Molecular genetics and molecular biology advances in brain tumors

Current Opinion in Oncology

Volumn 8, Issue 3, 1996, Pages 188-195

  James, C David ^a   Olson, Jeffrey J ^b  

^a MAYO CLINIC   (United States)

^b EMORY UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BRAIN TUMOR; HUMAN; MOLECULAR BIOLOGY; MOLECULAR GENETICS; ONCOGENE; PRIORITY JOURNAL; REVIEW; TUMOR SUPPRESSOR GENE;

EID: 0029992897     PISSN: 10408746     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001622-199605000-00004     Document Type: Review

References (64)

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18. Hoang-Xuan K, Merel P, Vega F, Hugot JP, Cornu P, Delattre J, Poisson M, Thomas G, Delattre O: Analysis of the NF2 tumor-suppressor gene and of chromosome 22 deletions in gliomas. Int J Cancer 1995, 60:478-481. A study showing a lack of NF2 gene alterations in various types of glial tumors.
19. Slavc I, MacCollin MM, Dunn M, Jones S, Sutton L, Gusella JF, Biegel JA: Exon scanning for mutations of the NF2 gene in pediatric ependymomas, rhabdoid tumors and meningiomas. Int J Cancer 1995, 64:243-247. An analysis of NF2 gene alterations that reveal inactivating NF2 gene alterations in some pediatric meningiomas, but not in ependymomas or rhabdoid tumors.
20. Jensen S, Paderanga DC, Chen P, Olson K, Edwards M, Iavorone A, Israel MA, Shannon K: Molecular analysis at the NF1 locus in astrocytic brain tumors. Cancer 1995, 76:674-677. A study indicating that LOH at the NF1 locus is uncommon in sporadic malignant astrocytomas.
21. Scheurlen WG, Senf L: Analysis of the gap-related domain of the neurofibromatosis type 1 (NF1) gene in childhood brain tumors. Int J Cancer 1995, 64:234-238. An analysis of a portion of the NF1 gene, encoding a portion of the corresponding protein critical to ras protein inactivation, that reveals a lack of involvement of inactivating NF1 gene alterations in childhood brain tumors.
22. Kanno H, Kondo K, Ito S, Yamamoto I, Fujii S, Torigoe S, Sakai N, Hosaka M, Shuin T, Yao M: Somatic mutations of the von Hippel-Lindau tumor suppressor gene in sporadic central nervous system hemangioblastomas. Cancer Res 1994, 54:4845-4847. An investigation demonstrating the involvement of inactivating mutations of the von Hippel-Lindau gene in sporadic hemangioblastomas.
23. Bello MJ, Vaquero J, de Campos JM, Kusak ME, Sarasa JL, Saez-Castresana J, Pestana A, Rey JA: Molecular analysis of chromosome 1 abnormalities in human gliomas reveals frequent loss of 1p in oligodendroglial tumors. Int J Cancer 1994, 57:172-175. A study in which the frequent loss of genetic material from chromosome 1p is restricted to glial tumors with oligodendroglial differentiation.
24. Kraus JA, Koopmann J, Kaskel P, Maintz D, Brandner S, Schramm J, Louis DN, Wiestler OD, von Deimling A: Shared allelic losses on chromosomes 1p and 19q suggest a common origin of oligoden-droglioma and oligoastrocytoma. J Neuropath Exp Neurol 1995, 54:91-95. A LOH analysis that limits frequent loss of genetic material from chromosome 1p to gliomas with oligodendroglial composition.
25. Sonoda Y, Iizuka M, Yasuda J, Makino R, Ono T, Kayama T, Yoshimoto T, Sekiya T: Loss of heterozygosity at 11p15 in malignant glioma. Cancer Res 1995, 55:2166-2168. An LOH analysis demonstrating loss of genetic material in approximately 30% of malignant gliomas for the 11p15.5-pter region.
26. Reifenberger G, Reifenberger J, Ichimura K, Collins VP: Amplification at 12q13-14 in human malignant gliomas is frequently accompanied by loss of heterozygosity at loci proximal and distal to the amplification site. Cancer Res 1995, 55:731-734. An LOH analysis of malignant gliomas that reveals that loss of genetic material from chromosome 12q is frequently associated with the amplification of chromosome 12q-localized genes.
27. Kim DH, Mohapatra G, Bollen A, Waldman FM, Feuerstein BG: Chromosomal abnormalities in glioblastoma multiforme tumors and glioma cell lines detected by comparative genomic hybridization. Int J Cancer 1995, 60:612-819. An application of a molecular cytogenetic technique to the analysis of malignant glial tumors and cell lines that indicates several regions of loss of genetic material not generally revealed by LOH analysis.
28. Collins VP: Amplified genes in human gliomas. Semin Cancer Biol 1993, 4:27-32.
29. Ekstrand AJ, Longo N, Hamid ML, Olson JJ, Collins VP, James CD: Functional characterization of an EGF receptor with a truncated extracellular domain expressed in glioblastomas with EGFR gene amplification. Oncogene 1994, 9:2313-2320. A study addressing in vitro functional properties of a glioma-specific mutant EGF receptor.
