Abstract

Abstract Abstract #4034 Background: The IGF-IR overexpression is reported to be detectable in 43-50% of primary breast cancers, its clinical and prognostic significance remains undetermined. Insulin growth factor type I (IGF-IR) is induced by estrogens in estrogens receptor (ER) positive cells that could explain why the IGF-IR overexpression is strongly related to ER positive breast cancer. However a small proportion of ER/PR negative cases overexpressed IGF-IR. The aim of this study was to correlate IGF-IR status by three techniques on a series of breast carcinomas : DNA microarrays ,CGH arrays and Immunohistochemistry.
 Material and Methods: Immunohistochemical phenotypes were studied in a series of 72 cases of breast carcinoma (40 basal and 32 luminal A). A series of 13 Markers was also studied IGF-IR, ER, PR, AR441, bcl2, FoxA1, Ki67, Gata3, P53, EGFR, ERBB2, CAV1 and MS110(BRCA1). Gene expression profiling with DNA microarrays (Affymetrix) and 244k CGH microarray was done on the same cases.
 Results: The IGF-IR expression was observed in IHC in 61% of the cases, overexpression in 25% and Gain or amplification in 7% .The IHC IGF-IR positivity was strongly correlated to the IGF-IR expression ( R=0.28 p<0.016) and IGF-IR DNA status (R=0.53 p= 5.610-6 ). IGF-IR over-expression in DNA microarrays is the only one results to be strongly associated to the luminal A subtype : 15/18 of the over expressed cases p=1.56 e-7. However the IHC expression of the ER related biomarkers is significantly associated to the IGF-IR overexpression.
 
 Discussion: The IGF-IR overexpression is representative of the Luminal A subtype, and to the ER regulated gene in IHC. Exploration of a panel of IGF-IR antibody is mandated before to best evaluate this target gene in IHC, who could contribute to the hormonal response. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 4034.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.