisms of glioma invasion: role of matrix-metalloproteinases. Can. J. Neural. Sci 24,3–15 (1997).
   PubMed Web of Science ®Google Scholar
• Fowler JE Total dose in fractionated radiotherapy: implications of new radiobiologic data. Int. J. Radiat. Biol. 46, 103–122 (1984).
   Google Scholar
• Walker MD, Breen SB, Byar DP etal. Randomized comparisons of radiotherapy and nitrosoureas for the treatment of malignant glioma after surgery N Engl. Med. 303,1323–1329 (1980)
   Google Scholar
• Fine HA, Dear CB, Loeffler JS et al Meta-analysis of radiation therapy with and without adjuvant chemotherapy for malignant gliomas in adults. Cancer 71, 2585–2597 (1993).
   PubMed Web of Science ®Google Scholar
• Brown JM. Exploiting the hypoxic cancer cell: mechanisms and therapeutic strategies. Mal Med. Today6, 157–162 (2000).
   PubMedGoogle Scholar
• Berger MS, Leibel SA, Bruner JM et al Primary central nervous system tumors of the supratentorial compartment. In: Cancer in the Nervous System. Levin VA (Ed.). Churchill Livingstone, NY, USA 57–126, (1996).
   Google Scholar
• Pardridge WM. CNS drug design based on principles of blood—brain barrier transport. Neurochem. 70,1781–1792 (1998).
   PubMed Web of Science ®Google Scholar
• Engelhard HH. Antisense oligodeoxynucleotide technology: potential use for the treatment of malignant brain tumors. Cancer ControI5, 163–170 (1998).
   PubMedGoogle Scholar
• Groothuis DR. The blood—brain and blood—tumor barriers: a review of strategies for increasing drug delivery. Neum-Oncology2,45–59 (2000).
   PubMed Web of Science ®Google Scholar
• Blasberg R, Molnar P, Groothius D et al Concurrent measurements of blood flow and transcapillary transport in avian sarcoma virus-induced experimental brain tumors: implications for chemotherapy. Pharmacol Exp. Ther 231,724–735 (1984).
   PubMedGoogle Scholar
• Strasser JF, Fung LK, Eller S et al Distribution of 1,3-bis (2-chloroethy0-1-nitrosourea and tracers in the rabbit brain after interstitial delivery by biodegradable polymer implants. I Pharmacol Exp. Ther 275,1647–1655 (1995).
   Google Scholar
• Bouvier G, Penn RD, Kroin JS et al Direct delivery of medication into a brain tumor through multiple chronically implanted catheters. Neurosurgery20, 286–291 (1987).
   PubMedGoogle Scholar
• Walter IKA, Tamargo RJ, Olivi A et al Intratumoral chemotherapy. Neurosurgery 37,1129–1145 (1995).
   Web of Science ®Google Scholar
• Bobo R, Laske D, Akbasak A et al Convection-enhanced delivery of macromolecules in the brain. Proc. Natl Acad. Sci. USA 91,2076–2080 (1994).
   PubMed Web of Science ®Google Scholar
• Morrison PF, Chen MY, Chadwick RS et al Focal delivery during direct infusion to brain: role of flow rate, catheter diameter and tissue mechanics. Am. J. Physiol 277(4 Pt 2), R1218—R1229 (1999).
   Google Scholar
• Chen MY, Lonser RR, Morrison PF et al Variables affecting convection-enhanced delivery to the striatum: a systematic examination of rate of infusion, cannula size, infusate concentration and tissue-cannula sealing time. j Neumsurg 90(2), 315–320 (1999).
   PubMedGoogle Scholar
• Lieberman D, Laske K, Morrison P et al. Convection-enhanced distribution of large molecules in gray matter during interstitial drug infusion. Neurosurg. 82,1021–1029 (1995).
   Web of Science ®Google Scholar
• Laske DW, Morrison PF, Lieberman DM et al Chronic interstitial infusion of protein to primate brain: determination of drug distribution and clearance with single-photon emission computerized tomography imaging. Neurosurg. 87,586–594 (1997).
   Web of Science ®Google Scholar
• Laske D, Youle R, Oldfield E et al. Tumor regression with regional distribution of the targeted toxin TF-CRM107 in patients with malignant brain tumors. Nature Med. 12,1362–1368 (1997).
   Google Scholar
• •First report in new technology of convection-enhanced delivery on brain tumor.
   Google Scholar
• Debinski W Local treatment of brain tumors with targeted chimera toxin proteins. Cancer Invest. 20,801–809 (2002).
   Google Scholar
• Hall WA, Fostad 0. Immunotoxins and central nervous system neoplasia. Neurosurg. 76,1-12 (1992).
   Google Scholar
• Debnski W, Obiri H, Pastan I et al A novel chimeric protein composed of interleukin-13 and Pseudomonas exotoxin is highly cytotoxic to human carcinoma cells expressing receptors for interleukin-13 and interleukin-4. j Biol. Chem. 270, 16775–16780 (1995).
   Google Scholar
• Debinski W, Miner R, Leland P et al Receptor for interleukin-13 does not interact with IL4 but receptor for IL4 interacts with IL13 in human glioma cells. .1. Biol. Chem. 271,22428-22433 (1996).