30. Nishikawa R, Ji XD, Harmon RC, Lazar CS, Gill GN, Cavenee WK, Huang HJ: A mutant epidermal growth factor receptor common in human glioma confers enhanced tumorigenicity. Proc Natl Acad Sci USA 1994, 91:7727-7731. A study addressing biological properties of a glioma-specific mutant EGFR.
31. Ekstrand AJ, Liu L, He J, Hamid ML, Longo N, Collins VP, James CD: Altered subcellular location of an activated and tumour-associated epidermal growth factor receptor. Oncogene 1995, 10:1455-1460. An investigation of the cellular localization, processing, and half-life of a glioma-specific mutant EGF receptor.
32. Reifenberger G, Reifenberger J, Ichimura K, Meltzer PS, Collins VP: Amplification of multiple genes from chromosomal region 12q13-14 in human malignant gliomas: preliminary mapping of the amplicons shows preferential involvement in CDK4, SAS, and, MDM2. Cancer Res 1994, 54:4299-4303. An analysis of genes residing in close proximity in 12q13-14 for their frequency of amplification in human gliomas.
33. Fischer U, Muller HW, Sattler HP, Feiden K, Zang KD, Meese E: Amplification of the MET gene in glioma. Genes Chromosom Cancer 1995, 12:63-65. A study in which MET gene amplification is demonstrated in four of 18 gliomas.
34. Fleming TP, Saxena A, Clark WC, Robertson JT, Oldfield EH, Aaronson SA, Ali IU: Amplification and/or overexpression of platelet-derived growth factor receptors and epidermal growth factor receptor in human glial tumors. Cancer Res 1992, 52:4550-4553. A study in which platelet-derived growth factor receptor-alpha amplification is determined in eight of 50 glioblastomas.
35. James CD, He J, Collins VP, Allalunis-Turner MJ, Day RS: Localization of chromosome 9p homozygous deletions in glioma cell lines with markers constituting a continuous linkage group. Cancer Res 1993, 53:3674-3676.
36. Ichimura K, Schmidt EE, Yamaguch N, James CD, Collins VP: A common region of homozygous deletion in malignant human gliomas lie between the IFN-α/ω gene cluster and the D9S171 locus. Cancer Res 1994, 54:3127-3130. A study similar in purpose and results to those associated with James et al. (Cancer Res 1993, 53:3674-3676) but involving primary glial tumors.
37. Kamb A, Gruis NA, Weaver-Feldhaus J, Liu Q, Harshman K, Tavtigian SV, Stockert E, Day RS III, Johnson BE, Skolnick MH: A cell cycle regulator potentially involved in the genesis of many tumor types. Science 1994, 264:436-440. A key report establishing the frequency and prevalence of p16 gene inactivation in human cancers.
38. Nobori T, Miura K, Wu DJ, Lois A, Takabayashi K, Carson DA: Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers. Nature 1994, 368:753-756. A key report establishing the frequency and prevalence of p16 gene inactivation in human cancers.
39. INK4B Is a potential effector of TGF-β-induced cell cycle arrest Nature 1994, 371:257-260. A report establishing the existence of a second 9p-localized cdk4 and cdk6 inhibitory protein, p15, residing in close proximity to p16.
40. Schmidt EE, Ichimura K, Reifenberger G, Collins VP: CDKN2 (p16/MTS1) gene deletion or CDK4 amplification occurs in the majority of glioblastomas. Cancer Res 1994, 54:6321-6324. An analysis of p16 gene inactivations and CDK4 gene amplifications, in glial tumors, as alternative mechanisms for inactivation of Rb protein function.
41. Jen J, Harper JW, Bigner SH, Bigner DD, Papadopoulos N, Markowitz S, Wilson JK, Kinzler KW, Vogelstein B: Deletion of p16 and p15 genes in brain tumors. Cancer Res 1994, 54:6353-6358. An analysis of human glioma xenografts showing the frequent codeletion of the p16 and p15 genes.
42. He J, Allen JR, Collins VP, Allalunis-Turner MJ, Godbout R, Day RS III, James CD: CDK4 amplification is an alternative mechanisms to p16 gene homozygous deletion in glioma cell lines. Cancer Res 1994, 54:5804-5807. Similar to reference 40, but involving the analysis of glioma cell lines.
43. Nishikawa R, Furnari FB, Lin H, Arap W, Berger MS, Cavenee WK, Huang H-JS: Loss of p16ink4 expression is frequent in high grade gliomas. Cancer Res 1995, 55:1941-1945. An investigation demonstrating frequent lack of p16 expression in malignant gliomas without corresponding p16 gene alterations.
44. Serrano M, Hannon GJ, Beach D: A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4. Nature 1993, 366:704-707. A key paper involving the isolation of the p16 gene and characterization of its protein product.
45. Weinberg RA: The retinoblastoma protein and cell cycle control. Cell 1995, 81:323-330. An outstanding review of a protein with ubiquitous involvement in human cancer.
