Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-2-6
pubmed:abstractText
Acute promyelocytic leukemia (APL) is characterized by reciprocal chromosomal translocations that always Involve the retinoic acid receptor-alpha (RARalpha) gene on chromosome 17. RARalpha variably fuses to the PML, PLZF, NPM, NuMA, and STAT 5b genes (X genes), leading to the generation of X-RARalpha and RARalpha-X fusion genes. The aberrant X-RARalpha proteins retain the dimerization domains of their parental proteins and therefore can act as dominant negative oncogenic products on both RARalpha/RXR and X pathways. Studies in transgenic mice harboring X-RARalpha and RARalpha-X fusion genes and In mice lacking X genes have helped unravel the molecular mechanisms underlying APL leukemogenesis, which lead to the development of novel therapeutic strategies. Moreover, transgenic mouse models of APL were useful to test in vivo the efficacy of these novel therapeutic approaches as well as of drug combinations such as retinoic acid and As2O3 that were previously known to be effective as single agents in human APL.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0037-1963
pubmed:author
pubmed:issnType
Print
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
54-70
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Analysis of the molecular genetics of acute promyelocytic leukemia in mouse models.
pubmed:affiliation
Department of Human Genetics, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.
pubmed:publicationType
Journal Article, Review