PMID- 10029066
OWN - NLM
STAT- MEDLINE
DCOM- 19990304
LR  - 20220519
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 59
IP  - 4
DP  - 1999 Feb 15
TI  - Survey of gene amplifications during prostate cancer progression by 
      high-throughout fluorescence in situ hybridization on tissue microarrays.
PG  - 803-6
AB  - Prostate cancer development and progression is driven by the accumulation of 
      genetic changes, the nature of which remains incompletely understood To 
      facilitate high-throughput analysis of molecular events taking place in primary, 
      recurrent, and metastat prostate cancer, we constructed a tissue microarray 
      containing small 0.6-mm cylindrical samples acquired from 371 formalin-fixed 
      blocks, including benign prostatic hyperplasia (n = 32) and primary tumors (n = 
      223), as well as both locally recurrent tumors (n = 54) and metastases (n = 62) 
      from patients with hormone-refractory disease. Fluorescence in situ hybridization 
      (FISH) was applied to the analysis of consecutive tissue microarray sections with 
      probes for five different genes. High-level (> or =3X) amplifications were very 
      rare (<2%) in primary prostate cancers However, in metastases from patients with 
      hormone-refractory disease, amplification of the androgen receptor gene was seen 
      in 22%, MYC in 11%, and Cyclin-D1 in 5% of the cases. In specimens from locally 
      recurrent tumors, the corresponding percentages were 23, 4, and 8%. ERBB2 and 
      NMYC amplifications were never detected at any stage of prostate cancer 
      progression. In conclusion, FISH to tissue microarray sections enables 
      high-throughput analysis of genetic alterations contributing to cancer 
      development and progression. Our results implicate a role for amplification of 
      androgen receptor in hormonal therapy failure and that of MYC in the metastatic 
      progression of human prostate cancer.
FAU - Bubendorf, L
AU  - Bubendorf L
AD  - Laboratory of Cancer Genetics, National Human Genome Research Institute, NIH, 
      Bethesda, Maryland 20892-4470, USA.
FAU - Kononen, J
AU  - Kononen J
FAU - Koivisto, P
AU  - Koivisto P
FAU - Schraml, P
AU  - Schraml P
FAU - Moch, H
AU  - Moch H
FAU - Gasser, T C
AU  - Gasser TC
FAU - Willi, N
AU  - Willi N
FAU - Mihatsch, M J
AU  - Mihatsch MJ
FAU - Sauter, G
AU  - Sauter G
FAU - Kallioniemi, O P
AU  - Kallioniemi OP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (Receptors, Androgen)
RN  - 136601-57-5 (Cyclin D1)
SB  - IM
EIN - Cancer Res 1999 Mar 15;59(6):1388
MH  - Cyclin D1/genetics
MH  - *Gene Amplification
MH  - Genes, erbB-2
MH  - Genes, myc
MH  - Humans
MH  - *In Situ Hybridization, Fluorescence
MH  - Male
MH  - Prostatic Neoplasms/*genetics
MH  - Receptors, Androgen/genetics
EDAT- 1999/02/24 00:00
MHDA- 1999/02/24 00:01
CRDT- 1999/02/24 00:00
PHST- 1999/02/24 00:00 [pubmed]
PHST- 1999/02/24 00:01 [medline]
PHST- 1999/02/24 00:00 [entrez]
PST - ppublish
SO  - Cancer Res. 1999 Feb 15;59(4):803-6.