Detection of p16, RB, CDK4, and p53 gene deletion and amplification by fluorescence in situ hybridization in 96 gliomas

American Journal of Clinical Pathology

Volumn 112, Issue 6, 1999, Pages 801-809

  Perry, Arie ^a   Anderl, Kari ^b   Borell, Tom J ^b   Kimmel, David W ^b   Wang, Chiao H ^b   O'Fallon, Judith R ^b   Feuerstein, Burt G ^b   Scheithauer, Bernd W ^b   Jenkins, Robert B ^b  

^a WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b NONE

Author keywords

Astrocytoma; Cyclin dependent kinases; Fluorescence in situ hybridization; Glioma; p16 gene; p53 gene; Retinoblastoma gene

Indexed keywords

CREATINE KINASE; PROTEIN P16; PROTEIN P53;

ADULT; AGED; ARTICLE; DNA PROBE; FEMALE; FLUORESCENCE IN SITU HYBRIDIZATION; GENE AMPLIFICATION; GENE DELETION; GLIOMA CELL; HISTOPATHOLOGY; HUMAN; HUMAN CELL; HUMAN TISSUE; MAJOR CLINICAL STUDY; MALE; PHENOTYPE; PRIORITY JOURNAL; PROTEIN EXPRESSION;

EID: 0033491737     PISSN: 00029173     EISSN: None     Source Type: Journal    
DOI: 10.1093/ajcp/112.6.801     Document Type: Article

References (42)

