A dose response relationship has been shown in prostate cancer.
Furthermore, hyperactivation of AKT signalling has been shown in prostate cells as well as in advanced PCa tissues (Kreisberg et al, 2004).
The tumor growth inhibitory activity of DCN gene therapy has also been shown in prostate and pancreatic cancer models [ 79, 80].
In keeping with this notion, increased levels of CB2 have been shown in prostate cancer cells compared with normal prostate (Sarfaraz et al, 2008), and a correlation between CB2 expression and the histological grade of breast tumours has also been observed (Caffarel et al, 2006).
Both acetylation and ubiquitination marks of H2A.Z have been potentially shown to play an important role in transcriptional regulation by the AR [ 12, 67, 68] (Fig. 1) and deregulation of histone acetylation and histone H2A.Z composition has been shown in prostate cancer [ 12, 68].
Also, decreased expression of CYP2B6 is shown in prostate cancer, and it has been recognized as growth inhibitory [ 43].
Additionally, transactivation and the critical involvement of metalloproteinases for this cross-communication were shown in prostate cancer cells, which are known to regulate their growth via autocrine pathways requiring either the bombesin or the EGFR [ 52**].
To study peptide distribution and accumulation in solid tumors, we choose to study GRPr-targeting radiopeptides that bind with high affinity to GRPr-expressing tumor cells It has been shown in several prostate cancers and in PDX models of prostate cancer that the GRPr expression is high [9, 11, 13, 20, 21].
EMT has been induced in prostate cancer cell lines, but has previously not been shown in primary prostate cells.
The presence of TU-1, -1A, -1B, -1C, -1D, and -1E has been shown in human prostate [2], [5].
More recently, an important role for hedgehog signaling has been shown in medulloblastoma, prostate, and pancreatic carcinomas [ 33, 34].
