PMID- 7654340
OWN - NLM
STAT- MEDLINE
DCOM- 19951005
LR  - 20190913
IS  - 0829-8211 (Print)
IS  - 0829-8211 (Linking)
VI  - 72
IP  - 11-12
DP  - 1994 Nov-Dec
TI  - Identification of chromosomes implicated in suppression of apoptosis in somatic 
      cell hybrids.
PG  - 655-62
AB  - In vitro exposure of tumorigenic cell lines to the chemotherapeutic agent PALA 
      (N-(phosphonoacetyl)-L-aspartate) usually results in cell death (shown here to be 
      apoptosis), followed by clonal growth of rare survivors. On the other hand, 
      normal diploid cells respond to PALA by arresting in G1 and G2 of the cell cycle. 
      It was previously suggested that growth control mechanisms might exist to prevent 
      cells from entering S phase under toxic conditions and that genes involved in 
      such mechanisms were mutated or deleted in tumor cells. Interestingly, the tumor 
      suppressor gene p53, a putative G1 control gene, was shown to mediate 
      PALA-induced growth arrest. However, growth arrest occurs in cells that lack 
      wild-type p53, suggesting that other genes are involved as well. To identify 
      these genes, we have generated whole cell hybrids between mouse melanoma and 
      normal human fibroblast cells. At early passage, a whole cell hybrid (BHF12) 
      responds to PALA with growth arrest, while at later passage, the same hybrid 
      undergoes apoptosis. To determine which human chromosomes are required for the 
      PALA-induced growth arrest phenotype, we isolated subclones of the hybrid and 
      tested them for their PALA response. FISH (fluorescence in situ hybridization) 
      and PCR (polymerase chain reaction) amplification have been used to identify the 
      human chromosome content of BHF12 and its subclones. Several human chromosomes, 
      in addition to chromosome 17 (the location of p53), are consistently associated 
      with the growth arrest phenotype.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Speevak, M D
AU  - Speevak MD
AD  - University of Ottawa, Department of Biochemistry, Faculty of Medicine, ON, 
      Canada.
FAU - Chevrette, M
AU  - Chevrette M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Canada
TA  - Biochem Cell Biol
JT  - Biochemistry and cell biology = Biochimie et biologie cellulaire
JID - 8606068
RN  - 30KYC7MIAI (Aspartic Acid)
RN  - 78QVZ7RG8L (sparfosic acid)
RN  - 9007-49-2 (DNA)
RN  - N919E46723 (Phosphonoacetic Acid)
SB  - IM
GS  - p53
MH  - Animals
MH  - Apoptosis/drug effects/*genetics
MH  - Aspartic Acid/*analogs & derivatives/pharmacology
MH  - Cell Cycle/drug effects
MH  - *Chromosomes, Human
MH  - Clone Cells
MH  - DNA/analysis
MH  - Fibroblasts/pathology
MH  - Flow Cytometry
MH  - Genes, p53
MH  - Humans
MH  - Hybrid Cells
MH  - Karyotyping
MH  - Male
MH  - Melanoma, Experimental/pathology
MH  - Mice
MH  - Phosphonoacetic Acid/*analogs & derivatives/pharmacology
MH  - Polymerase Chain Reaction
MH  - Tumor Cells, Cultured
EDAT- 1994/11/01 00:00
MHDA- 1994/11/01 00:01
CRDT- 1994/11/01 00:00
PHST- 1994/11/01 00:00 [pubmed]
PHST- 1994/11/01 00:01 [medline]
PHST- 1994/11/01 00:00 [entrez]
AID - 10.1139/o94-086 [doi]
PST - ppublish
SO  - Biochem Cell Biol. 1994 Nov-Dec;72(11-12):655-62. doi: 10.1139/o94-086.