Linked Life Data

8558945

Source:http://linkedlifedata.com/resource/pubmed/id/8558945

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-2-26
pubmed:abstractText
The cells from patients with acute promyelocytic leukemia (AML M3) undergo terminal differentiation when treated with all-trans retinoic acid (ATRA). We have analyzed the expression of the mRNA for cathepsin G, a promyelocyte stage-specific transcript, in the leukemia and in retinoic acid responsive cell lines. We showed that the transcript is perpetually synthesized in patients' cells and that it rapidly disappears when the cells are treated with ATRA. In ATRA-sensitive (HL-60, NB4) cell lines and an ATRA-resistant (HL-60R) cell line we have shown that this process is dependent on proteins synthesized during the first 6h of ATRA-triggered differentiation and may involve both pre- and post-transcriptional mechanisms. A corresponding decrease in cathepsin G protein synthesis then follows. These findings indicate that the maturation arrest in AML M3 results in cells that may constitutively continue to produce proteins whose production is temporally confined during normal hemopoiesis. This would explain the elevated plasma-free serine protease activity we have demonstrated in this disease, and has implications for both the coagulopathy and the 'retinoic acid syndrome' in AML M3.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0887-6924
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
95-101
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
All-trans retinoic acid rapidly decreases cathepsin G synthesis and mRNA expression in acute promyelocytic leukemia.
pubmed:affiliation
Laboratoire de Biologie Cellulaire Hématopoïétique, Hôpital Saint Louis, Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't