Molecular biology of gliomas

Current Neurology and Neuroscience Reports

Volumn 4, Issue 3, 2004, Pages 228-233

  Lassman, Andrew B ^a  

^a MEMORIAL SLOAN KETTERING CANCER CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ARF PROTEIN; CYCLIN DEPENDENT KINASE 4; CYCLIN DEPENDENT KINASE INHIBITOR; EPIDERMAL GROWTH FACTOR; EPIDERMAL GROWTH FACTOR RECEPTOR; ERLOTINIB; GEFITINIB; IMATINIB; PLATELET DERIVED GROWTH FACTOR; PLATELET DERIVED GROWTH FACTOR RECEPTOR; PROTEIN KINASE B; RAPAMYCIN; RAS PROTEIN;

ANTINEOPLASTIC ACTIVITY; CANCER GROWTH; CELL PROLIFERATION; CLINICAL TRIAL; DRUG DESIGN; DRUG TARGETING; GLIOMA; HUMAN; PATHOGENESIS; PROGNOSIS; REVIEW; SIGNAL TRANSDUCTION; BRAIN TUMOR; METABOLISM; MOLECULAR BIOLOGY; PATHOLOGY; PATHOPHYSIOLOGY;

BRAIN NEOPLASMS; GLIOMA; HUMANS; MOLECULAR BIOLOGY; SIGNAL TRANSDUCTION;

EID: 3042673613     PISSN: 15284042     EISSN: None     Source Type: Journal    
DOI: 10.1007/s11910-004-0043-3     Document Type: Review

References (50)

