Reliability of chromogenic in situ hybridization for epidermal growth factor receptor gene copy number detection in non-small-cell lung carcinomas: A comparison with fluorescence in situ hybridization study

Yoo, Seol Bong; Lee, Hyun Ju; Park, Jung Ok; Choe, Gheeyoung; Chung, Doo Hyun; Seo, Jeong‐Wook; Chung, Jin-Haeng

doi:10.1016/j.lungcan.2009.05.002

Cited by 23 publications

(24 citation statements)

References 9 publications

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“…Although a high correlation between EGFR FISH and CISH analyses has been shown,11 12 the success rate of FISH was 100% in both years (in total 150 results), but for CISH the success rate was 67% (34 /51) in 2008 and 95% (37/39) in 2009 (see table 6). The low success rate for ISH in 2008 was largely due to a single laboratory (with a success rate of 24%) that had just begun to use EGFR ISH.…”

Section: Discussionmentioning

confidence: 93%

“…For gene copy number changes, fluorescence in-situ hybridisation (FISH) analysis was preferred, as true amplification of the EGFR gene in NSCLC is less frequent as polysomy. Since then, high correlation between EGFR FISH and chromogenic in-situ hybridisation (CISH) analysis has been shown 11 12. For colorectal cancer, a norm for mutation analysis has been published recently,13 and the required level of minimum performance was based on arbitrary grounds.…”

Section: Introductionmentioning

confidence: 99%

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EGFR and KRAS quality assurance schemes in pathology: generating normative data for molecular predictive marker analysis in targeted therapy

et al. 2011

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EGFR and KRAS quality assurance schemes in pathology: generating normative data for molecular predictive marker analysis in targeted therapy Thunnissen, E.; Bovée, J.V.M.G.; Bruinsma, H.; van den Brule, A.J.C.; Dinjens, W.; Heideman, D.A.M.; Meulemans, E.; Nederlof, P.; van Noesel, C.; Prinsen, C.F.M.; Scheidel, K.; van de Ven, P.M.; de Weger, R.; Schuuring, E.; Ligtenberg, M. Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible.

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

EGFR and KRAS quality assurance schemes in pathology: generating normative data for molecular predictive marker analysis in targeted therapy

et al. 2011

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“…EGFR is composed of 28 exons and is located on the short arm of chromosome 7. EGFR has been shown to be widely distributed in the membranes of epidermal cells and is composed of three regions that include the intracellular, transmembrane, and extracellular domains (Yoo et al, 2010). EGFR has mainly been implicated in the following four signaling pathways: JAK-STAT, PI3K-PDK, PLC-γ, and RAS-RAF-MEK-ERK-MAPK (Qi et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Comparison of EGFR mutation rates in lung adenocarcinoma tissue and pleural effusion samples

Guan

Wang

et al. 2016

Genet. Mol. Res.

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ABSTRACT.The goal of the current study was to investigate the differences in epidermal growth factor receptor (EGFR) mutation rates in tumor tissue and pleural effusion specimens from patients with lung adenocarcinoma. PCR amplification and gene sequencing were used to detect EGFR mutations in exons 18, 19, 20, and 21 in tumor tissue and pleural effusion samples from 50 patients with advanced lung adenocarcinoma. The EGFR mutation rate was 34.0% in tissue samples from patients with advanced lung adenocarcinoma. There were 11 cases with exon 19 mutations and 6 cases with exon 21 mutations. The EGFR mutation rate was 30.0% in pleural effusion specimens, including 10 cases with exon 19 mutation and 5 cases with exon 21 mutations. Although the tissue samples had a slightly higher mutation rate compared to the pleural effusion samples, the difference was not statistically significant. These results indicate that the EGFR mutation rate detected in pleural effusion specimens from patients with advanced lung adenocarcinoma is similar to that detected in tumor tissue samples. Therefore, pleural effusion specimens can potentially be used for EGFR mutation detection in advanced lung adenocarcinoma.

