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HER2, TOP2A, CCND1, EGFR and C-MYC oncogene amplification in colorectal cancer.

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HER2, TOP2A, CCND1, EGFR and C-MYC oncogene amplification in colorectal cancer. / Al-Kuraya, Khawla; Novotny, Hedvika; Bavi, Prashant; Siraj, Abdul K; Uddin, Shahab; Ezzat, Adnan; Sanea, Nasser Al; Al-Dayel, Fouad; Al-Mana, Hadeel; Sheikh, Salwa S; Mirlacher, Martina; Tapia, Coya; Simon, Ronald; Sauter, Guido; Terracciano, Luigi; Tornillo, Luigi.

In: J CLIN PATHOL, Vol. 60, No. 7, 7, 2007, p. 768-772.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Al-Kuraya, K, Novotny, H, Bavi, P, Siraj, AK, Uddin, S, Ezzat, A, Sanea, NA, Al-Dayel, F, Al-Mana, H, Sheikh, SS, Mirlacher, M, Tapia, C, Simon, R, Sauter, G, Terracciano, L & Tornillo, L 2007, 'HER2, TOP2A, CCND1, EGFR and C-MYC oncogene amplification in colorectal cancer.', J CLIN PATHOL, vol. 60, no. 7, 7, pp. 768-772. <http://www.ncbi.nlm.nih.gov/pubmed/16882699?dopt=Citation>

APA

Al-Kuraya, K., Novotny, H., Bavi, P., Siraj, A. K., Uddin, S., Ezzat, A., Sanea, N. A., Al-Dayel, F., Al-Mana, H., Sheikh, S. S., Mirlacher, M., Tapia, C., Simon, R., Sauter, G., Terracciano, L., & Tornillo, L. (2007). HER2, TOP2A, CCND1, EGFR and C-MYC oncogene amplification in colorectal cancer. J CLIN PATHOL, 60(7), 768-772. [7]. http://www.ncbi.nlm.nih.gov/pubmed/16882699?dopt=Citation

Vancouver

Al-Kuraya K, Novotny H, Bavi P, Siraj AK, Uddin S, Ezzat A et al. HER2, TOP2A, CCND1, EGFR and C-MYC oncogene amplification in colorectal cancer. J CLIN PATHOL. 2007;60(7):768-772. 7.

Bibtex

@article{e99c912d3d5c49af85ab240a4fcb8cd4,
title = "HER2, TOP2A, CCND1, EGFR and C-MYC oncogene amplification in colorectal cancer.",
abstract = "AIM: Recent studies had suggested substantial molecular differences between tumours from different ethnic groups. In this study, the molecular differences between the incidences of colorectal carcinoma in Saudi and Swiss populations are investigated. Method: 518 cases of colon cancer tumours (114 from Saudi Arabia and 404 from Switzerland) were analysed in a tissue microarray format. Fluorescence in situ hybridisation (FISH) was used to estimate frequencies of copy number changes of known oncogenes, including HER2, TOPO2A, CCND1, EGFR and C-MYC. RESULTS: Using FISH, amplifications were mostly low level (gene-to-centromere ratio 2 to 4), which is in contrast with other tumour types with more frequent gene amplifications. The amplifications were particularly frequent for MYC (Saudi 9% and Swiss 14.2%) but unrelated to clinical outcome and pathological information. Remarkably, there were four tumours exhibiting classic high-level gene amplification for HER2 (Swiss 1.3%), a pattern often accompanied by response to trastuzumab (Herceptin) in breast cancer. Occasional high-level amplifications were also observed for CCND1 (Saudi 1/106, 0.9%; Swiss 2/373, 0.5%) and EGFR (Swiss 2/355; 0.6%). CONCLUSIONS: Rare high-level amplifications of therapeutic target genes were found in patients with colon cancer. Although no molecular differences were found between incidences of colon cancer cases in Swiss and Saudi populations, these observations emphasise the urgent need for clinical studies investigating the effect of targeted therapies.",
author = "Khawla Al-Kuraya and Hedvika Novotny and Prashant Bavi and Siraj, {Abdul K} and Shahab Uddin and Adnan Ezzat and Sanea, {Nasser Al} and Fouad Al-Dayel and Hadeel Al-Mana and Sheikh, {Salwa S} and Martina Mirlacher and Coya Tapia and Ronald Simon and Guido Sauter and Luigi Terracciano and Luigi Tornillo",
year = "2007",
language = "Deutsch",
volume = "60",
pages = "768--772",
journal = "J CLIN PATHOL",
issn = "0021-9746",
publisher = "BMJ PUBLISHING GROUP",
number = "7",

}

RIS

TY - JOUR

T1 - HER2, TOP2A, CCND1, EGFR and C-MYC oncogene amplification in colorectal cancer.

