Detection of HER-2/neu gene amplification in breast carcinomas using quantitative real-time PCR — A comparison with immunohistochemical and FISH results

2006 ◽  
Vol 12 (4) ◽  
pp. 197-204 ◽  
Author(s):  
Janina Kulka ◽  
Anna-Mária Tokés ◽  
Pál Kaposi-Novák ◽  
Nóra Udvarhelyi ◽  
Anikó Keller ◽  
...  
Keyword(s):  
Real Time ◽  
Gene Amplification ◽  
Real Time Pcr ◽  
Breast Carcinomas ◽  
Quantitative Real Time Pcr ◽  
Her 2

scholarly journals Comparing MicroRNA Profilings of Purified HER-2-Negative and HER-2-Positive Cells Validates miR-362-5p/Sema3A as Characteristic Molecular Change in Triple-Negative Breast Cancers

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Xiaoqing Zhang ◽  
Qi He ◽  
Leiqin Sun ◽  
Yanfei Zhang ◽  
Shengying Qin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Expression ◽  
Real Time ◽  
Differential Expression ◽  
Real Time Pcr ◽  
Therapeutic Target ◽  
Triple Negative ◽  
Quantitative Real Time Pcr ◽  
Her 2 ◽  
Tnbc Subtype

Background. HER-2 is a key molecule serving as the therapeutic target, prognostic biomarker, and classification marker in breast cancer. Accurate microRNA profilings had not been conducted in purified tumor cells of HER-2-negative and HER-2-positive tissue specimens obtained from breast cancer patients. Methods. (i) Differential expression microRNA discovery using laser capture microdissection- (LCM-) assisted specimen preparation and microRNA array chips on HER-2 overexpressing and triple-negative breast carcinoma (TNBC) subtype tissues, (ii) differential expression microRNA validation by quantitative real-time PCR, and (iii) independent validation on tissue microarray. Results. Five microRNAs (miR-20a-5p, miR-221-3p, miR-362-5p, miR-502-3p, and miR-222-3p) were screened and validated as upregulated microRNAs in TNBC cells comparing to HER-2 overexpressing cells using a microRNA array (5 cases in each group) and quantitative real-time PCR (20 cases in each group). The expression difference of miR-362-5p had the most significant statistical significance (p=0.0016) among the five microRNAs. The expression of miR-362-5p and its target gene Sema3A was further analyzed using in situ hybridization (ISH) and immunohistochemistry on standard tissue sections (n=150). 70.8% of HER-2-negative cells showed moderate expression of miR-362-5p whereas 20.4% HER-2-negative cells correlated with strong expression of miR-362-5p (p<0.0001). The proportion of patients with moderate/strong miR-362-5p expression in luminal, HER-2 overexpressing, and TNBC subtypes were 53.2%, 22.2%, and 74.3%, respectively (p=0.0002). High miR-362-5p expressers had shorter overall survival in the univariate analysis (p=0.046). There was a significant negative correlation between miR-362-5p and Sema3A expression (p<0.0001). The patients with negative/weak Sema3A protein expression had poorer prognosis than those with moderate (HR: 3.723, p=0.021) or strong (HR: 3.966, p=0.013) Sema3A protein expression in the multivariate analysis. Conclusions. miR-362-5p/Sema3A might provide a promising therapeutic pathway and represents a candidate therapeutic target of the TNBC subtype.

The prognostic impact of EGFR, ErbB2 and MET gene amplification in human gastric carcinomas as measured by quantitative Real-Time PCR

2015 ◽  
Vol 141 (11) ◽  
pp. 1945-1952 ◽  
Author(s):  
Ghasem Janbabai ◽  
Ziaeddin Oladi ◽  
Touraj Farazmandfar ◽  
Tarang Taghvaei ◽  
Farshad Naghshvar
Keyword(s):  
Real Time ◽  
Gene Amplification ◽  
Real Time Pcr ◽  
Prognostic Impact ◽  
Quantitative Real Time Pcr ◽  
Gastric Carcinomas

Preoperative assessment of HER-2/neu status in breast carcinoma: The role of quantitative real-time PCR on core-biopsy specimens

