EGF had no effect on AC activity in cancers or fibroblasts, and no effect on cAMP concentration in cancer, although EGF incubation did increase intracellular cAMP in fibroblasts.
The maximal increase was observed at 10(-6) M around 48 h. Previously, we demonstrated the autocrine growth of HSG cells mediated by epidermal growth factor (EGF) receptors and EGF-like molecules (Kurokawa et al.(1989) Cancer Res.
The present study was designed to investigate the messenger ribonucleic acid (mRNA) expression of transforming growth factor (TGF)-alpha, TGF-beta 1, TGF-beta 2, TGF- beta 3, keratinocyte growth factor (KGF), epidermal growth factor (EGF), EGF receptor (EGF-R), and KGF receptor (KGF-R) in human fetal and adult prostatic tissues and cancer cell lines by reverse-transcriptase-polymerase chain reaction-(RT-PCR) using specific oligonucleotide primers.
We then examined the expression of mRNAs of such cytokines as TNF-alpha, TGF-alpha, EGF, and TGF-beta, in cancer tissue specimens from these three different groups.
On the contrary, there was a significant correlation between EGF and TGF-alpha (p < 0.001), EGF and EGF-R (p = 0.028), EGF-R and c-erb B-2 (p = 0.0009), and-inversely related-between TGF-alpha and tumor stage (p = 0.047) and between EGF-R and malignancy grade (p = 0.03).
Enhanced activity of receptor tyrosine kinases such as the PDGF beta-receptor and EGF receptor has been implicated as a contributing factor in the development of malignant and nonmalignant proliferative diseases such as cancer and atherosclerosis.
Targeting retrovirus to cancer cells expressing a mutant EGF receptor by insertion of a single chain antibody variable domain in the envelope glycoprotein receptor binding lobe.
Thus, AS/D1 may be a candidate for use as a novel cancer therapy specifically targeted against the over-expression of cyclin D1 enhanced by EGF in malignant cells.
Cancer cells have also been shown to express mutated EGF receptors; these are potentially highly specific targets for cancer therapeutics, as they have not been detected in any normal adult tissues.
Up-regulation of thrombospondin-1 gene by epidermal growth factor and transforming growth factor beta in human cancer cells--transcriptional activation and messenger RNA stabilization.
Animal studies have confirmed efficacy in the use of specific targeting of molecules regulating cancer growth (EGF receptor [EGFR], super oxide dismutase [SOD], cyclin D1, E1A and Bcl-2).These approaches are discussed.
Finally, to understand the mechanisms of resistance to EGF-R inhibitors, which have been shown to be useful in many different types of cancer, the Src-STAT signaling pathways are described here in detail.
In this paper, a nonviral gene delivery system GE7, which was designed to target EGF receptor (EGF R) overexpressed on the surface of cancer cel Is through an EGF R-binding oligopeptide (GE7), was used for in vivo gene therapy in a murine subcutaneous hepatoma model.
Therefore, we hypothesized that identification of potential EGF target genes in normal cells will provide a basis for unbiased genetic analysis of this signaling pathway in cancer.
The abnormal activation of the epidermal growth factor (EGF) pathway is one of the most common findings in human cancer, and a number of molecular devices of laboratory and clinical relevance have been designed to block this transduction pathway.
The two analytic approaches used in the study provide evidence against a strong association between EGF 61*G and melanoma and demonstrate the potential utility of case-case designs for evaluating the role of single nucleotide polymorphisms and cancer.
The ligands of the epidermal growth factor family and their receptors, the ErbB proteins, have been linked to the development of different types of cancer.