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Article: Melatonin slowed the early biochemical progression of hormone-refractory prostate cancer in a patient whose prostate tumor tissue expressed MT 1 receptor subtype

TitleMelatonin slowed the early biochemical progression of hormone-refractory prostate cancer in a patient whose prostate tumor tissue expressed MT 1 receptor subtype
Authors
Issue Date2003
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPI
Citation
Journal Of Pineal Research, 2003, v. 35 n. 3, p. 177-182 How to Cite?
AbstractMelatonin inhibited the proliferation of hormone-independent LNCaP prostate cancer cells partly via MT 1 receptor activation both in vitro and in nude mice xenograft model. In this study, the melatonin receptor expression in the prostate cancer tissue of a patient with bone metastases and the effect of melatonin on the biochemical progression of hormone-refractory prostate tumor which later developed in the same patient were reported. Saturation and competition 2-[ 125I]iodomelatonin binding assays were conducted on prostate tumor tissue obtained by transurethral resection of the prostate from the index patient. The receptor subtype identity of melatonin receptor expressed in the cancer tissue was determined by comparison of the rank order of inhibition constants (K i) of various melatonergic ligands and the affinity of 4-phenyl-2-propionamidotetraline relative to melatonin in inhibiting 2-[ 125I]iodomelatonin binding to the tumor sample and to human cell lines stably transfected with MT 1 or MT 2 melatonin receptor subtype. MT 1 receptor expression in the cancer tissue was also examined by immunohistochemistry. The surgically castrated patient later developed biochemical relapse of his disease. His serum total prostate-specific antigen (PSA) level was monitored before and during treatment with 5 mg/day oral melatonin at 20:00 hr. High-affinity (K d = 103.7 pM) MT 1 melatonin receptor subtype was expressed by the patient's prostate cancer. As indicated by his PSA levels, melatonin induced stabilization of his hormone-refractory disease for 6 wk. This report validates melatonin's oncostatic action on prostate cancer and the potential involvement of MT 1 receptor subtype in the attendant antiproliferative signal transduction as suggested by recent preclinical laboratory findings in a human.
Persistent Identifierhttp://hdl.handle.net/10722/171716
ISSN
2015 Impact Factor: 9.314
2015 SCImago Journal Rankings: 2.655
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShiu, SYWen_US
dc.contributor.authorLaw, ICen_US
dc.contributor.authorLau, KWen_US
dc.contributor.authorTam, PCen_US
dc.contributor.authorYip, AWCen_US
dc.contributor.authorNg, WTen_US
dc.date.accessioned2012-10-30T06:16:34Z-
dc.date.available2012-10-30T06:16:34Z-
dc.date.issued2003en_US
dc.identifier.citationJournal Of Pineal Research, 2003, v. 35 n. 3, p. 177-182en_US
dc.identifier.issn0742-3098en_US
dc.identifier.urihttp://hdl.handle.net/10722/171716-
dc.description.abstractMelatonin inhibited the proliferation of hormone-independent LNCaP prostate cancer cells partly via MT 1 receptor activation both in vitro and in nude mice xenograft model. In this study, the melatonin receptor expression in the prostate cancer tissue of a patient with bone metastases and the effect of melatonin on the biochemical progression of hormone-refractory prostate tumor which later developed in the same patient were reported. Saturation and competition 2-[ 125I]iodomelatonin binding assays were conducted on prostate tumor tissue obtained by transurethral resection of the prostate from the index patient. The receptor subtype identity of melatonin receptor expressed in the cancer tissue was determined by comparison of the rank order of inhibition constants (K i) of various melatonergic ligands and the affinity of 4-phenyl-2-propionamidotetraline relative to melatonin in inhibiting 2-[ 125I]iodomelatonin binding to the tumor sample and to human cell lines stably transfected with MT 1 or MT 2 melatonin receptor subtype. MT 1 receptor expression in the cancer tissue was also examined by immunohistochemistry. The surgically castrated patient later developed biochemical relapse of his disease. His serum total prostate-specific antigen (PSA) level was monitored before and during treatment with 5 mg/day oral melatonin at 20:00 hr. High-affinity (K d = 103.7 pM) MT 1 melatonin receptor subtype was expressed by the patient's prostate cancer. As indicated by his PSA levels, melatonin induced stabilization of his hormone-refractory disease for 6 wk. This report validates melatonin's oncostatic action on prostate cancer and the potential involvement of MT 1 receptor subtype in the attendant antiproliferative signal transduction as suggested by recent preclinical laboratory findings in a human.en_US
dc.languageengen_US
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPIen_US
dc.relation.ispartofJournal of Pineal Researchen_US
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.subject.meshAgeden_US
dc.subject.meshCell Division - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshIodine Radioisotopes - Metabolismen_US
dc.subject.meshLigandsen_US
dc.subject.meshMaleen_US
dc.subject.meshMelatonin - Pharmacologyen_US
dc.subject.meshProstatic Neoplasms - Drug Therapy - Metabolismen_US
dc.subject.meshReceptor, Melatonin, Mt1 - Metabolismen_US
dc.titleMelatonin slowed the early biochemical progression of hormone-refractory prostate cancer in a patient whose prostate tumor tissue expressed MT 1 receptor subtypeen_US
dc.typeArticleen_US
dc.identifier.emailShiu, SYW:sywshiu@hkucc.hku.hken_US
dc.identifier.authorityShiu, SYW=rp00384en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1034/j.1600-079X.2003.00074.xen_US
dc.identifier.pmid12932201-
dc.identifier.scopuseid_2-s2.0-0042412174en_US
dc.identifier.hkuros93929-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0042412174&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume35en_US
dc.identifier.issue3en_US
dc.identifier.spage177en_US
dc.identifier.epage182en_US
dc.identifier.isiWOS:000185114600006-
dc.publisher.placeDenmarken_US
dc.identifier.scopusauthoridShiu, SYW=7005550655en_US
dc.identifier.scopusauthoridLaw, IC=7005327712en_US
dc.identifier.scopusauthoridLau, KW=7401560179en_US
dc.identifier.scopusauthoridTam, PC=7202539419en_US
dc.identifier.scopusauthoridYip, AWC=7004871369en_US
dc.identifier.scopusauthoridNg, WT=7401613569en_US

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