[1]
|
D. S. Kong, J. I. Lee, J. H. Kim, et al., “Phase II Trial of Low-Dose Continuous (Metronomic) Treatment of Temozolomide for Recurrent Glioblastoma,” Neurology Oncology, Vol. 12, No. 3, 2010, pp. 289-296.
|
[2]
|
J. E. Chang, D. Khuntia, H. I. Robins, et al., “Radiotherapy and Radiosensitizers in the Treatment of Glioblastoma Multiforme,” Clinical Advanced Hematology Oncology, Vol. 5, No. 11, 2007, pp. 894-902, 907-915.
|
[3]
|
H. L. Liu, M. Y. Hua, P. Y. Chen, et al., “Blood-Brain Barrier Disruption with Focused Ultrasound Enhances Delivery of Chemotherapeutic Drugs for Glioblastoma Treatment,” Radiology, Vol. 255, No. 2, 2010, pp. 415- 425. doi:10.1148/radiol.10090699
|
[4]
|
T. Nagasaka, M. Gunji, N. Hosokai, et al., “FISH 1p/19q Deletion/Imbalance for Molecular Subclassification of Glioblastoma,” Brain Tumor Pathology, Vol. 24, No. 1, 2007, pp. 1-5. doi:10.1007/s10014-006-0209-6
|
[5]
|
B. Klink, B. Schlingelhof, M. Klink, et al., “Glioblastomas with Oligodendroglial Component-Common Origin of the Different Histological Parts and Genetic Subclassification,” Cell Oncology, May 25, 2010.
|
[6]
|
T. Miyanaga, J. Hirato and Y. Nakazato, “Amplification of the Epidermal Growth Factor Receptor Gene in Glioblastoma: An Analysis of the Relationship between Genotype and Phenotype by CISH Method,” Neuropathology, Vol. 28, No. 2, 2007, pp. 116-126. doi:10.1111/j.1440-1789.2007.00853.x
|
[7]
|
H. Ohgaki and P. Kleihues, “Genetic Pathways to Primary and Secondary Glioblastoma,” American Journal of Pathology, Vol. 170, No. 5, 2007, pp. 1445-1453. doi:10.2353/ajpath.2007.070011
|
[8]
|
M. Kanamori, T. Kawaguchi, J. M. Nigro, et al., “Contribution of Notch Signaling Activation to Human Glioblastoma Multiforme,” Journal Neurosurg, Vol. 106, No. 3, 2007, pp. 417- 427.
doi:10.3171/jns.2007.106.3.417
|
[9]
|
C. B. Knobbe and G. Reifenberger, “Genetic Alterations and Aberrant Expression of Genes Related to the PhosPhatidyl-Inositol-3’-Kinase/protein Kinase B (Akt) Signal Transduction Pathway in Glioblastomas,” Brain Pathology, Vol. 13, No. 4, 2003, pp. 507-518. doi:10.1111/j.1750-3639.2003.tb00481.x
|
[10]
|
R. Blum, I. Nakdimon, L. Goldberg, et al., “E2F1 Identified by Promoter and Biochemical Analysis as a Central Target of Glioblastoma Cell-Cycle Arrest in Response to Ras Inhibition,” International Journal of Cancer, Vol. 119, No. 3, 2006, pp. 527-538. doi:10.1002/ijc.21735
|
[11]
|
J. Guldenhaupt, Y. Adiguzel, J. Kuhlmann, et al., “Secondary Structure of Lipidated Ras Bound to a Lipid Bilayer,” FEBS Journal, Vol. 275, No. 23, 2008, pp. 5910-5918. doi:10.1111/j.1742-4658.2008.06720.x
|
[12]
|
A. C. Berzat, D. C. Brady, J. J. Fiordalisi, et al., “Using Inhibitors of Prenylation to Block Localization and Transforming Activity,” Methods in Enzymology, Vol. 407, 2006, pp. 575-597.
