scholarly journals ERBB2 gene amplification increases during the transition of proximal EGFR+ to distal HLA-G+ first trimester cell column trophoblasts

Placenta ◽  
2015 ◽  
Vol 36 (8) ◽  
pp. 803-808 ◽  
Author(s):  
G. Meinhardt ◽  
S. Kaltenberger ◽  
C. Fiala ◽  
M. Knöfler ◽  
J. Pollheimer
Keyword(s):  
Gene Amplification ◽  
First Trimester ◽  
Cell Column ◽  
Erbb2 Gene

The characterization of ERBB family mutations in Chinese biliary tract cancers.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e15595-e15595
Author(s):  
Tianqiang Song ◽  
Wei Zhang ◽  
Huikai Li ◽  
Ping Chen ◽  
Xiaoqian Chen ◽  
...  
Keyword(s):  
Gene Amplification ◽  
Biliary Tract ◽  
Copy Number Variations ◽  
High Rate ◽  
Chinese Patients ◽  
Common Mutation ◽  
Biliary Tract Cancers ◽  
Erbb Family ◽  
Erbb2 Gene ◽  
Major Mutation

e15595 Background: Next generation sequencing has been applied to identify actionable mutations in biliary tract cancers (BTCs). ERBB family genes, especially ERBB2 and ERBB3, serve as effective biomarkers for BTCs targeted therapy as shown in MyPathway and SUMMIT clinical trials. However, the distribution and major mutation types of ERBB family genes were not clear in Chinese BTC patients. Methods: Deep sequencing targeting 450 cancer genes was performed on FFPE and matching blood samples collected from a cohort of 716 Chinese BTC patients. Genomic alterations including single nucleotide variations (SNV), short and long insertions/deletions (Indels), copy number variations, gene rearrangements and fusions were analyzed. Results: A total of 14% (101/716) of patients with a median age of 62 years old, including 45 males and 56 females, were identified harboring ERBB family mutations. Somatic ERBB family mutations occurred with a rate of 29% in gallbladder carcinoma (GBCA), 13% in extrahepatic cholangiocarcinoma (EHCCA), 12% in hilar cholangiocarcinoma (HCCA) and 8% in intrahepatic cholangiocarcinoma (IHCCA). No germline mutation was detected. A high rate of ERBB2 gene amplification was observed in GBCA (17%). In IHCCA and EHCCA, SNV/Indel accounted for 3% and 5%, respectively, and was the major variation in ERBB2. In HCCA, SNV/Indel was the most common mutation in ERBB3 (8%). In BTC patients, TP53 (81%) and CDK12 (36%) were the top-ranked co-mutant genes with ERBB2. The mutant frequency of CDK12 was significantly different between patients with or without an ERBB2 mutation ( p< 0.001). ERBB2 S310F/Y, ERBB3 V104L/M were hotspot mutations within the ERBB family in BTCs. Conclusions: ERBB family mutations were detected in 14% of Chinese BTC patients. Similar to Western populations (PMID: 27622582), ERBB2 gene amplification was the most common mutation in GBCA in Chinese patients. Unlike ERBB2/ ERBB3 amplification which has been reported as the major mutation in previous studies, our study of other BTC types revealed ERBB2/ ERBB3 SNV/Indel as the major mutation. BTC patients harboring ERBB family mutations have the potential to benefit from pan-HER inhibitors.

scholarly journals 26. Prognostic value of c-erbB2 gene amplification detected in archival human breast carcinomas by quantitative differential PCR

The Breast ◽  
1996 ◽  
Vol 5 (3) ◽  
pp. 167
Author(s):  
H.G. Schniirch ◽  
H.X. An ◽  
D. Niederacher ◽  
S.I. Dominik ◽  
S. Scharl ◽  
...  
Keyword(s):  
Gene Amplification ◽  
Prognostic Value ◽  
Breast Carcinomas ◽  
Human Breast ◽  
Erbb2 Gene ◽  
Human Breast Carcinomas

Detection of c-erbB2 gene amplification in 195 archival human breast carcinomas by the quantitative differential PCR

1995 ◽  
Vol 121 (S1) ◽  
pp. A33-A33
Author(s):  
C. R. C. van Roeyen ◽  
M. W. Beckman ◽  
H X An ◽  
F. Picard ◽  
D. Niederacher
Keyword(s):  
Gene Amplification ◽  
Breast Carcinomas ◽  
Human Breast ◽  
Erbb2 Gene ◽  
Human Breast Carcinomas

AP-1 Transcription Factors c-FOS and c-JUN Mediate GnRH-Induced Cadherin-11 Expression and Trophoblast Cell Invasion

