scholarly journals Low Level ofHer-2Locus Amplification by Fluorescent In Situ Hybridization Does Not Correlate with Her-2 Protein Overexpression by Immunohistochemistry in Barrett's Esophagus

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Agnieszka M. Rygiel ◽  
Francesca Milano ◽  
Fiebo J. ten Kate ◽  
Jacques J. G. H. M. Bergman ◽  
Kausillia K. Krishnadath
Keyword(s):  
In Situ Hybridization ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Fluorescent In Situ Hybridization ◽  
Chromosome 17 ◽  
Protein Overexpression ◽  
Therapeutic Implications ◽  
Low Level ◽  
Her 2

An accurate evaluation of theHer-2status has important prognostic and therapeutic implications in many carcinomas. The aim of the study was to correlateHer-2locus (17q11.2) amplification and chromosome 17 gains as assessed by fluorescent in situ hybridization (FISH) with Her-2 protein overexpression by immunohistochemistry (IHC) in patients with Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). We analyzed 34 patients withHer-2amplification and/or chromosome 17gains using FISH on brush cytology specimens. Seven patients (21%) showed highHer-2locus amplification (Her-2: Cep17≥5 : 1), 5 (15%) showed lowHer-2locus amplification (Her-2: Cep17≥2<5 : 1), and 22 (65%) displayed gains of chromosome 17 only. Further, we confirmedHer-2amplification on corresponding biopsies that were taken at the same occasion as the cytologybrushings. Then, we compared the FISH results with IHC data obtained from the corresponding biopsies and showed that low level of Her-2 amplification does not correlate with Her-2 protein overexpression (score+3/+2;P=1), in contrast to the high amplification level (P=.001). Thus, in our population of BE and EAC patients, low level ofHer-2amplification does not result in detectable level of Her-2 protein as assessed by IHC.

Aneuploidies of chromosome 17 in breast cancer: Relative prevalence in a series of 170 patients from Córdoba, Argentina, studied with fluorescent in-situ hybridization (FISH)

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e22195-e22195
Author(s):  
A. Sturich ◽  
P. Calafat ◽  
M. Botterón ◽  
A. Borello ◽  
A. Diller ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Fluorescent In Situ Hybridization ◽  
Clinical Effect ◽  
Immunohistochemical Analysis ◽  
Chromosome 17 ◽  
Fish Technique ◽  
Polysomy 17 ◽  
Her 2 ◽  
Relative Prevalence

e22195 Background: The amplification of HER-2 oncogen, located in 17q11.2–12, occurs in 20–30% of invasive breast cancer. Numerical anomalies of chromosome 17 are frequent findings in these patients, during the study of the amplification of HER-2 oncogen with FISH technique, though clinical implications are yet not defined. Objectives: To determine the presence of chromosome 17 aneuploidies in a series of patients with histological diagnosis of breast cancer and to correlate these data with amplification and overexpression of HER-2 oncogen. Methods: Samples of 170 patients included in paraffin were analyzed with FISH technique, using the PathVysion system. We analyzed the number of HER-2 oncogen specific signals and chromosome 17 centromere (CEP 17) signals. We followed the ASCO 2007 guidelines to evaluate FISH and immunohistochemical analysis (IHC). Criteria for aneuploidy: diploid at 1.5–2.25 average CEP 17 signals /cell; hyperdiploidy: values over 2.25 and hypodiploidy: lower than 1.5. Results: We found 73 cases of chromosome 17 aneuploidies (42.9%), 68/73 polysomies (93%) and 5/73 monosomies (7%). The monosomies were observed in 4/5 patients with HER-2 amplification. Polysomies occurred simultaneously with HER-2 amplification in 48% (35/73), 45% (33/73) were not amplified and 7% (5/73) were equivocal. FISH and IHC could be correlated in 136 patients: the higher percentage of polysomies observed corresponded to groups IHC+3/HER-2+ (46%) and IHC+2/HER- (29%). Polysomy 17 was detected in 3 cases IHC+3/HER-2-. Conclusions: The relative prevalence of chromosome 17 aneuploidy in our series was 43%. According to the literature, this finding in 3 patients IHC+3/HER-2- could be responsible for the overexpression of protein cerbB2. The clinical effect of chromosome 17 aneuploidy continues under study. No significant financial relationships to disclose.

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