1. Louis DN. A molecular genetic model of astrocytoma histopathology. Brain Pathol. 1997;7:755-764.
2. Collins VP. Genetic alterations in gliomas. J Neurooncol. 1995;24:37-38.
3. Ohgaki H, Schauble B, zur Hausen A, et al. Genetic alterations associated with the evolution and progression of astrocytic brain tumors. Virchow Arch. 1995;427:113-118.
4. Von Deimling A, Louis DN, Wiestler OD. Molecular pathways in the formation of gliomas. Glia. 1995;15:328-338.
5. Dalrymple SJ, Jenkins RB. Molecular genetics of astrocytomas and meningiomas. Curr Opin Neurol. 1994;7:477-483.
6. Kamb A, Gruis NA, Weaver-Feldhaus J, et al. A cell cycle regulator potentially involved in genesis of many tumor types. Science. 1994;264:436-440.
7. Nobori T, Miura K, Wu DJ, et al. Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers. Nature. 1994;368:753-756.
8. Schmidt EE, Ichimura K, Reifenberger G, et al. CDKN2 (p16/MTS1) gene deletion or CDK4 amplification occurs in the majority of glioblastomas. Cancer Res. 1994;54:6321-6324.
9. Jen J, Harper JW, Bigner SH, et al. Deletion of p16 and p15 genes in brain tumors. Cancer Res. 1994;54:6353-6358.
10. Sonoda Y, Yoshimoto T, Sekiya T. Homozygous deletion of the MTS1/p16 and MTS2/p15 genes and amplification of the CDK4 gene in glioma. Oncogene. 1995;11:2145-2149.
11. Izumoto S, Arita N, Ohnishi T, et al. Homozygous deletions of p16INK4A/MTS1 and p15INK4B/MTS2 genes in glioma cells and primary glioma tissues. Cancer Lett. 1995;97:241-247.
12. 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.
13. 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;56:15-53.
14. Walker DG, Duan W, Popovic EA, et al. Homozygous deletions of the multiple tumor suppressor gene 1 in the progression of human astrocytomas. Cancer Res. 1995;55:20-23.
15. Dreyling MH, Bohlander SK, Adeyanju MO, et al. Detection of CDKN2 deletions in tumor cell lines and primary glioma by interphase fluorescence in situ hybridization. Cancer Res. 1995;55:984-988.
16. Nishikawa R, Fumari FB, Lin H, et al. Loss of p16INK4 expression is frequent in high grade gliomas. Cancer Res. 1995;55:1941-1945.
17. Henson JW, Schnitker BL, Correa KM, et al. The retinoblastoma gene is involved in malignant progression of astrocytomas. Ann Neurol. 1994;36:714-721.
18. Perry A, Nobori T, Ru N, et al. Detection of p16 gene deletions in gliomas: a comparison of fluorescence in situ hybridization (FISH) versus quantitative PCR. J Neuropathol Exp Neurol. 1997;56:999-1008.
19. Kleihues P, Burger PC, Scheithauer BW. Histological Typing of Tumours of the Central Nervous System. Berlin, Germany: World Health Organization, Springer-Verlag; 1993.
20. Dalrymple SJ, Herath JF, Borell TJ, et al. Correlation of cytogenetic and fluorescence in situ hybridization (FISH) studies in normal and gliotic brain. J Neuropathol Exp Neurol. 1994;53:448-456.
21. Arnoldus EPJ, Noordermeer IA, Peters AC, et al. Interphase cytogenetics reveals somatic pairing of chromosome 17 centromeres in normal human brain tissue, but no trisomy 7 or sex-chromosome loss. Cytogenet Cell Genet. 1991;56:214-216.
22. Kaplan EL, Meier P. Nonparametric estimation from incomplete observations. J Am Stat Assoc. 1958;53:457-481.
23. Mantel N. Evaluation of survival data and two new rank order statistics arising in its consideration. Cancer Chemother Rep. 1966;50:163-170.
24. Cox DR. Regression models and life tables (with discussion). J R Stat Soc B. 1972;34:187-220.
25. Park SH, Maeda T, Mohapatra G, et al. Heterogeneity, polyploidy, aneusomy, and 9p deletion in human glioblastoma multiforme. Cancer Gen Cytogenet. 1995;83:127-135.
26. James CD, Carlbom E, Nordenskjold M, et al. Mitotic recombination of chromosome 17 in astrocytomas. Proc Natl Acad Sci U S A. 1989;86:2858-2862.
27. Pollack IF, Hamilton RL, Finkelstein SD, et al. The relationship between TP53 mutations and overexpression of p53 and prognosis in malignant gliomas of childhood. Cancer Res. 1997;57:304-309.
28. Rasheed BKA, McLendon RE, Herndon JE, et al. Alterations of the TP53 gene in human gliomas. Cancer Res. 1994;54:1324-1330.
29. Al-Sarraj S, Bridges LR. p53 immunoreactivity in astrocytomas and its relationship to survival. Br J Neurosurg. 1995;9:143-149.
30. Chozick BS, Pezzullo JC, Epstein MH, et al. Prognostic implications of p53 overexpression in supratentorial astrocytic tumors. Neurosurgery. 1994;35:831-837.
31. Bhattacharjee MB, Bruner JM. p53 protein in pediatric malignant astrocytomas: a study of 21 patients. J Neurooncol. 1997;32:225-233.
32. Jaros E, Perry RH, Adam L, et al. Prognostic implications of p53 protein, epidermal growth factor receptor, and Ki-67 labelling in brain tumors. Br J Cancer. 1992;66:373-385.
33. Childhood Brain Tumor Consortium. Intraobserver reproducibility in assigning brain tumors to classes in the World Health Organization diagnostic scheme. J Neurooncol. 1989;7:211-224.
34. Rorke LB. Pathologic diagnosis as the gold standard [editorial]. Cancer. 1997;79:665-667.
35. Bruner JM, Inouye L, Fuller GN, et al. Diagnostic discrepancies and their clinical impact in a neuropathology referral practice. Cancer. 1997;79:796-803.
36. Caimcross JG, Ueki K, Zlatescu MC, et al. Specific genetic predictors of chemotherapeutic response and survival in patients with anaplastic oligodendrogliomas. J Natl Cancer Inst. 1998;90:1473-1479.
37. Perry A, Smith JS, Borell TJ, et al. Alterations of chromosome arms 1p and 19q as predictors of survival in diffuse gliomas [abstract]. J Neuropathol Exp Neurol. 1999;58:512.
38. Reifenberger J, Riefenberger G, Liu L, et al. Molecular genetic analysis of oligodendroglial tumors shows preferential allelic deletions on 19q and 1p. Am J Pathol. 1994;145:1175-1190.
39. Bello MJ, Leone PE, Vaquero J, et al. Allelic loss at 1p and 19q frequently occurs in association and may represent early oncogenic events in oligodendroglial tumors. Int J Cancer. 1995;64:207-210.
40. Smith JS, Alderete B, Minn Y, et al. Localization of common deletion regions on 1p and 19q in human gliomas and their association with histological subtype. Oncogene. 1999;18:4144-4152.
41. Ono Y, Tamiya T, Ichikawa T, et al. Malignant astrocytomas with homozygous CDKN2/p16 gene deletions have higher Ki-67 proliferation indices. J Neuropathol Exp Neurol. 1996;55:1026-1031.
42. 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 bcl-2 genes. Brain Pathol. 1998;8:655-667.