PMID- 12603425
OWN - NLM
STAT- MEDLINE
DCOM- 20030428
LR  - 20220321
IS  - 1464-4096 (Print)
IS  - 1464-4096 (Linking)
VI  - 91
IP  - 4
DP  - 2003 Mar
TI  - Loss of CD38 correlates with simultaneous up-regulation of human leukocyte 
      antigen-DR in benign prostatic glands, but not in fetal or androgen-ablated 
      glands, and is strongly related to gland atrophy.
PG  - 409-16
AB  - OBJECTIVE: To determine whether CD38 loss in benign and malignant prostatic 
      disease is related to human leukocyte antigen (HLA)-DR up-regulation, by 
      assessing the histopathology of the prostate and the effect of androgen 
      deprivation. MATERIALS AND METHODS: Serial sections of frozen fetal (eight), 
      infant (six), normal adult (10), benign hyperplastic (BPH, 24), and primary (10) 
      and hormone-treated (11) carcinomatous human prostatic tissues were analysed by 
      immunohistology for anti-CD38 and HLA-DR antigens. RESULTS: In BPH samples there 
      was a significant correlation between CD38 loss (mean 21% of acini) and HLA-DR 
      up-regulation (mean 20%; P < 0.001). Moreover, 76% of all CD38-negative acini in 
      BPH had HLA-DR up-regulation in the same prostate epithelial cells, predominantly 
      in atrophic and cystic glands, and in cells with retained secretions (74%). In 
      contrast to the uniform expression in normal adult prostate, CD38 was negative or 
      partly expressed in fetal acini (mean 19%) and almost completely negative in 
      acini of the early infant period (mean 0.7%). In contrast to BPH, cancer cells 
      did not selectively up-regulate HLA-DR when CD38 was lost. In patients with 
      cancer treated by androgen deprivation, cancer cells were CD38-negative. 
      CONCLUSIONS: The absence of CD38 and presence of HLA-DR expression in prostatic 
      epithelium is consistent in BPH and tissue surrounding tumour, and strongly 
      related to gland atrophy. This is particularly interesting as HLA-DR triggering 
      can induce apoptosis of cells, whereas CD38 prevents it. A permissive role for 
      androgens to maintain full CD38 expression in epithelial cells is suggested.
FAU - Kramer, G
AU  - Kramer G
AD  - Department of Urology, University of Vienna, Austria. gero_kramer@hotmail.com
FAU - Steiner, G E
AU  - Steiner GE
FAU - Sokol, P
AU  - Sokol P
FAU - Mallone, R
AU  - Mallone R
FAU - Amann, G
AU  - Amann G
FAU - Marberger, M
AU  - Marberger M
LA  - eng
PT  - Journal Article
PL  - England
TA  - BJU Int
JT  - BJU international
JID - 100886721
RN  - 0 (Androgens)
RN  - 0 (Antigens, CD)
RN  - 0 (HLA Antigens)
RN  - 0 (Membrane Glycoproteins)
RN  - EC 3.2.2.5 (ADP-ribosyl Cyclase)
RN  - EC 3.2.2.5 (CD38 protein, human)
RN  - EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
SB  - IM
MH  - ADP-ribosyl Cyclase/*metabolism
MH  - ADP-ribosyl Cyclase 1
MH  - Adolescent
MH  - Adult
MH  - Androgens/metabolism
MH  - Antigens, CD/*metabolism
MH  - Atrophy/metabolism
MH  - Child
MH  - Child, Preschool
MH  - HLA Antigens/*metabolism
MH  - Humans
MH  - Immunoblotting
MH  - Infant
MH  - Infant, Newborn
MH  - Male
MH  - Membrane Glycoproteins
MH  - Prostate/*embryology/pathology
MH  - Prostatic Hyperplasia/*immunology
MH  - Prostatitis/metabolism
MH  - Up-Regulation
EDAT- 2003/02/27 04:00
MHDA- 2003/04/29 05:00
CRDT- 2003/02/27 04:00
PHST- 2003/02/27 04:00 [pubmed]
PHST- 2003/04/29 05:00 [medline]
PHST- 2003/02/27 04:00 [entrez]
AID - 4091 [pii]
AID - 10.1046/j.1464-410x.2003.04091.x [doi]
PST - ppublish
SO  - BJU Int. 2003 Mar;91(4):409-16. doi: 10.1046/j.1464-410x.2003.04091.x.