Activation of Akt signaling in prostate induces a TGFβ-mediated restraint on cancer progression and metastasis - Bjerke, G A; Yang, C-S; Frierson, H F; Paschal, B M; Wotton, D (Oncogene, 2014)
Keywords: 631/67/581; 631/80/86; 692/420/755; 692/699/67/589/466; Adenocarcinoma - genetics; Adenocarcinoma - metabolism; Adenocarcinoma - pathology; AKT protein; AKT1 protein; Animals; Apoptosis; Cell Biology; Development and progression; Disease Progression; Epithelial cells; Epithelial Cells - pathology; Epithelium; Gene Deletion; Genetic aspects; Homozygote; Human Genetics; Humans; Internal Medicine; Invasiveness; Lung Neoplasms - secondary; Lymph nodes; Lymphatic Metastasis; Male; Medicine; Medicine & Public Health; Metastases; Metastasis; Mice; Neoplasm Invasiveness; Oncology; original-article; Properties; Prostate - metabolism; Prostate - pathology; Prostate cancer; Prostatic Neoplasms - genetics; Prostatic Neoplasms - metabolism; Prostatic Neoplasms - pathology; Prostatic Neoplasms, Castration-Resistant - genetics; Prostatic Neoplasms, Castration-Resistant - metabolism; Prostatic Neoplasms, Castration-Resistant - pathology; Protein-Serine-Threonine Kinases - deficiency; Protein-Serine-Threonine Kinases - genetics; Proto-Oncogene Proteins c-akt - metabolism; PTEN Phosphohydrolase - deficiency; PTEN Phosphohydrolase - genetics; PTEN protein; Receptors, Transforming Growth Factor beta - deficiency; Receptors, Transforming Growth Factor beta - genetics; Signal Transduction; Transforming Growth Factor beta - metabolism; Tumor suppressor genes; Tumorigenesis; TGFβ; prostate cancer; signaling; Akt; Pten