doi:10.1016/S0076-6879(05)07046-1
|
[13]
|
N. Saxena, S. S. Lahiri, S. Hambarde, et al., “RAS: Target for Cancer Therapy,” Cancer Investigation, Vol. 26, No. 9, November 2008, pp. 948-955. doi:10.1080/07357900802087275
|
[14]
|
B. H. Chung, H. Y. Lee, J. S. Lee, et al., “Perillyl Alcohol Inhibits the Expression and Function of the Androgen Receptor in Human Prostate Cancer Cells,” Cancer Letter, Vol. 236, No. 2, May 18, 2006, pp. 222-228. doi:10.1016/j.canlet.2005.05.023
|
[15]
|
S. C. Chaudhary, M. S. Alam, M. S. Siddiqui, et al., “Perillyl Alcohol Attenuates Ras-ERK Signaling to Inhibit Murine Skin Inflammation and Tumorigenesis,” Chemical Biology Interact, Vol. 179, No. 2-3, 15, 2009, pp. 145-153. doi:10.1016/j.cbi.2008.12.016
|
[16]
|
C. O. da Fonseca, J. A. Landeiro, S. S. Clark, et al., “Recent Advances in the Molecular Genetics of Malignant Gliomas Disclose Targets for Antitumor Agent Perillyl Alcohol,” Surgery Neurology, Vol. 65, Suppl. 1, 2006, pp. 2-9.
|
[17]
|
J. Fernandes, C. O. da Fonseca, A. Teixeira, et al., “Perillyl Alcohol Induces Apoptosis in Human Glioblastoma Multiforme Cells,” Oncology Reports, Vol. 13, No. 5, 2005, pp. 943-947.
|
[18]
|
M. M. Patel, B. R. Goyal, S. V. Bhadada, et al., “Getting into the Brain: Approaches to Enhance Brain Drug Delivery,” CNS Drugs, Vol. 23, No. 1, 2009, pp. 35-58. doi:10.2165/0023210-200923010-00003
|
[19]
|
H. Wu, K. Hu and X. Jiang, “From Nose to Brain: Understanding Transport Capacity and Transport Rate of Drugs,” Expert Opinion on Drug Delivery, Vol. 5, 2008, pp. 1159-1168. doi:10.1517/17425247.5.10.1159
|
[20]
|
C. da Fonseca, M. Sim?o, I. Lins, et al., “Efficacy of Monoterpene Perillyl Alcohol upon Survival Rate of Patients with Recurrent Glioblastoma,” Journal of Cancer Research and Clinical Oncology, 2010, pp. 1-7.
|
[21]
|
C. O. da Fonseca, R. Linden, D. Futuro, et al., “Ras Pathway Activation in Gliomas: A Strategic Target for Intranasal Administration of Perillyl Alcohol,” Archivum Immunologiae et Therapia Experimentalis (Warsz), Vol. 56, No. 4, 2008, pp. 267-276. doi:10.1007/s00005-008-0027-0
|
[22]
|
H. Colman, L. Zhang, E. P. Sulman, et al., “A Multigene Predictor of Outcome in Glioblastoma,” Neuro Oncology, Vol. 12, No. 1, 2010, pp. 49-57.
|
[23]
|
S. S. Clark, L. Zhong, D. Filiault, et al., “Anti-Leukemia Effect of Perillyl Alcohol in Bcr/Abl-Transformed Cells Indirectly Inhibits Signaling through Mek in a Ras- and Raf-Independent Fashion,” Clinical Cancer Research, Vol. 9, No. 12, 2003, pp. 4494-4504.
|
[24]
|
C. O. da Fonseca, G. Schwartsmann, J. Fischer, et al., “Preliminary Results from a Phase I/II Study of Perillyl Alcohol Intranasal Administration in Adults with Recurrent Malignant Gliomas,” Surgery Neurology, Vol. 70, No. 3, 2008, pp. 259-266. doi:10.1016/j.surneu.2007.07.040
|
[25]
|
C. O. Da Fonseca, J. T. Silva, I. R. Lins, et al., “Correlation of Tumor Topography and Peritumoral Edema of Recurrent Malignant Gliomas with Therapeutic Response to Intranasal Administration of Perillyl Alcohol,” Investigational New Drugs, January 13, 2009.
|
[26]
|
P. Kleihues and H. Ohgaki, “Primary and Secondary Glioblastomas: From Concept to Clinical Diagnosis,” Neuro Oncology, Vol. 1, No. 1, January 1999, pp. 44-51.
|
[27]
|
Y. Zhu, F. Guignard, D. Zhao, et al., “Early Inactivation of P53 Tumor Suppressor Gene Cooperating with NF1 Loss Induces Malignant Astrocytoma,” Cancer Cell, Vol. 8, No. 2, 2005, pp. 119-130.
doi:10.1016/j.ccr.2005.07.004
|