Document Detail


The novel tryptamine derivative JNJ-26854165 induces wild-type p53- and E2F1-mediated apoptosis in acute myeloid and lymphoid leukemias.
MedLine Citation:
PMID:  20736344     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The development of small-molecule activators of p53 is currently focused on malignancies containing a wild-type p53 genotype, which is present in most leukemias. JNJ-26854165 is one such p53-activating agent, but its mechanism of action remains to be elucidated. Here, we report the effects of JNJ-26854165 in acute leukemias. JNJ-26854165 treatment induced p53-mediated apoptosis in acute leukemia cells with wild-type p53, in which p53 rapidly drives transcription-independent apoptosis followed by activation of a transcription-dependent pathway. JNJ-26854165 accelerated the proteasome-mediated degradation of p21 and antagonized the transcriptional induction of p21 by p53. Interestingly, JNJ-26854165 induced S-phase delay and upregulated E2F1 expression in p53 mutant cells, resulting in apoptosis preferentially of S-phase cells. E2F1 knockdown blocked apoptosis induced by JNJ-26854165 in p53 mutant cells. Apoptotic activity of JNJ-26854165 against primary acute leukemia cells was maintained in leukemia/stroma cocultures, unlike doxorubicin, which has reduced cytrotoxicity in coculture systems. JNJ-26854165 synergizes with 1-β-arabinofuranosylcytosine or doxorubicin to induce p53-mediated apoptosis. Our data suggest that JNJ-26854165 may provide a novel therapeutic approach for the treatment of acute leukemias. The presence of p53-independent apoptotic activity in addition to p53-mediated apoptosis induction, if operational in vivo, may prevent the selection of p53 mutant subclones during therapy.
Authors:
Kensuke Kojima; Jared K Burks; Janine Arts; Michael Andreeff
Related Documents :
15255934 - Inhibition of the e2f-1/p53/bax pathway by tauroursodeoxycholic acid in amyloid beta-pe...
20423464 - Deregulation of apoptosis mediators' p53 and bcl2 in lung tissue of copd patients.
20840854 - Non-dioxin-like pcbs interact with benzo[a]pyrene-induced p53-responses and inhibit apo...
15064714 - Progesterone prevents radiation-induced apoptosis in breast cancer cells.
18309904 - Pharmacological intervention to the inflammatory response from decompression sickness i...
17996064 - The role of ifn-gamma in regulation of ifn-gamma-inducible protein 10 (ip-10) expressio...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-08-24
Journal Detail:
Title:  Molecular cancer therapeutics     Volume:  9     ISSN:  1538-8514     ISO Abbreviation:  Mol. Cancer Ther.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-10     Completed Date:  2011-02-17     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  101132535     Medline TA:  Mol Cancer Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2545-57     Citation Subset:  IM    
Affiliation:
Section of Molecular Hematology and Therapy, Department of Stem Cell Transplantation and Cellular Therapy, M.D. Anderson Cancer Center, The University of Texas, Houston, Texas 77030, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*,  genetics
Cell Line, Tumor
E2F1 Transcription Factor / genetics,  metabolism*
Genes, p53*
Humans
Leukemia, Myeloid, Acute / drug therapy*,  genetics,  metabolism,  pathology
Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy,  genetics,  metabolism,  pathology
Transfection
Tryptamines / pharmacology*
Grant Support
ID/Acronym/Agency:
CA16672/CA/NCI NIH HHS; CA49639/CA/NCI NIH HHS; CA55164/CA/NCI NIH HHS; CA89346/CA/NCI NIH HHS; P01 CA049639-09A19007/CA/NCI NIH HHS; P01 CA055164-08/CA/NCI NIH HHS; P01 CA055164-09/CA/NCI NIH HHS; P30 CA016672-22S29015/CA/NCI NIH HHS; R01 CA089346-03/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/E2F1 Transcription Factor; 0/Tryptamines
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Detecting two-locus associations allowing for interactions in genome-wide association studies.
Next Document:  Substitution of adenovirus serotype 3 hexon onto a serotype 5 oncolytic adenovirus reduces factor X ...