PMID- 10655059
OWN - NLM
STAT- MEDLINE
DCOM- 20000228
LR  - 20061115
IS  - 1061-4036 (Print)
IS  - 1061-4036 (Linking)
VI  - 24
IP  - 2
DP  - 2000 Feb
TI  - A genome-wide survey of RAS transformation targets.
PG  - 144-52
AB  - An important aspect of multi-step tumorigenesis is the mutational activation of
      genes of the RAS family, particularly in sporadic cancers of the pancreas, colon,
      lung and myeloid system. RAS genes encode small GTP-binding proteins that affect 
      gene expression in a global way by acting as major switches in signal
      transduction processes, coupling extracellular signals with transcription
      factors. Oncogenic forms of RAS are locked in their active state and transduce
      signals essential for transformation, angiogenesis, invasion and metastasis via
      downstream pathways involving the RAF/MEK/ERK cascade of cytoplasmic kinases, the
      small GTP-binding proteins RAC and RHO, phosphatidylinositol 3-kinase and others.
      We have used subtractive suppression hybridization (SSH), a PCR-based cDNA
      subtraction technique, to contrast differential gene expression profiles in
      immortalized, non-tumorigenic rat embryo fibroblasts and in HRAS- transformed
      cells. Sequence and expression analysis of more than 1,200 subtracted cDNA
      fragments revealed transcriptional stimulation or repression of 104 ESTs, 45
      novel sequences and 244 known genes in HRAS- transformed cells compared with
      normal cells. Furthermore, we identified common and distinct targets in cells
      transformed by mutant HRAS, KRAS and NRAS, as well as 61 putative target genes
      controlled by the RAF/MEK/ERK pathway in reverted cells treated with the
      MEK-specific inhibitor PD 98059.
FAU - Zuber, J
AU  - Zuber J
AD  - [1] Laboratory of Molecular Tumour Pathology, Institute of Pathology, Charite,
      Humboldt-University D-10117, Berlin, Germany.
FAU - Tchernitsa, O I
AU  - Tchernitsa OI
FAU - Hinzmann, B
AU  - Hinzmann B
FAU - Schmitz, A C
AU  - Schmitz AC
FAU - Grips, M
AU  - Grips M
FAU - Hellriegel, M
AU  - Hellriegel M
FAU - Sers, C
AU  - Sers C
FAU - Rosenthal, A
AU  - Rosenthal A
FAU - Schafer, R
AU  - Schafer R
LA  - eng
SI  - GENBANK/AB000220
SI  - GENBANK/AF023451
SI  - GENBANK/AF058922
SI  - GENBANK/AF061749
SI  - GENBANK/AF131207
SI  - GENBANK/AF141386
SI  - GENBANK/D38496
SI  - GENBANK/E08769
SI  - GENBANK/L11932
SI  - GENBANK/U17032
SI  - GENBANK/U79550
SI  - GENBANK/X65627
SI  - GENBANK/Z29651
SI  - RefSeq/NM_004398
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Nat Genet
JT  - Nature genetics
JID - 9216904
RN  - EC 3.6.1.- (GTP-Binding Proteins)
SB  - IM
MH  - Animals
MH  - Cell Division
MH  - *Cell Transformation, Neoplastic
MH  - Cells, Cultured
MH  - Cloning, Molecular
MH  - GTP-Binding Proteins/metabolism
MH  - *Gene Expression Regulation
MH  - *Genes, ras
MH  - *Genome
MH  - Genome, Human
MH  - Humans
MH  - Mice
MH  - Molecular Sequence Data
MH  - Rats
MH  - Transfection
EDAT- 2000/02/02 09:00
MHDA- 2000/03/04 09:00
CRDT- 2000/02/02 09:00
PHST- 2000/02/02 09:00 [pubmed]
PHST- 2000/03/04 09:00 [medline]
PHST- 2000/02/02 09:00 [entrez]
AID - 10.1038/72799 [doi]
PST - ppublish
SO  - Nat Genet. 2000 Feb;24(2):144-52. doi: 10.1038/72799.