AU - Al-Kuraya, Khawla

AU - Novotny, Hedvika

AU - Bavi, Prashant

AU - Siraj, Abdul K

AU - Uddin, Shahab

AU - Ezzat, Adnan

AU - Sanea, Nasser Al

AU - Al-Dayel, Fouad

AU - Al-Mana, Hadeel

AU - Sheikh, Salwa S

AU - Mirlacher, Martina

AU - Tapia, Coya

AU - Simon, Ronald

AU - Sauter, Guido

AU - Terracciano, Luigi

AU - Tornillo, Luigi

PY - 2007

Y1 - 2007

N2 - AIM: Recent studies had suggested substantial molecular differences between tumours from different ethnic groups. In this study, the molecular differences between the incidences of colorectal carcinoma in Saudi and Swiss populations are investigated. Method: 518 cases of colon cancer tumours (114 from Saudi Arabia and 404 from Switzerland) were analysed in a tissue microarray format. Fluorescence in situ hybridisation (FISH) was used to estimate frequencies of copy number changes of known oncogenes, including HER2, TOPO2A, CCND1, EGFR and C-MYC. RESULTS: Using FISH, amplifications were mostly low level (gene-to-centromere ratio 2 to 4), which is in contrast with other tumour types with more frequent gene amplifications. The amplifications were particularly frequent for MYC (Saudi 9% and Swiss 14.2%) but unrelated to clinical outcome and pathological information. Remarkably, there were four tumours exhibiting classic high-level gene amplification for HER2 (Swiss 1.3%), a pattern often accompanied by response to trastuzumab (Herceptin) in breast cancer. Occasional high-level amplifications were also observed for CCND1 (Saudi 1/106, 0.9%; Swiss 2/373, 0.5%) and EGFR (Swiss 2/355; 0.6%). CONCLUSIONS: Rare high-level amplifications of therapeutic target genes were found in patients with colon cancer. Although no molecular differences were found between incidences of colon cancer cases in Swiss and Saudi populations, these observations emphasise the urgent need for clinical studies investigating the effect of targeted therapies.

AB - AIM: Recent studies had suggested substantial molecular differences between tumours from different ethnic groups. In this study, the molecular differences between the incidences of colorectal carcinoma in Saudi and Swiss populations are investigated. Method: 518 cases of colon cancer tumours (114 from Saudi Arabia and 404 from Switzerland) were analysed in a tissue microarray format. Fluorescence in situ hybridisation (FISH) was used to estimate frequencies of copy number changes of known oncogenes, including HER2, TOPO2A, CCND1, EGFR and C-MYC. RESULTS: Using FISH, amplifications were mostly low level (gene-to-centromere ratio 2 to 4), which is in contrast with other tumour types with more frequent gene amplifications. The amplifications were particularly frequent for MYC (Saudi 9% and Swiss 14.2%) but unrelated to clinical outcome and pathological information. Remarkably, there were four tumours exhibiting classic high-level gene amplification for HER2 (Swiss 1.3%), a pattern often accompanied by response to trastuzumab (Herceptin) in breast cancer. Occasional high-level amplifications were also observed for CCND1 (Saudi 1/106, 0.9%; Swiss 2/373, 0.5%) and EGFR (Swiss 2/355; 0.6%). CONCLUSIONS: Rare high-level amplifications of therapeutic target genes were found in patients with colon cancer. Although no molecular differences were found between incidences of colon cancer cases in Swiss and Saudi populations, these observations emphasise the urgent need for clinical studies investigating the effect of targeted therapies.

M3 - SCORING: Zeitschriftenaufsatz

VL - 60

SP - 768

EP - 772

JO - J CLIN PATHOL

JF - J CLIN PATHOL

SN - 0021-9746

IS - 7

M1 - 7

ER -