scholarly journals High EGFR gene copy number predicts poor outcome in triple-negative breast cancer

2014 ◽  
Vol 27 (9) ◽  
pp. 1212-1222 ◽  
Author(s):  
Heae Surng Park ◽  
Min Hye Jang ◽  
Eun Joo Kim ◽  
Hyun Jeong Kim ◽  
Hee Jin Lee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Copy Number ◽  
Triple Negative ◽  
Gene Copy Number ◽  
Gene Copy ◽  
Egfr Gene ◽  
Poor Outcome

Abstract 2396: High EGFR gene copy number predicts poor outcome in triple-negative breast cancer.

2013 ◽  
Author(s):  
Heae Surng Park ◽  
Min Hye Jang ◽  
Eun Joo Kim ◽  
Hyun Jeong Kim ◽  
Hee Jin Lee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Copy Number ◽  
Triple Negative ◽  
Gene Copy Number ◽  
Gene Copy ◽  
Egfr Gene ◽  
Poor Outcome

scholarly journals Spectrum of EGFR Gene Copy Number Changes and KRAS Gene Mutation Status in Korean Triple Negative Breast Cancer Patients

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e79014 ◽  
Author(s):  
Yoonjung Kim ◽  
Juwon Kim ◽  
Hy-De Lee ◽  
Joon Jeong ◽  
Woochang Lee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Copy Number ◽  
Triple Negative ◽  
Gene Copy Number ◽  
Gene Copy ◽  
Breast Cancer Patients ◽  
Kras Gene ◽  
Mutation Status ◽  
Egfr Gene ◽  
Copy Number Changes

scholarly journals Importance of Copy Number Alterations of FGFR1 and C-MYC Genes in Triple Negative Breast Cancer

2018 ◽  
Vol 0 (0) ◽  
Author(s):  
Milica Nedeljković ◽  
Nikola Tanić ◽  
Tatjana Dramićanin ◽  
Zorka Milovanović ◽  
Snežana Šušnjar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Prognostic Marker ◽  
Triple Negative Breast Cancer ◽  
Copy Number ◽  
Triple Negative ◽  
Clinical Course ◽  
Copy Number Gain ◽  
Gene Copy ◽  
Copy Number Alterations ◽  
The Impact

Summary Background: Triple negative breast cancer (TNBC) is characterized by aggressive clinical course and is unresponsive to anti-HER2 and endocrine therapy. TNBC is difficult to treat and is often lethal. Given the need to find new targets for therapy we explored clinicopathological significance of copy number gain of FGFR1 and c-MYC. Our aim was to determine the impact of FGFR1 and c-MYC copy number gain on clinical course and outcome of TNBC. Methods: FGFR1 and c-MYC gene copy number alterations were evaluated in 78 archive TNBC samples using TaqMan based quantitative real time PCR assays. Results: 50% of samples had increased c-MYC copy number. c-MYC copy number gain was associated with TNBC in contrast to ER positive cancers. Our results showed significant correlation between c-MYC copy number gain and high grade of TNBCs. This suggests that c-MYC copy number could be an useful prognostic marker for TNBC patients. c-MYC copy number gain was associated with high pTNM stage as well as lobular and medullary tumor subtypes. 43% of samples had increased FGFR1 copy number. No correlations between FGFR1 copy number gain and clinicopathological variables were observed. Conclusions: We identified c-MYC copy number gain as a prognostic marker for TNBC. Our results indicate that c- MYC may contribute to TNBC progression. We observed no significant association between c-MYC and/or FGFR1 copy number status and patient survival.

scholarly journals Importance of Copy Number Alterations of FGFR1 and C-MYC Genes in Triple Negative Breast Cancer

2019 ◽  
Vol 38 (1) ◽  
pp. 63-70
Author(s):  
Milica Nedeljković ◽  
Nikola Tanić ◽  
Tatjana Dramićanin ◽  
Zorka Milovanović ◽  
Snežana Šušnjar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Prognostic Marker ◽  
Triple Negative Breast Cancer ◽  
Copy Number ◽  
Triple Negative ◽  
Clinical Course ◽  
Copy Number Gain ◽  
Gene Copy ◽  
Copy Number Alterations ◽  
The Impact

