We conclude that IGF1R and IGF2R differential expression may contribute to the increased risk of malignant transformation in young AA women and to the more aggressive breast cancer phenotype observed among AA breast cancer patients and represent, along with IGF-II, potential therapeutic targets in breast cancer.
It is probable, therefore, that posttranscriptional dysregulation of M6P/IGF2r is a contributing mechanism in breast cancer development and breast cancer response to therapy.
IGF2R promoter-driven expression was USF-independent in both MCF-7 and MDA-MB-231 breast cancer cell lines, suggesting that a defect in USF function may contribute to down-regulation of IGF2R expression in cancer cells.
Increased expression of the mannose 6-phosphate/insulin-like growth factor-II receptor in breast cancer cells alters tumorigenic properties in vitro and in vivo.
Differential expression of the mannose 6-phosphate/ insulin-like growth factor-II receptor in human breast cancer cell lines of different invasive potential.
We have sought to confirm that allelic loss of IGF2R is an early event in the aetiology of breast cancer by screening a group of 'early' lesions for LOH at a polymorphic microsatellite marker within the IGF2R gene using polymerase chain reaction (PCR).
These findings provide evidence that M6P/IGF2r allelic loss is an early event in the etiology of breast cancer, that this gene functions as a tumor suppressor gene in the breast.
In order to determine whether the Man-6-P/IGF-II receptor gene copy number is altered in breast cancer we analysed specimens of invasive breast carcinoma from 51 patients by Southern blotting.
We have studied the regulation by estradiol of the mannose-6-phosphate (Man-6-P)/insulin-like growth factor-II (IGF-II) receptor concentration in different breast cancer cell lines.