   Google Scholar
• Kunwar S, Pai L, Pastan I et al Cytotoxicity and antitumor effects of growth factor-toxin fusion proteins on human glioblastoma multiforme cells. j Neurosurg. 79,569–576 (1993).
   PubMed Web of Science ®Google Scholar
• Debinski W, Obiri N, Powers S et al Human glioma cells overexpress receptors for interleukin-13 and are extremely sensitive to a novel chimeric protein composed of interleukin-13 and pseudomonas exotoxin. Clin. Cancer Res. 1, 1253–1258 (1995).
   Google Scholar
• Sampson JH, Akabani G, Archer GE et al Progress report of a Phase I study of the intracerebral microinfusion of a recombinant chimeric protein composed of transforming growth factor (TGF)-a and a mutated form of the Pseudomonas exotoxin termed PE-38 (TP-38) for the treatment of malignant brain tumors. j Neuro-Oncology 65,27–35, (2003).
   PubMed Web of Science ®Google Scholar
• Weingart J, Strauss L, Grossman S et al Phase VII study: intra-tumoral infusion of IL-13PE38QQR cytotoxin for recurrent supratentorial malignant glioma. Neuro-oncology4\(Suppl. 1), S79 (2002).
   Google Scholar
• Prados M, Lang F, Sherman J et al Convection-enhanced delivery (CED) by positive pressure infusion for intra-tumoral and peritumoral administration of IL13-PE38QQR, a recombinant tumor-targeted cytotoxin in recurrent malignant gliomas. Neuro-oncology 4\(Suppl. 1)578, (2002).
   Google Scholar
• Wong AJ, Bigner SH, Bigner DD et al Increased expression of the epidermal growth factor receptor gene in malignant gliomas is invariably associated with gene amplification. Proc. Natl Acad. Sci. USA 84, 6899–6903 (1987).
   PubMed Web of Science ®Google Scholar
• Libermann TA, Razon N, Bartal D et al Expression of epidermal growth factor receptors in human brain tumors. Cancer Res. 44,753–760 (1984).
   PubMed Web of Science ®Google Scholar
• Torp SH, Halsted E, Dalen A et al Epidermal growth factor receptor expression in human gliomas. Cancer Immunal Immunother. 33,61–64 (1991).
   PubMed Web of Science ®Google Scholar
• Mesri EA, Kreitman RJ, Fu YM et al Heparin-binding transforming growth factor a-Pseudomonas exotoxin A. A heparin modulated recombinant toxin cytotoxic to cancer cells and proliferation smooth muscle cells. j Biol. Chem. 268, 4853–4862 (1993).
   Google Scholar
• Lonser RR, Gogate N, Morrison P et al Direct convective delivery of macromolecules to the spinal cord. Neurosurg. 89,616–622 (1998).
   Google Scholar
• Scherer H. Cerebral astrocytomas and their derivative. Ainj Cancer 40,159–198 (1940).
   Google Scholar
• Lonser RR, Walbridge S, Garmestani K et al Successful and safe perfusion of the primate brainstem: in vivo magnetic resonance imaging of macromolecular distribution during infusion. j Neurosurg. 9,905–913 (2002).
   Google Scholar
• Rand R, Kreitman R, Patronas N et al Intratumoral administration of recombinant circularly permuted interleukin-4-pseudomaonas exotoxin in patients with high-grade glioma. Clin. Cancer Res. 6,2157-2165 (2000).
   Google Scholar
• Kim D, Uttley D, Bell B et al. Comparisons of rates of infection of two methods of emergency ventricular drainage. j Neural Neurosurg. Pwchiatry58, 444–446 (1995).
   PubMedGoogle Scholar
• Samson JH, Akabani G, Archer G et al Clinical outcome and distribution of a recombinant chimeric protein composed of transforming growth factor-a and a mutated Pseudomonas exotoxin (TP-38) via convection-enhanced microinfusion on a Phase I study for a malignant brain tumor. Proc. Am Soc. Clin. Oncol 22,99 (2003).
   Google Scholar
• Lorimer IAJ, Wikstrand CJ, Batra SK et al. Immunotoxins that target an oncogenic mutant epidermal growth factor receptor expressed in human tumors. Clin. Cancer Res. 1,859–864 (1995).
   PubMed Web of Science ®Google Scholar
• Newton FIB. Molecular neuro-oncology and development of targeted therapeutic strategies for brain tumors. Part 2. Expert Rev AntiCancer Ther. 4(1) 105–128 (2004).
   Google Scholar
• ••Provides a good review of angiogenesisinhibitors; P13 /Aluiphosphatidylinositol phosphate 3'-phosphatase, mTOR, SIIIIPTCH and angiogenesis.
   Google Scholar
• Van Meir EG, Bellail A, Phuphanich S. Emerging molecular therapies for brain tumors. Semin. Oncol 31(2 Suppl. 4), 38–46 (2004).
   Google Scholar
• ••Excellent review of cell cycle control,angiogenesis, prodrug/suicide gene therapy and immunotherapy.
   Google Scholar