1. Kleihues P, Cavanee W: Pathology and Genetics of Tumours of the Nervous System. Lyon, France: International Agency for Research on Cancer, 2000.
2. Bailey P, Cushing H: A Classification of the Tumors of the Glioma Group on a Histo-genetic Basis with a Correlated Study of Prognsosis. Philadelphia: JB Lippincott; 1926.
3. Scherer HJ: Structural development in gliomas. Am J Cancer 1938, 34:333-351.
4. Jelsma RK, Bucy PC: The treatment of glioblastoma multiforme. Trans Am Neurol Assoc 1967, 92:90-93.
5. Blume-Jensen P, Hunter T: Oncogenic kinase signalling. Nature 2001, 411:355-365.
6. Downward J, Yarden Y, Mayes E, et al.: Close similarity of epidermal growth factor receptor and v-erb-B oncogene protein sequences. Nature 1984, 307:521-527.
7. Ullrich A, Coussens L, Hayflick JS, et al.: Human epidermal growth factor receptor cDNA sequence and aberrant expression of the amplified gene in A431 epidermoid carcinoma cells. Nature 1984, 309:418-425.
8. Schlegel J, Stumm G, Brandle K, et al.: Amplification and differential expression of members of the erbB-gene family in human glioblastoma. J Neuro-oncol 1994, 22:201-207.
9. Kleihues P, Ohgaki H: Primary and secondary glioblastomas: from concept to clinical diagnosis. J Neuro-oncol 1999, 1:44-51.
10. Kuan CT, Wikstrand CJ, Bigner DD: EGF mutant receptor vIII as a molecular target in cancer therapy. Endocr Relat Cancer 2001, 8:83-96.
11. Frederick L, Wang XY, Eley G, James CD: Diversity and frequency of epidermal growth factor receptor mutations in human glioblastomas. Cancer Res 2000, 60:1383-1387.
12. Hermanson M, Funa K, Koopmann J, et al.: Association of loss of heterozygosity on chromosome 17p with high platelet-derived growth factor alpha receptor expression in human malignant gliomas. Cancer Res 1996, 56:164-171.
13. Nister M, Libermann T, Betsholtz C, et al.: Expression of messenger RNAs for platelet-derived growth factor and transforming growth factor-alpha and their receptors in human malignant glioma cell lines. Cancer Res 1988, 48:3910-3918.
14. Guha A, Dashner K, Black PM, et al.: Expression of PDGF and PDGF receptors in human astrocytoma operation specimens supports the existence of an autocrine loop. Int J Cancer 1995, 60:168-173.
15. Di Rocco F, Carroll RS, Zhang J, Black PM: Platelet-derived growth factor and its receptor expression in human oligodendrogliomas. Neurosurgery 1998, 42:341-346.
16. Staal SP: Molecular cloning of the akt oncogene and its human homologues AKT1 and AKT2: amplification of AKT1 in a primary human gastric adenocarcinoma. Proc Natl Acad Sci U S A 1987, 84:5034-5037.
17. Rajasekhar VK, Viale A, Socci ND, et al.: Oncogenic Ras and Akt signaling contribute to glioblastoma formation by differential recruitment of existing mRNAs to polysomes. Mol Cell 2003, 12:889-901.
18. Alessi DR, James SR, Downes CF, et al.: Characterization of a 3-phosphoinositide-dependent protein kinase which phosphorylates and activates protein kinase Balpha. Curr Biol 1997, 7:261-269.
19. Datta K, Bellacosa A, Chan TO, Tsichlis PN: Akt is a direct target of the phosphatidylinositol 3-kinase. Activation by growth factors, v-src and v-Ha-ras, in Sf9 and mammalian cells. J Biol Chem 1996, 271:30835-30839.
20. Schmelzle T, Hall MN: TOR, a central controller of cell growth. Cell 2000, 103:253-262.
21. Haas-Kogan D, Shalev N, Wong M, et al.: Protein kinase B (PKB/Akt) activity is elevated in glioblastoma cells due to mutation of the tumor suppressor PTEN/MMAC. Curr Biol 1998, 8:1195-1198.
22. Stambolic V, Suzuki A, de la Pompa JL, et al.: Negative regulation of PKB/Akt-dependent cell survival by the tumor-suppressor PTEN. Cell 1998, 95:29-39.
23. Wu X, Senechal K, Neshat MS, et al.: The PTEN/MMAC1 tumor suppressor phosphatase functions as a negative regulator of the phosphoinositide 3-kinase/Akt pathway. Proc Natl Acad Sci U S A 1998, 95:15587-15591.
24. Tohma Y, Gratas C, Biernat W, et al.: PTEN (MMAC1) mutations are frequent in primary glioblastomas (de novo) but not in secondary glioblastomas. J Neuropathol Exp Neurol 1998, 57:684-689.
25. Guha A, Feldkamp MM, Lau N, et al.: Proliferation of human malignant astrocytomas is dependent on Ras activation. Oncogene 1997, 15:2755-2765.