Endocrinology ◽  
2015 ◽  
Vol 156 (6) ◽  
pp. 2269-2277 ◽  
Author(s):  
Bo Peng ◽  
Hua Zhu ◽  
Liyang Ma ◽  
Yan-ling Wang ◽  
Christian Klausen ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Cell Invasion ◽  
Gnrh Antagonist ◽  
First Trimester ◽  
Nuclear Accumulation ◽  
Activator Protein 1 ◽  
Cell Column ◽  
Protein Levels ◽  
Extravillous Cytotrophoblasts ◽  
Interfering Rna

Abstract GnRH is expressed in first-trimester human placenta and increases cell invasion in extravillous cytotrophoblasts (EVTs). Invasive phenotypes have been reported to be regulated by transcription factor activator protein 1 (AP-1) and mesenchymal cadherin-11. The aim of our study was to investigate the roles of AP-1 components (c-FOS/c-JUN) and cadherin-11 in GnRH-induced cell invasion in human EVT cells. Phosphorylated c-FOS and phosphorylated c-JUN were detected in the cell column regions of human first-trimester placental villi by immunohistochemistry. GnRH treatment increased c-FOS, c-JUN, and cadherin-11 mRNA and protein levels in immortalized EVT (HTR-8/SVneo) cells. Moreover, GnRH treatment induced c-FOS and c-JUN protein phosphorylation and nuclear accumulation. Pretreatment with antide, a GnRH antagonist, attenuated GnRH-induced cadherin-11 expression. Importantly, basal and GnRH-induced cadherin-11 expression and cell invasion were reduced by small interfering RNA-mediated knockdown of c-FOS, c-JUN, and cadherin-11 in HTR-8/SVneo cells. Our results suggest that GnRH induces the expression and phosphorylation of the AP-1 transcription factors c-FOS and c-JUN in trophoblast cells, which contributes to GnRH-induced elevation of cadherin-11 expression and cell invasion.

Association of c-erbB2-gene amplification with poor prognosis in non-inflammatory breast carcinomas but not in carcinomas of the inflammatory type

1994 ◽  
Vol 58 (6) ◽  
pp. 763-768 ◽  
Author(s):  
Monique G. Lě ◽  
Sétha Douc-Rasy ◽  
Jean Charles Ahomadegbe ◽  
Marc Spielmann ◽  
Martine Guérin ◽  
...  
Keyword(s):  
Gene Amplification ◽  
Poor Prognosis ◽  
Breast Carcinomas ◽  
Erbb2 Gene

scholarly journals Liquid-Based Fluorescence In Situ Hybridization Assay for Detection of ERBB2 Gene Amplification in Patients with Breast Cancer3

2008 ◽  
Vol 54 (11) ◽  
pp. 1831-1839
Author(s):  
Chen-Hsiung Yeh ◽  
William A Whitmire ◽  
Maher Albitar
Keyword(s):  
Breast Cancer ◽  
Flow Cytometry ◽  
In Situ Hybridization ◽  
Gene Amplification ◽  
Ffpe Tissue ◽  
Breast Cancer Patients ◽  
Serum Samples ◽  
Erbb2 Gene ◽  
Erbb2 Amplification

Abstract Background: Current reference methods for evaluating gene amplification and expression of ERBB2 (also known as HER-2)—cell-based fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC)—are subjective and influenced by methods of tissue preparation and fixation. We developed and evaluated a novel, quantitative liquid-based FISH (L-FISH) assay that uses flow cytometry to detect ERBB2 gene amplification in breast cancer patients. Methods: DNA was extracted from serum or tissue, biotinylated, hybridized to differentially labeled probes for ERBB2 and a chromosome 17–specific single-copy sequence (17-SSC), and immobilized to streptavidin-coated microspheres. The ERBB2/17-SSC signal ratio measured by flow cytometry was used to evaluate ERBB2 amplification. We used L-FISH to test 122 stored formalin-fixed, paraffin-embedded (FFPE) tissue samples and 22 serum samples from randomly selected breast cancer patients; results were compared with those obtained with conventional FISH and IHC. Results: The inter- and intraassay imprecisions were 3.7%–18.9% for FFPE tissue and 2.8%–6.3% for serum. Overall, L-FISH analyses of FFPE tissues demonstrated 84.4% concordance with results obtained with conventional FISH (P &lt; 0.001) and 78.8% concordance with IHC results (P &lt; 0.001). L-FISH analyses of serum samples showed 91% concordance with tissue-based IHC/FISH results (P = 0.038). Conclusions: Our data indicate that this PCR-free L-FISH method can be used to evaluate ERBB2 amplification in both cell-containing (paraffin-embedded tissue) and cell-free (serum) samples. This approach provides more objective results and is amenable to automation and quantitative measurement.

Sign in / Sign up

Export Citation Format

Share Document