Maximum androgen blockade in advanced prostate cancer: an overview of the randomised trials
Background: In advanced prostatic adenocarcinoma , androgen suppression (AS) by surgery or drugs controls testicular hormone secretion, and therefore the further addition of an antiandrogen like nilutamide, flutamide, or cyproterone acetate is mentioned as maximum androgen blockade (MAB). The aim of this overview was to match the consequences on the duration of survival of MAB and of AS alone.
Methods: The collaborative meta–analysis of 27 randomised trials involved central reanalysis of the info on each of 8275 men (98% of these ever randomised in trials of MAB vs AS) with metastatic (88%) or locally advanced (12%) prostatic adenocarcinoma. Half were over 70 years aged , and follow–up was typically for about 5 years. 
Prostate cancer in a transgenic mouse.
Progress toward understanding the biology of prostatic adenocarcinoma has been slow thanks to the few animal research models available to review the spectrum of this uniquely human disease. To develop an animal model for prostatic adenocarcinoma , several lines of transgenic mice were generated by using the prostate-specific rat probasin promoter to derive expression of the simian virus 40 large tumor antigen-coding region. Mice expressing high levels of the transgene display progressive sorts of prostatic disease that histologically resemble human prostatic adenocarcinoma , starting from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. Prostate tumors are detected specifically within the prostate as early as 10 weeks aged . Immunohistochemical analysis of tumor tissue has demonstrated that dorsolateral prostate-specific secretory proteins were confined to well-differentiated ductal epithelial cells adjacent to, or within, the poorly differentiated tumor mass. 
Prospective Identification of Tumorigenic Prostate Cancer Stem Cells
Existing therapies for prostatic adenocarcinoma eradicates the majority of cells within a tumor. However, most patients continue to develop androgen-independent disease that is still incurable by current treatment strategies. there’s now increasing evidence in some malignancies that the tumor cells are organized as a hierarchy originating from rare stem cells that are liable for maintaining the tumor. We report here the identification and characterization of a cancer somatic cell population from human prostate tumors, which possess a big capacity for self-renewal. These cells also are ready to regenerate the phenotypically mixed populations of nonclonogenic cells, which express differentiated cell products, like androgen receptor and prostatic acid phosphatase. 
Tumour innervation and neurosignalling in prostate cancer
Prostate cancer progression has been shown to be hooked in to the event of autonomic nerves into the tumour microenvironment. Sympathetic nerves activate adrenergic neurosignalling that’s necessary in early stages of tumour progression and for initiating an angiogenic switch, whereas parasympathetic nerves activate cholinergic neurosignalling leading to tumour dissemination and metastasis. The innervation of prostatic adenocarcinoma seems to be initiated by neurotrophic growth factors, like the precursor to nerve protein secreted by tumour cells, and therefore the contribution of brain-derived neural progenitor cells has also been reported. Current experimental, epidemiological and clinical evidence shows the stimulatory effect of tumour innervation and neurosignalling in prostatic adenocarcinoma. 
New Therapy Strategy for Prostate Cancer: Amanita phalloides Treatment Stabilizes Best Without Pre-treatments (Observational Study Pre-protocol)
Background: death cap (Amanita) contains amanitin, inhibiting RNA polymerase II. Partial inhibition with amanitin influences tumor cell – but not normal cell – activity. Patients treated with Amanita often gain a stable disease state without further tumor growth.
Aim: Several therapies for prostatic adenocarcinoma are in use thus far . This study evaluates the implementation of the Amanita therapy into the therapeutic regimen of today.
Methods: 38 Patients with diagnosed prostatic adenocarcinoma were treated with Amanita alone. Prostate specific antigen (PSA) was used as a parameter for tumor cell growth. Data about previous therapies like anti androgen treatment, prostatectomy, chemotherapy or radiation and progression state of the disease were collected, and relationships analyzed. 
 Group, P.C.T.C., 2000. Maximum androgen blockade in advanced prostate cancer: an overview of the randomised trials. The Lancet, 355(9214), (Web Link)
 Greenberg, N.M., DeMayo, F., Finegold, M.J., Medina, D., Tilley, W.D., Aspinall, J.O., Cunha, G.R., Donjacour, A.A., Matusik, R.J. and Rosen, J.M., 1995. Prostate cancer in a transgenic mouse. Proceedings of the National Academy of Sciences, 92(8), (Web Link)
 Collins, A.T., Berry, P.A., Hyde, C., Stower, M.J. and Maitland, N.J., 2005. Prospective identification of tumorigenic prostate cancer stem cells. Cancer research, 65(23), (Web Link)
 Tumour innervation and neurosignalling in prostate cancer
Brayden March, Sam Faulkner, Phillip Jobling, Allison Steigler, Alison Blatt, Jim Denham & Hubert Hondermarck
Nature Reviews Urology (2020) (Web Link)
 Riede, I. (2017) “New Therapy Strategy for Prostate Cancer: Amanita phalloides Treatment Stabilizes Best Without Pre-treatments (Observational Study Pre-protocol)”, Journal of Advances in Medicine and Medical Research, 21(3), (Web Link)