This specific suppression of IGF-IEc expression was evident and positively correlated with the histological and/or clinical characteristics of an advanced disease, referring to clinical stage, tumor grade and disease recurrence (p<0.05); however, in situ carcinomas exhibited an increased expression of all IGF-I transcripts.
Several studies have shown that PPAR<i>γ</i>/TZDs decrease IGF-1 levels and, thus, reduce cancer growth in carcinomas such as the pancreas, colon, liver, and prostate.
CAF from low-grade but not high-grade carcinomas required insulin-like growth factor 1 and transforming growth factor beta 1 to stimulate carcinoma growth.
Although the association between IGF1 gene polymorphisms and cancer risk has been evaluated for several carcinomas, this association has not yet been examined for stomach cancer.
Now IGF-1R, the receptor tyrosine kinase for IGF-II, has been found to be variably upregulated, first uniformly in dysplastic and angiogenic progenitors and then focally at the margins and in invasive regions of carcinomas.
We documented increased IGF-1 and IGF-1rec immunoreactivity in adenomas (31 of 50 and 40 of 50 cases, respectively) and carcinomas (38 of 53 and 42 of 53 cases) compared with normal thyroid, which only showed minimal immunoreactivity for the ligand and its receptor.
IGF-1 may interact with function and proliferation of the human adrenal cortex with particular reference to cortical carcinomas lacking discernible aldosterone excess.
The purposes of this study are to characterize the gene expression of IGF-II at the mRNA and protein level in seven different epithelial cell lines derived from colon carcinomas and to determine the action of IGF-II and IGF-receptors on a colon carcinoma cell line.
The percentage of follicular carcinomas and Hürthle cell carcinomas that stained positively for the different oncogenes was as follows and respectively: Pan-ras 8% versus 63%; TGF-alpha 17% versus 63%; TGF-beta 25% versus 88%; IGF-1 17% versus 88%; and N-myc 17% versus 100%.