title: Changes of protein expression in prostate cancer having lost its androgen sensitivity.
abstract: OBJECTIVE
  The majority of prostate cancers require androgen hormones for growth, and androgen ablation is an important part of the systemic treatment of advanced prostate cancer. Nevertheless, most of these cancers eventually relapse as they become less sensitive to androgen ablation and anti-androgen treatment. Elucidating the molecular events that are responsible for the conversion of androgen-sensitive cancers to androgen-refractory tumors may reveal new therapeutic opportunities.
  
  
  METHODS
  In the present study, we investigated nine androgen-sensitive and nine androgen-refractory prostate cancer samples to evaluate the expression levels of 10 selected proteins that have been implicated in oncogenesis and cancer progression.
  
  
  RESULTS
  Our immunohistochemical data show that three of the investigated proteins (i.e., minichromosome maintenance-2, methylguanine-DNA methyltransferase, and androgen receptor) are expressed at significantly different levels in the androgen-refractory cancer samples than in the androgen-sensitive tumors, whereas the expression levels of the seven other studied proteins (i.e., β-catenin, p27, p21, p16, Ki67, hypoxia-inducible factor 1 alpha, and geminin) are not significantly different regarding the two groups.
  
  
  CONCLUSIONS
  Our data suggest that the increased expression of minichromosome maintenance-2 and decreased expression of methylguanine-DNA methyltransferase related to androgen receptor are indicative of the androgen-refractory stage in prostate cancer. Further studies are required to determine whether these expression changes play a causative role in the transition of androgen-sensitive to androgen-refractory prostate cancer.
authors.affiliation: Department of Urology, Semmelweis University, Budapest, Hungary, banfigergely@hotmail.com.
authors.forename: Gergely
authors.initials: G
authors.lastname: Bánfi
authors.forename: Ivett
authors.initials: I
authors.lastname: Teleki
authors.forename: Péter
authors.initials: P
authors.lastname: Nyirády
authors.forename: Attila
authors.initials: A
authors.lastname: Keszthelyi
authors.forename: Imre
authors.initials: I
authors.lastname: Romics
authors.forename: Attila
authors.initials: A
authors.lastname: Fintha
authors.forename: Tibor
authors.initials: T
authors.lastname: Krenács
authors.forename: Béla
authors.initials: B
authors.lastname: Szende
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D000368:Aged; D000726:Androgen Antagonists / Q000378:metabolism / Q000494:pharmacology; D015254:DNA Modification Methylases / Q000378:metabolism; D045643:DNA Repair Enzymes / Q000378:metabolism; D018450:Disease Progression; D064248:Geminin / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D064111:Minichromosome Maintenance Complex Component 2 / Q000378:metabolism; D009367:Neoplasm Staging; D011467:Prostate / Q000378:metabolism / Q000473:pathology; D011471:Prostatic Neoplasms / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D064129:Prostatic Neoplasms, Castration-Resistant / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D011944:Receptors, Androgen / Q000378:metabolism*; D015398:Signal Transduction; D020728:Transurethral Resection of Prostate / Q000379:methods; D025521:Tumor Suppressor Proteins / Q000378:metabolism
chemical_list: D000726:Androgen Antagonists; D064248:Geminin; D011944:Receptors, Androgen; D025521:Tumor Suppressor Proteins; D015254:DNA Modification Methylases; C515491:MGMT protein, human; C084859:MCM2 protein, human; D064111:Minichromosome Maintenance Complex Component 2; D045643:DNA Repair Enzymes