2010 ◽  
Vol 116 (2) ◽  
pp. 234-239 ◽  
Author(s):  
Tommaso Susini ◽  
Cecilia Bussani ◽  
Giulia Marini ◽  
Jacopo Nori ◽  
Simone Olivieri ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Real Time ◽  
Real Time Pcr ◽  
Core Biopsy ◽  
Preoperative Assessment ◽  
Quantitative Real Time Pcr ◽  
Biopsy Specimens ◽  
Her 2

HER-2 DNA quantification of paraffin-embedded breast carcinomas with LightCycler real-time PCR in comparison to immunohistochemistry and chromogenic in situ hybridization

2006 ◽  
Vol 39 (9) ◽  
pp. 942-946 ◽  
Author(s):  
Maria Ntoulia ◽  
Loukas Kaklamanis ◽  
Christos Valavanis ◽  
Maria Kafousi ◽  
Efstathios Stathopoulos ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Real Time ◽  
Real Time Pcr ◽  
Dna Quantification ◽  
Breast Carcinomas ◽  
Her 2 ◽  
Chromogenic In Situ Hybridization

Detection of Gene Amplification in Intraductal and Infiltrating Breast Cancer by Laser-Assisted Microdissection and Quantitative Real-Time PCR

Pathobiology ◽  
2000 ◽  
Vol 68 (4-5) ◽  
pp. 173-179 ◽  
Author(s):  
Sabine Glöckner ◽  
Ulrich Lehmann ◽  
Nadine Wilke ◽  
Wolfram Kleeberger ◽  
Florian Länger ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Real Time ◽  
Gene Amplification ◽  
Real Time Pcr ◽  
Quantitative Real Time Pcr

scholarly journals KLK11 promotes the activation of mTOR and protein synthesis to facilitate cardiac hypertrophy

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yi Wang ◽  
Hongjuan Liao ◽  
Yueheng Wang ◽  
Jinlin Zhou ◽  
Feng Wang ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Western Blot ◽  
Real Time ◽  
Real Time Pcr ◽  
Mtor Signaling ◽  
Heart Weight ◽  
Cardiomyocyte Hypertrophy ◽  
Quantitative Real Time Pcr

Abstract Background Cardiovascular diseases have become the leading cause of death worldwide, and cardiac hypertrophy is the core mechanism underlying cardiac defect and heart failure. However, the underlying mechanisms of cardiac hypertrophy are not fully understood. Here we investigated the roles of Kallikrein 11 (KLK11) in cardiac hypertrophy. Methods Human and mouse hypertrophic heart tissues were used to determine the expression of KLK11 with quantitative real-time PCR and western blot. Mouse cardiac hypertrophy was induced by transverse aortic constriction (TAC), and cardiomyocyte hypertrophy was induced by angiotensin II. Cardiac function was analyzed by echocardiography. The signaling pathway was analyzed by western blot. Protein synthesis was monitored by the incorporation of [3H]-leucine. Gene expression was analyzed by quantitative real-time PCR. Results The mRNA and protein levels of KLK11 were upregulated in human hypertrophic hearts. We also induced cardiac hypertrophy in mice and observed the upregulation of KLK11 in hypertrophic hearts. Our in vitro experiments demonstrated that KLK11 overexpression promoted whereas KLK11 knockdown repressed cardiomyocytes hypertrophy induced by angiotensin II, as evidenced by cardiomyocyte size and the expression of hypertrophy-related fetal genes. Besides, we knocked down KLK11 expression in mouse hearts with adeno-associated virus 9. Knockdown of KLK11 in mouse hearts inhibited TAC-induced decline in fraction shortening and ejection fraction, reduced the increase in heart weight, cardiomyocyte size, and expression of hypertrophic fetal genes. We also observed that KLK11 promoted protein synthesis, the key feature of cardiomyocyte hypertrophy, by regulating the pivotal machines S6K1 and 4EBP1. Mechanism study demonstrated that KLK11 promoted the activation of AKT-mTOR signaling to promote S6K1 and 4EBP1 pathway and protein synthesis. Repression of mTOR with rapamycin blocked the effects of KLK11 on S6K1 and 4EBP1 as well as protein synthesis. Besides, rapamycin treatment blocked the roles of KLK11 in the regulation of cardiomyocyte hypertrophy. Conclusions Our findings demonstrated that KLK11 promoted cardiomyocyte hypertrophy by activating AKT-mTOR signaling to promote protein synthesis.

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