Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2006-1-11
pubmed:abstractText
To investigate the potential role and the mechanism of PLZF-RARalpha/RARalpha-PLZF double fusion gene in the pathogenesis of acute promyelocytic leukemia (APL) in vivo at systematic biological level, PLZF-RARalpha/RARalpha-PLZF double transgenic mouse model was established by intercross; the integration and expression of fusion genes were analyzed by PCR and RT-PCR; the disease phenotype was detected by morphological and pathological examination of peripheral blood and bone marrow cells, as well as flow cytometry assays; the effects of ATRA with or without tricostatin A on bone marrow blast cells from PLZF-RARalpha/RARalpha-PLZF double TM were observed. The results showed that leukemia occurred in 5 PLZF-RARalpha/RARalpha-PLZF double TM 7, 7, 9, 11 and 11 months respectively, out of them two (40%) with classic APL features, the others (60%) with chronic myeloid leukemia through an observation period of 18 months. The leukemia occurrence of PLZF-RARalpha/RARalpha-PLZF TM was about 10%, which was similar to PLZF-RARalpha TM as that reported before. The latency was over 6 months, not earlier than PLZF-RARalpha TM only. No morphologic changes of PLZF-RARalpha/RARalpha-PLZF double TM blast cells to ATRA were observed, but increased cytoplasmic-nuclear ratio and nuclear condensation in bone marrow blast cells were found in combination of ATRA with tricostatin A. It is concluded that PLZF-RARalpha/RARalpha-PLZF double fusion gene transgenic mice have heterogeneity of pathogenesis. HDAC inhibitors such as trichostatin A, in combination with ATRA, induce differentiation of the blast/promyelocytic cells from PLZF-RARa/RARa-PLZF double TM, but not ATRA alone.
pubmed:language
chi
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1009-2137
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
924-31
pubmed:meshHeading
pubmed-meshheading:16403252-Animals, pubmed-meshheading:16403252-Antigens, CD34, pubmed-meshheading:16403252-Bone Marrow Cells, pubmed-meshheading:16403252-Cell Differentiation, pubmed-meshheading:16403252-Chorionic Gonadotropin, pubmed-meshheading:16403252-Disease Models, Animal, pubmed-meshheading:16403252-Female, pubmed-meshheading:16403252-Flow Cytometry, pubmed-meshheading:16403252-Humans, pubmed-meshheading:16403252-Hydroxamic Acids, pubmed-meshheading:16403252-Leukemia, Promyelocytic, Acute, pubmed-meshheading:16403252-Male, pubmed-meshheading:16403252-Mice, pubmed-meshheading:16403252-Mice, Inbred C57BL, pubmed-meshheading:16403252-Mice, Inbred CBA, pubmed-meshheading:16403252-Mice, Transgenic, pubmed-meshheading:16403252-Oncogene Proteins, Fusion, pubmed-meshheading:16403252-Pedigree, pubmed-meshheading:16403252-Receptors, Chemokine, pubmed-meshheading:16403252-Tretinoin
pubmed:year
2005
pubmed:articleTitle
[hCG-PLZF-RARalpha/hCG-RARalpha-PLZF transgenic mice developing into leukemia].
pubmed:affiliation
State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital, The Shanghai Second Medical University, Shanghai 200025, China.
pubmed:publicationType
Journal Article, English Abstract, Research Support, Non-U.S. Gov't