PMID- 9010025
OWN - NLM
STAT- MEDLINE
DCOM- 19970220
LR  - 20190515
IS  - 0007-0920 (Print)
IS  - 1532-1827 (Electronic)
IS  - 0007-0920 (Linking)
VI  - 75
IP  - 2
DP  - 1997
TI  - Genetic changes associated with the acquisition of androgen-independent growth, 
      tumorigenicity and metastatic potential in a prostate cancer model.
PG  - 190-5
AB  - Genetic changes underlying the progression of human prostate cancer are 
      incompletely understood. Recently, an experimental model system that resembles 
      human prostate cancer progression was developed based on the serial passage of an 
      androgen-responsive, non-tumorigenic LNCaP prostate cancer cell line into athymic 
      castrated mice. Six different sublines, derived after one, two or three rounds of 
      in vivo passage, sequentially acquired androgen independence and tumorigenicity 
      as well as metastatic capacity. Here, we used comparative genomic hybridization 
      (CGH) and locus-specific fluorescence in situ hybridization (FISH) analysis to 
      search for genetic changes that may underlie the phenotypic progression events in 
      this model system. Six genetic aberrations were seen by CGH in the parental LNCaP 
      cell line. The derivative sublines shared virtually all these changes, indicating 
      a common clonal origin, but also contained 3-7 additional genetic changes. Gain 
      of the 13q12-q13 chromosomal region as well as losses of 4, 6q24-qter, 20p and 
      21q were associated with androgen independence and tumorigenicity with additional 
      changes correlating with metastasis. In conclusion, an accumulation of genetic 
      changes correlates with tumour progression in this experimental in vivo model of 
      prostate cancer progression. It is possible that the specific chromosomal 
      aberrations involved in this model system may provide clues to the location of 
      genes involved in human prostate cancer progression and metastasis.
FAU - Hyytinen, E R
AU  - Hyytinen ER
AD  - Laboratory of Cancer Genetics, Tampere University Hospital, Finland.
FAU - Thalmann, G N
AU  - Thalmann GN
FAU - Zhau, H E
AU  - Zhau HE
FAU - Karhu, R
AU  - Karhu R
FAU - Kallioniemi, O P
AU  - Kallioniemi OP
FAU - Chung, L W
AU  - Chung LW
FAU - Visakorpi, T
AU  - Visakorpi T
LA  - eng
GR  - CA57361/CA/NCI NIH HHS/United States
GR  - CA64863/CA/NCI NIH HHS/United States
GR  - DK47596/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Br J Cancer
JT  - British journal of cancer
JID - 0370635
RN  - 0 (Androgens)
SB  - IM
MH  - Androgens/physiology
MH  - Animals
MH  - Cell Division
MH  - Chromosome Aberrations/pathology
MH  - Chromosome Deletion
MH  - Chromosome Disorders
MH  - Chromosome Mapping
MH  - Chromosomes, Human, Pair 1
MH  - Chromosomes, Human, Pair 3
MH  - Chromosomes, Human, Pair 6
MH  - Clone Cells
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Mice
MH  - Mice, Nude
MH  - *Neoplasm Metastasis
MH  - Neoplasm Transplantation
MH  - Orchiectomy
MH  - Prostatic Neoplasms/*genetics/pathology
MH  - Transplantation, Heterologous
PMC - PMC2063274
EDAT- 1997/01/01 00:00
MHDA- 1997/01/01 00:01
CRDT- 1997/01/01 00:00
PHST- 1997/01/01 00:00 [pubmed]
PHST- 1997/01/01 00:01 [medline]
PHST- 1997/01/01 00:00 [entrez]
AID - 10.1038/bjc.1997.32 [doi]
PST - ppublish
SO  - Br J Cancer. 1997;75(2):190-5. doi: 10.1038/bjc.1997.32.