PMID- 12563308
OWN - NLM
STAT- MEDLINE
DCOM- 20030326
LR  - 20071115
IS  - 1474-175X (Print)
IS  - 1474-175X (Linking)
VI  - 3
IP  - 2
DP  - 2003 Feb
TI  - Disruption of differentiation in human cancer: AML shows the way.
PG  - 89-101
AB  - Although much is understood about the ways in which transcription factors 
      regulate various differentiation systems, and one of the hallmarks of many human 
      cancers is a lack of cellular differentiation, relatively few reports have linked 
      these two processes. Recent studies of acute myeloid leukaemia (AML), however, 
      have indicated how disruption of transcription-factor function can disrupt normal 
      cellular differentiation and lead to cancer. This model involves lineage-specific 
      transcription factors, which are involved in normal haematopoietic 
      differentiation. These factors are often targeted in AML--either by direct 
      mutation or by interference from translocation proteins. Uncovering these 
      underlying pathways will improve the diagnosis and treatment of AML, and provide 
      a working model for other types of human cancer, including solid tumours.
FAU - Tenen, Daniel G
AU  - Tenen DG
AD  - Harvard Institutes of Medicine, 77 Avenue Louis Pasteur, Boston, Massachusetts 
      02115, USA. dtenen@caregroup.harvard.edu
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - England
TA  - Nat Rev Cancer
JT  - Nature reviews. Cancer
JID - 101124168
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Cell Differentiation/*physiology
MH  - Humans
MH  - Leukemia, Myeloid, Acute/*genetics/pathology
MH  - Mutation
MH  - Neoplasms/genetics
MH  - Transcription Factors/*genetics/metabolism
RF  - 125
EDAT- 2003/02/04 04:00
MHDA- 2003/03/27 05:00
CRDT- 2003/02/04 04:00
PHST- 2003/02/04 04:00 [pubmed]
PHST- 2003/03/27 05:00 [medline]
PHST- 2003/02/04 04:00 [entrez]
AID - nrc989 [pii]
AID - 10.1038/nrc989 [doi]
PST - ppublish
SO  - Nat Rev Cancer. 2003 Feb;3(2):89-101. doi: 10.1038/nrc989.