Mechanisms involved in the progression of androgen-independent prostate cancers: it is not only the cancer cell's fault.

摘要: The acquisition of an androgen-independent phenotype by prostate cancer cells is presently a death sentence for patients. In order to have realistic chance changing this outcome, understanding what drives the progression androgen independence critical. We review here working hypothesis based on position that development epithelial result series cellular and molecular events within whole tissue culminates in loss normal tissue-maintained growth control. This includes stromal cells, supporting extracellular matrix circulating hormones. discusses characteristics these malignant role involved differentiation as mediator phenotypes cells. addition, environmental, neuroendocrine immune factors may contribute disturbance fine balance epithelial–stromal–extracellular connection are considered. While goal many therapeutic approaches has been ablation or targeting receptor (AR) therapies become ineffective progress beyond dependence Twenty years ago Sir David Smithers debated tolerance tissues organizational failure growth-control mechanisms. precipitated prolonged abnormal demands regeneration repair, rather than any inherent disorder peculiar each individual components involved. He wrote ‘It not cell itself disorderly, but its relationship with rest tissue’. gained significantly large amounts precise data effects androgenic cancerous AR cancer. need come compile information towards perspective dysregulation whole, develop experimental systems address broader find treatment prevention.