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“…The TMA blocks were manufactured from the most representative areas of individual paraffin blocks, as previously described (Superbiochips Laboratories, Seoul, Korea) (Yoo et al , 2010). Briefly, the representative tumour area was selected by two experienced pulmonary pathologists (HK and SBY), and the single core of 2 mm in diameter for each case was taken to TMA block.…”

Section: Methodsmentioning

confidence: 99%

Clinicopathologic and prognostic significance of c-MYC copy number gain in lung adenocarcinomas

Yuan

Kim

et al. 2014

Br J Cancer

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Background:c-MYC copy number gain (c-MYC gain) has been associated with aggressive behaviour in several cancers. However, the role of c-MYC gain has not yet been determined in lung adenocarcinomas classified by genetic alterations in epidermal growth factor receptor (EGFR), KRAS, and anaplastic lymphoma kinase (ALK) genes. We investigated the clinicopathologic and prognostic significance of c-MYC gain for disease-free survival (DFS) and overall survival (OS) according to EGFR, KRAS, and ALK gene status and stages in lung adenocarcinomas.Methods:In 255 adenocarcinomas resected in Seoul National University Bundang Hospital from 2003 to 2009, fluorescence in situ hybridisation (FISH) with c-MYC probe and centromeric enumeration probe 8 (CEP8) was analysed using tissue microarray containing single representative core per each case. EGFR (codon 18 to 21) and KRAS (codon 12, 13, and 61) mutations were analysed by polymerase chain reaction and direct sequencing method from formalin-fixed, paraffin-embedded tissue sections. ALK rearrangement was determined by FISH method. c-MYC gain was defined as >2 copies per nucleus, chromosome 8 gain as ⩾3 copies per nucleus, and gain of c-MYC:CEP8 ratio (hereafter, c-MYC amplification) as ⩾2.Results:We observed c-MYC gain in 20% (51 out of 255), chromosome 8 gain in 5.5% (14 out of 255), c-MYC amplification in 2.4% (6 out of 255), EGFR mutation in 49.4% (118 out of 239), KRAS mutation in 5.7% (7 out of 123), and ALK rearrangement in 4.9% (10 out of 205) of lung adenocarcinomas. c-MYC gain was observed in 19% (22 out of 118) of patients with lung adenocarcinomas with an EGFR mutation, but not in any patients with a KRAS mutation, or an ALK rearrangement. c-MYC gain (but not chromosome 8 gain or c-MYC amplification) was an independent poor-prognostic factor in the full cohort of lung adenocarcinoma (P=0.022, hazard ratio (HR)=1.71, 95% confidence interval (CI), 1.08–2.69 for DFS; P=0.032, HR=2.04, 95% CI, 1.06–3.91 for OS), as well as in stage I subgroup (P=0.023, HR=4.70, 95% CI, 1.24–17.78 for DFS; P=0.031, HR=4.65, 95% CI, 1.15–18.81 for OS), and in EGFR-mutant subgroup (P=0.022; HR=2.14; 95% CI, 1.11–4.10 for DFS).Conclusions:c-MYC gain (but not chromosome 8 gain or c-MYC amplification) was an independent poor-prognostic factor for DFS and OS in lung adenocarcinomas, both in full cohort and stage I cancer, and possibly for DFS in EGFR-mutant adenocarcinomas. Additional studies are required to determine if patients with lung adenocarcinoma with c-MYC gain are candidates for additional first-line treatment to mitigate their increased risk for disease progression and death.

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Reliability of chromogenic in situ hybridization for epidermal growth factor receptor gene copy number detection in non-small-cell lung carcinomas: A comparison with fluorescence in situ hybridization study

Cited by 23 publications

References 9 publications

EGFR and KRAS quality assurance schemes in pathology: generating normative data for molecular predictive marker analysis in targeted therapy

EGFR and KRAS quality assurance schemes in pathology: generating normative data for molecular predictive marker analysis in targeted therapy

Comparison of EGFR mutation rates in lung adenocarcinoma tissue and pleural effusion samples

Clinicopathologic and prognostic significance of c-MYC copy number gain in lung adenocarcinomas

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