Please use this identifier to cite or link to this item:
Title: Gene expression analysis of matched ovarian primary tumors and peritoneal metastasis
Authors: Malek, J.A
Martinez, A
Mery, E
Ferron, G
Huang, R 
Raynaud, C
Jouve, E
Thiery, J.-P
Querleu, D
Rafii, A
Keywords: 1 (1 cyano 1 methylethyl) 3 methyl 8 (3 quinolinyl)imidazo[4,5 c]quinolin 2(1h,3h) one
4 diallylaminomethylene 1,3,4,7,10,11,12,13,14,15,16,17 dodecahydro 6 hydroxy 1 methoxymethyl 10,13 dimethyl 3,7,17 trioxo 2 oxacyclopenta[a]phenanthren 11 yl acetate
[1 (4 oxo 8 phenyl 4h 1 benzopyran 2 yl)morpholinio]methoxysuccinylarginylglycylaspartylserine acetate
interleukin 6
Janus kinase
mitogen activated protein kinase kinase kinase 4
phosphatidylinositol 3 kinase
STAT protein
xl 147
adjuvant therapy
clinical article
copy number variation
enzyme activation
enzyme inhibition
gene expression
gene expression profiling
gene targeting
haplotype map
human tissue
immune response
multiple cycle treatment
nucleotide sequence
ovary cancer
peritoneum metastasis
personalized medicine
signal transduction
Gene Expression Profiling
Ovarian Neoplasms
Peritoneal Neoplasms
Issue Date: 2012
Citation: Malek, J.A, Martinez, A, Mery, E, Ferron, G, Huang, R, Raynaud, C, Jouve, E, Thiery, J.-P, Querleu, D, Rafii, A (2012). Gene expression analysis of matched ovarian primary tumors and peritoneal metastasis. Journal of Translational Medicine 10 (1) : 121. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Background: Ovarian cancer is the most deadly gynecological cancer due to late diagnosis at advanced stage with major peritoneal involvement. To date most research has focused on primary tumor. However the prognosis is directly related to residual disease at the end of the treatment. Therefore it is mandatory to focus and study the biology of meatastatic disease that is most frequently localized to the peritoneal caivty in ovarian cancer.Methods: We used high-density gene expression arrays to investigate gene expression changes between matched primary and metastatic (peritoneal) lesions.Results: Here we show that gene expression profiles in peritoneal metastasis are significantly different than their matched primary tumor and these changes are affected by underlying copy number variation differences among other causes. We show that differentially expressed genes are enriched in specific pathways including JAK/STAT pathway, cytokine signaling and other immune related pathways. We show that underlying copy number variations significantly affect gene expression. Indeed patients with important differences in copy number variation displayed greater gene expression differences between their primary and matched metastatic lesions.Conclusions: Our analysis shows a very specific targeting at both the genomic and transcriptomic level to upregulate certain pathways in the peritoneal metastasis of ovarian cancer. Moreover, while primary tumors use certain pathways we identify distinct differences with metastatic lesions. The variation between primary and metastatic lesions should be considered in personalized treatment of ovarian cancer. © 2012 Malek et al.; licensee BioMed Central Ltd.
Source Title: Journal of Translational Medicine
ISSN: 14795876
DOI: 10.1186/1479-5876-10-121
Rights: Attribution 4.0 International
Appears in Collections:Elements
Staff Publications

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_1186_1479-5876-10-121.pdf2.51 MBAdobe PDF



Google ScholarTM



This item is licensed under a Creative Commons License Creative Commons