26. Feldkamp MM, Lala P, Lau N, et al.: Expression of activated epidermal growth factor receptors, Ras-guanosine triphosphate, and mitogen-activated protein kinase in human glioblastoma multiforme specimens. Neurosurgery 1999, 45:1442-1453.
27. Prigent SA, Nagane M, Lin H, et al.: Enhanced tumorigenic behavior of glioblastoma cells expressing a truncated epidermal growth factor receptor is mediated through the Ras-Shc-Grb2 pathway. J Biol Chem 1996, 271:25639-25645.
28. Ballester R, Marchuk D, Boguski M, et al.: The NF1 locus encodes a protein functionally related to mammalian GAP and yeast IRA proteins. Cell 1990, 63:851-859.
29. Xu GF, Lin B, Tanaka K, et al.: The catalytic domain of the neurofibromatosis type 1 gene product stimulates ras GTPase and complements ira mutants of S. cerevisiae. Cell 1990, 63:835-841.
30. Pardee AB: G1 events and regulation of cell proliferation. Science 1989, 246:603-608.
31. Chellappan SP, Hiebert S, Mudryj M, et al.: The E2F transcription factor is a cellular target for the RB protein. Cell 1991, 65:1053-1061.
32. Johnson DG, Schwarz JK, Cress WD, Nevins JR: Expression of transcription factor E2F1 induces quiescent cells to enter S phase. Nature 1993, 365:349-352.
33. Fakharzadeh SS,Trusko SP, George DL: Tumorigenic potential associated with enhanced expression of a gene that is amplified in a mouse tumor cell line. EMBO J 1991, 10:1565-1569.
34. Momand J, Zambetti GP, Olson DC, et al.: The mdm-2 oncogene product forms a complex with the p53 protein and inhibits p53-mediated transactivation. Cell 1992, 69:1237-1245.
35. Oliner JD, Kinzler KW, Meltzer PS, et al.: Amplification of a gene encoding a p53-associated protein in human sarcomas. Nature 1992, 358:80-83.
36. Pomerantz J, Schreiber-Agus N, Liegeois NJ, et al.: The Ink4a tumor suppressor gene product, p19Arf, interacts with MDM2 and neutralizes MDM2's inhibition of p53. Cell 1998, 92:713-723.
37. Kamijo T, Weber JD, Zambetti G, et al.: Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2. Proc Natl Acad Sci U S A 1998, 95:8292-8297.
38. Tao W, Levine AJ: P19(ARF) stabilizes p53 by blocking nucleo-cytoplasmic shuttling of Mdm2. Proc Natl Acad Sci U S A 1999, 96:6937-6941.
39. Ashcroft M, Kubbutat MH, Vousden KH: Regulation of p53 function and stability by phosphorylation. Mol Cell Biol 1999, 19:1751-1758.
40. el-Deiry WS, Tokino T, Velculescu VE, et al.: WAF1, a potential mediator of p53 tumor suppression. Cell 1993, 75:817-825.
41. Harper JW, Adami GR, Wei N, et al.: The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. Cell 1993, 75:805-816.
42. Fueyo J, Gomez-Manzano C, Bruner JM, et al.: Hypermethylation of the CpG island of p16/CDKN2 correlates with gene inactivation in gliomas. Oncogene 1996, 13:1615-1619.
43. Reilenberger G, Reifenberger J, Ichimura K, et al.: Amplification of multiple genes from chromosomal region 12q13-14 in human malignant gliomas: preliminary mapping of the amplicons shows preferential involvement of CDK4, SAS, and MDM2. Cancer Res 1994, 54:4299-4303.
44. Moulton T, Samara G, Chung WY, et al.: MTS1/p16/CDKN2 lesions in primary glioblastoma multiforme. Am J Pathol 1995, 146:613-619.
45. Ichimura K, Bolin MB, Goike HM, et al.: Deregulation of the p14ARF/MDM2/p53 pathway is a prerequisite for human astrocytic gliomas with G1-S transition control gene abnormalities. Cancer Res 2000, 60:417-424.
46. Costello JF, Berger MS, Huang HS, Cavenee WK: Silencing of p16/CDKN2 expression in human gliomas by methylation and chromatin condensation. Cancer Res 1996, 56:2405-2410.
47. Ichimura K, Schmidt EE, Goike HM, Collins VP: Human glioblastomas with no alterations of the CDKN2A (p16INK4A, MTS1) and CDK4 genes have frequent mutations of the retinoblastoma gene. Oncogene 1996, 13:1065-1072.
48. Fulci G, Labuhn M, Maier D, et al.: p53 gene mutation and ink4a-arf deletion appear to be two mutually exclusive events in human glioblastoma. Oncogene 2000, 19:3816-3822.
49. Ueki K, Ono Y, Henson JW, et al.: CDKN2/p16 or RB alterations occur in the majority of glioblastomas and are inversely correlated. Cancer Res 1996, 56:150-153.
50. Wolter M, Reifenberger J, Blaschke B, et al.: Oligodendroglial tumors frequently demonstrate hypermethylation of the CDKN2A (MTS1, p16INK4a), p14ARF, and CDKN2B(MTS2, p15INK4b) tumor suppressor genes. J Neuropathol Exp Neurol 2001, 60:1170-1180.