Summary Background: Triple negative breast cancer (TNBC) is characterized by aggressive clinical course and is unresponsive to anti-HER2 and endocrine therapy. TNBC is difficult to treat and is often lethal. Given the need to find new targets for therapy we explored clinicopathological significance of copy number gain of FGFR1 and c-MYC. Our aim was to determine the impact of FGFR1 and c-MYC copy number gain on clinical course and outcome of TNBC. Methods: FGFR1 and c-MYC gene copy number alterations were evaluated in 78 archive TNBC samples using TaqMan based quantitative real time PCR assays. Results: 50% of samples had increased c-MYC copy number. c-MYC copy number gain was associated with TNBC in contrast to ER positive cancers. Our results showed significant correlation between c-MYC copy number gain and high grade of TNBCs. This suggests that c-MYC copy number could be an useful prognostic marker for TNBC patients. c-MYC copy number gain was associated with high pTNM stage as well as lobular and medullary tumor subtypes. 43% of samples had increased FGFR1 copy number. No correlations between FGFR1 copy number gain and clinicopathological variables were observed. Conclusions: We identified c-MYC copy number gain as a prognostic marker for TNBC. Our results indicate that c- MYC may contribute to TNBC progression. We observed no significant association between c-MYC and/or FGFR1 copy number status and patient survival.

Correlation of efficacy between EGFR gene copy number and lapatinib/capecitabine therapy in HER2-positive metastatic breast cancer.

2010 ◽  
Vol 28 (15_suppl) ◽  
pp. 1059-1059 ◽  
Author(s):  
A. Fabi ◽  
A. Di Benedetto ◽  
R. Merola ◽  
G. Metro ◽  
M. Mottolese ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Copy Number ◽  
Gene Copy Number ◽  
Metastatic Breast ◽  
Gene Copy ◽  
Her2 Positive ◽  
Egfr Gene

scholarly journals Nongenotoxic ABCB1 activator tetraphenylphosphonium can contribute to doxorubicin resistance in MX-1 breast cancer cell line

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Raimonda Kubiliute ◽  
Indre Januskeviciene ◽  
Ruta Urbanaviciute ◽  
Kristina Daniunaite ◽  
Monika Drobniene ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Protein Level ◽  
Copy Number ◽  
Gene Copy Number ◽  
Gene Copy ◽  
Common Mechanism ◽  
Dna Hypomethylation ◽  
Mesenchymal Transition ◽  
Molecular Features

AbstractHyperactivation of ABC transporter ABCB1 and induction of epithelial–mesenchymal transition (EMT) are the most common mechanism of acquired cancer chemoresistance. This study describes possible mechanisms, that might contribute to upregulation of ABCB1 and synergistically boost the acquisition of doxorubicin (DOX) resistance in breast cancer MX-1 cell line. DOX resistance in MX-1 cell line was induced by a stepwise increase of drug concentration or by pretreatment of cells with an ABCB1 transporter activator tetraphenylphosphonium (TPP+) followed by DOX exposure. Transcriptome analysis of derived cells was performed by human gene expression microarrays and by quantitative PCR. Genetic and epigenetic mechanisms of ABCB1 regulation were evaluated by pyrosequencing and gene copy number variation analysis. Gradual activation of canonical EMT transcription factors with later activation of ABCB1 at the transcript level was observed in DOX-only treated cells, while TPP+ exposure induced considerable activation of ABCB1 at both, mRNA and protein level. The changes in ABCB1 mRNA and protein level were related to the promoter DNA hypomethylation and the increase in gene copy number. ABCB1-active cells were highly resistant to DOX and showed morphological and molecular features of EMT. The study suggests that nongenotoxic ABCB1 inducer can possibly accelerate development of DOX resistance.

scholarly journals Chromosomal Instability Selects Gene Copy-Number Variants Encoding Core Regulators of Proliferation in ER+ Breast Cancer

2014 ◽  
Vol 74 (17) ◽  
pp. 4853-4863 ◽  
Author(s):  
David Endesfelder ◽  
Rebecca A. Burrell ◽  
Nnennaya Kanu ◽  
Nicholas McGranahan ◽  
Mike Howell ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Copy Number ◽  
Chromosomal Instability ◽  
Copy Number Variants ◽  
Gene Copy Number ◽  
Gene Copy
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