Oncogenes amplification

Sestini, R., Orlando, C., Zentilin, L., Gelmini, S., Pinzani, P. et al.. Measuring c-erb B-2 oncogene amplification in fresh and paraffin-embedded tumors by competitive polymerase chain reaction. Clin. Chem. (Winston-Salem, N.C.) 40, 630-636 (1994). 

Ross, J. S., Sheehan, C. E., and Fletcher, J. A. 2001. HER-2/neu oncogene amplification determined by fluorescence in situ hybridization. In Molecular Pathology Protocols (A. A. Killeen, ed.), pp. 93-104. Humana Press, Totowa, NJ. 

Vona, G., Caldini, A., Sestini, R., Rapi, S., Bianchi, S., Fanelli, A., Pazzagli, M., and Orlando, C. 1999. The c-erbB2 oncogene amplification by competitive PCR in aneuploid cell clones stored from breast cancer samples. Clin. Chem. Lab. Med. 37 649-654. 

Schwab M (1999) Oncogene amplification in solid tumors. Semin Cancer Biol 9 319-325... 

Tanner M, Gancberg D, Di Leo A, Larsimont D, Rouas G, Piccart MJ, et al. Chromogenicinsitu hybridization apractical alternative forfluorescence in situ hybridization to detect HER-2/neu oncogene amplification in archival breast cancer samples. Am J Pathol 2000 157(5) 1467-72. 

Laakso M, Tanner M, Isola J. Dual-colour chromogenic in situ hybridization for testing of HER-2 oncogene amplification in archival breast tumours. J Pathol 2006 210(1) 3-9. 

Isola J, Tanner M, Forsyth A, Cooke TG, Watters AD, Bartlett JM. Interlaboratory comparison of HER-2 oncogene amplification as detected by chromogenic and fluorescence in situ hybridization. Clin Cancer Res 2004 10(14) 4793-8. 

Tong CY, Hui AB, Yin XL, et al. Detection of oncogene amplifications in medulloblastomas by comparative genomic hybridization and array-based comparative genomic hybridization. J Neurosurg Spine. 2004 100 187-193. 

Gene amplification 1 Many oncogenes are present in multiple copies erbB amplified in certain breast cancers Dihydrofolate reductase genes are amplified in some tumors, leading to drug resistance... 

As in cancer predisposing syndromes, these genetic alterations are sometimes carried in the germline. Among human tumours, heritable mutations are an exception. Most alterations are acquired in somatic life in the form of chromosomal translocations, deletions, inversions, amplifications or point mutations. Certain oncogenic viruses play important roles in a few human tumours. Examples are human papilloma-virus in cervical cancer and skin tumours, Ep-stein-Barr virus in nasopharyngeal carcinoma and Burkitt s lymphoma, and human T-cell leukaemia viruses (e.g. HTLV-I, HTLV-II) in T-cell leukaemia. 

Proto-oncogenes can be activated by mutations, chromosome translocations, gene amplifications, or promoter insertion. 

Wood et al. (1991) have used the Southern hybridization method for detecting DNA amplification and a possible structural rearrangement of the HER-2/nen oncogene in 1 of 12 bladder tumors. Amplification of this oncogene in the tumor was sixfold that of oncogene found in placental DNA. Approximately 36% of the tumors studied overexpressed HER-2 mRNA, which was 3- to 38-fold that of normal urothelium. HER-2 overexpression occurred in superficial and invasive tumors. Deoxyribonucleic acid amplification occurs infrequently in bladder carcinoma, in contrast to its occurrence in some other carcinomas. Immunohistochemical analysis has shown that pi85 HER-2 polyclonal antibody is specific for HER-2 protein overexpression in bladder carcinoma. This study was carried out prior to the use of Herceptin. 

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