Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-5-18
pubmed:abstractText
Murine models of human neoplasms are being used to expand our understanding of pathogenesis and to develop improved cancer therapies. MRP8-PMLRARalpha transgenic mice represent one model of human acute promyelocytic leukemia (APL). These mice develop leukemias that mirror characteristic features of human APL including responsiveness to retinoic acid and arsenic. This model is proving its value in elucidating mechanisms by which PMLRARalpha contributes to leukemia, identifying genetic changes that cooperate to cause leukemia, and investigating new molecular targets for leukemia therapy. These studies suggest that acute myeloid leukemias (AMLs) such as APL result from genetic changes that combine to both impair differentiation and allow immature cells to survive and proliferate outside of a normal microenvironment. Retinoic acid targets the central molecular lesion in human APL and has greatly improved survival. Molecularly targeted therapies that either restore maturation or abrogate growth autonomy represent a hope for improving survival of patients with other subtypes of AML.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1079-9796
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Academic Press.
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
620-5
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Acute promyelocytic leukemia: a view from a mouse.
pubmed:affiliation
Department of Laboratory Medicine, University of California San Francisco, San Francisco, CA 94143-0128, USA. skogan@cc.ucsf.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't