46. Henson JW, Schnitker BL, Correa KM, von Deimling A, Fassbender F, Xu HJ, Benedict WF, Yandell DW, Louis DN: The retinoblastoma gene is involved in malignant progression of astrocytomas. Ann Neurol 1994, 36:714-721. An investigation that reveals frequent inactivating retinoblastoma gene mutations in human astrocytomas.
47. He J, Olson JJ, James CD: Lack of p16ink4 or retinoblastoma protein (pRb) or amplification-associated overexpression of cdk4 is observed in distinct subsets of malignant glial tumors and cell lines. Cancer Res 1995, 55:4833-4836. A study demonstrating alternative mechanisms leading to the functional inactivation of retinoblastoma in the majority of human glial tumors.
48. Lukas J, Parry D, Aagaard L, Mann DJ, Bartkova J, Strauss M, Peters G, Bartek J: Retinoblastoma-protein-dependent cell-cycle inhibition by the tumour suppressor p16. Nature 1995, 375:503-506. An investigation demonstrating that the growth-suppressive effects of p16 are dependent on the presence of a functional retinoblastoma protein.
49. Medema RH, Herrera RE, Lam F, Weinberg RA: Growth suppression by p16ink4 requires functional retinoblastoma protein. Proc Natl Acad Sci U S A 1995, 92:6289-6293. An investigation demonstrating that the growth-suppressive effects of p16 are dependent on the presence of a functional retinoblastoma protein.
50. Peters G: The D-type cyclins and their role in tumorigenesis. J Cell Sci 1994, 18:89-96. Review containing information involving alterations of the cyclin D1 gene in cancer.
51. Sherr CJ: D-type cyclins. Trends Biochem Sci 1995, 20:187-190. Review article containing information about growth factor stimulation of D-type cyclin synthesis.
52. Louis DN: The p53 gene and protein in human brain tumors. J Neuropathol Exp Neurol 1994, 53:11-21. A thorough review of p53 gene and p53 protein abnormalities in brain tumors.
53. Bogler O, Huang HJ, Cavenee WK: Loss of wild-type p53 bestows a growth advantage on primary cortical astrocytes and facilitates their in vitro transformation. Cancer Res 1995, 55:2746-2751. A biological analysis of the consequences of loss of p53 function in astrocytes.
54. Yahamada AM, Bruner JM, Donehower LA, Morrison RS: Astrocytes derived from p53-deficient mice provide a multistep in vitro model for development of malignant gliomas. Mol Cell Biol 1995, 15:4249-4259. A biological analysis of the consequences of loss of p53 function in astrocytes.
55. Chen P, Iavarone A, Fick J, Edwards M, Prados M, Israel MA: Constitutional p53 mutations associated with brain tumors in young adults. Cancer Genet Cytogenet 1995, 82:106-115. A study in which the incidence of germline p53 mutations was examined in 22 adult glioma patients.
56. Oliner JD, Pietenpol JA, Thiagalingam S, Gyuris J, Kinzler KW, Vogelstein B: Oncuprotein MDM2 conceals the activation domain of tumor suppressor p53. Nature 1993, 362:857-860. A study demonstrating MDM2 binding to and transcriptional inhibition of p53.
57. Reifenberger G, Liu L, Ichimura K, Schmidt EE, Collins VP: Amplification and overexpression of the MDM2 gene in a subset of human malignant gliomas without p53 mutations. Cancer Res 1993, 53:2736-2739. An investigation in which MDM2 amplification is detected in about 10% of malignant gliomas.
58. Kondo S, Barnett GH, Hara H, Morimura T, Takeuchi J: MDM2 protein confers resistance of a human glioblastoma cell line to cisplatin-induced apoptosis. Oncogene 1995, 10:2001-2006. An investigation indicating that mdm-2 protein may act as a negative reulator of cisplatin-induced apoptosis.
59. Alderson LM, Castleberg RL, Harsh GR, Louis DN, Henson JW: Human gliomas with wild-type p53 express bcl-2. Cancer Res 1995, 55:999-1001. A study demonstrating that the expression of bcl-2 in human gliomas is usually associated with wild-type p53 expression.
60. el-Deiry WS, Harper JW, O'Connor PM, Velculescu VE, Canman CE, Jackman J, Pietenpol JA, Burrell M, Hill DE, Wang Y, et al.: WAF1/CIP1 is induced in p53-mediated G1 arrest and apoptosis. Cancer Res 1994, 54:1169-1174. A study in which the results support the idea that p21 is a critical downstream effector in the p53-specific pathway of growth control.
61. 1.
62. CKI gene in malignant gliomas. Int J Cancer 1995, 62:115-117. An analysis of 35 malignant gliomas in which no inactivating p21 gene mutations were evident.
63. Shiohara M, el-Deiry WS, Wada M, Nakamaki T, Takeuchi S, Yang R, Chen DL, Vogelstein B, Koeffler HP: Absence of WAF1 mutations in a variety of human malignancies. Blood 1994, 84:3781-3784. A study in which p21 gene mutations were not detected in 351 DNAs from 14 types of human malignancies.
64. Hunter T, Pines J: Cyclins and cancer II: cyclin D and CDK inhibitors come of age. Cell 1994, 79:573-582. An outstanding review that successfully integrates the concepts of cell-cycle regulation with cancer.