Gout is an inflammatory condition associated with a problem of purine metabolism that results in crystallization of uric acid. [1]
[2] Colchicine is sometimes prescribed for gout.
[2a] (1991 - U.S.) An anecdotal paper:
"Laboratory data indicate that colchicine has an antimetastatic effect in tissue culture and in tumor-transplantation experiments in animals. The present case report reveals a lack of perineural and capsular invasion as well as distant metastases from a large adenocarcinoma of the prostate in a 63-year-old patient who had taken colchicine daily for 25 years prior to lesion discovery. Failure to demonstrate metastasis was unexpected both because of lesion size (estimated volume 4.4 ml) as well as its histopathology (Gleason pattern 3S, grade 6). Colchicine may have inhibited metastasis of activated Ki-ras oncogenes during oncogenesis along neural microtubules in the area because of the known inhibitory effect of this drug on particle transport along the microtubule component of the cytoskeleton."
[2b] (2010 - Netherlands) Another anecdotal report, warning that:
"Colchicine must be stopped before imaging with [18F]-methylcholine PET/CT."
[2c] (1995 - U.S.)
"Hormone-refractory prostate cancer continues to be associated with a very poor prognosis. Agents that inhibit microtubule function have been found to be cytotoxic to prostate cancer cells in preclinical and clinical settings. It was the aim of this study to assess the activity of estramustine and colchicine, two microtubule inhibitors, in hormone-refractory prostate cancer. In clinically achievable concentrations, the combination of estramustine and colchicine was cytotoxic to both the Dunning rat prostate adenocarcinoma cell line MAT-LyLu (MLL) and human prostate cancer cells (PC-3). Microtubule function was assessed in vitro to evaluate possible mechanisms of action. In motility and cell cycle analysis assays, estramustine and colchicine inhibited cellular motility but not cell cycle transit. In vivo, these two agents both inhibited the growth of implanted Dunning rat prostate adenocarcinoma MLL cells but did not appear to have additive effects. The use of oral colchicine in the treatment of hormone-refractory prostate cancer requires further investigation."
[3] Allopurinol is sometimes prescribed for gout.
[3a] (1996 - Sweden)
"Allopurinol treatment results in elevated prostate-specific antigen levels in prostatic fluid and serum of patients with non-bacterial prostatitis."
Apparently, urate suppresses PSA production.
[3b] (1996 - U.S.)
"5-fluorouracil and allopurinol combined with recombinant interferon-alpha 2b in the treatment of patients with advanced prostate cancer: a phase I/II study."
[3c] (2008 - Japan)
"Allopurinol has been used for the treatment of gout and conditions associated with hyperuricemia for several decades. We explored the potential of allopurinol on cancer treatment. Allopurinol did not expose cytotoxicity as a single treatment in human hormone refractory prostate cancer cell lines, PC-3 and DU145. However, allopurinol drastically induced apoptosis of PC-3 and DU145 in combination with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which is a promising candidate for anticancer agent but its efficacy is limited by the existence of resistant cancer cells."
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No PubMed PCa hits for pegloticase, febuxostat, benzbromazone, probenacid and sulfinpyrazone.
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[4] Uric Acid / Urate
[4a] (2016 - New Zealand)
"Elevated serum uric acid (SUA) or urate is associated with inflammation and gout. Recent evidence has linked urate to cancers, but little is known about urate effects in prostate cancer. Activins are inflammatory cytokines and negative growth regulators in the prostate. A hallmark of prostate cancer progression is activin insensitivity; however, mechanisms underlying this are unclear. We propose that elevated SUA is associated with prostate cancer counteracting the growth inhibitory effects of activins. The expression of activins A and B, urate transporter GLUT9 and tissue urate levels were examined in human prostate disease. Intracellular and secreted urate and GLUT9 expression were assessed in human prostate cancer cell lines. Furthermore, the effects of urate and probenecid, a known urate transport inhibitor, were determined in combination with activin A. Activin A expression was increased in low-grade prostate cancer, whereas activin B expression was reduced in high-grade prostate cancer. Intracellular urate levels decreased in all prostate pathologies ..." etc.
-Patrick
[1] en.wikipedia.org/wiki/Gout
[2] en.wikipedia.org/wiki/Colch...
"Colchicine inhibits microtubule polymerization by binding to tubulin, one of the main constituents of microtubules. Availability of tubulin is essential to mitosis, so colchicine effectively functions as a "mitotic poison" or spindle poison.[17]
The mitosis-inhibiting function of colchicine has been of great use in the study of cellular genetics. To see the chromosomes of a cell under a light microscope, it is important that they be viewed near the point in the cell cycle in which they are most dense. This occurs near the middle of mitosis (specifically metaphase), so mitosis must be stopped before it completes. Adding colchicine to a culture during mitosis is part of the standard procedure for doing karyotype studies.
Apart from inhibiting mitosis (a process heavily dependent on cytoskeletal changes), colchicine also inhibits neutrophil motility and activity, leading to a net anti-inflammatory effect. This has proven useful in the treatment of acute gout flares."
[2a] ncbi.nlm.nih.gov/pubmed/176...
[2b] ncbi.nlm.nih.gov/pubmed/210...
[2c] ncbi.nlm.nih.gov/pubmed/778...
[3] en.wikipedia.org/wiki/Allop...
"Allopurinol, sold under the brand name Zyloprim and generics, is a medication used primarily to treat excess uric acid in the blood and its complications, including chronic gout. It is a xanthine oxidase inhibitor and is administered orally."
[3a] ncbi.nlm.nih.gov/pubmed/882...
Gout drug febuxostat may be useful as repurposed drug for CRPC
