Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
1995-8-29
|
| pubmed:abstractText |
A critical determinant of the efficacy of antineoplastic therapy is the response of malignant cells to DNA damage induced by anticancer agents. The p53 tumor-suppressor gene is a critical component of two distinct cellular responses to DNA damage, the induction of a reversible arrest at the G1/S cell cycle checkpoint, and the activation of apoptosis, a genetic program of autonomous cell death. Expression of the BCR-ABL chimeric gene produced by a balanced translocation in chronic myeloid leukemia, confers resistance to multiple genotoxic anticancer agents. BCR-ABL expression inhibits the apoptotic response to DNA damage without altering either the p53-dependent WAF1/CIP1-mediated G1 arrest or DNA repair. BCR-ABL-mediated inhibition of DNA damage-induced apoptosis is associated with a prolongation of cell cycle arrest at the G2/M restriction point; the delay of G2/M transition may allow time to repair and complete DNA replication and chromosomal segregation, thereby preventing a mitotic catastrophe. The inherent resistance of human cancers to genotoxic agents may result not only by the loss or inactivation of the wild-type p53 gene, but also by genetic alterations such as BCR-ABL that can delay G2/M transition after DNA damage.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Nucleotidylexotransferase,
http://linkedlifedata.com/resource/pubmed/chemical/Fusion Proteins, bcr-abl,
http://linkedlifedata.com/resource/pubmed/chemical/Oligonucleotides, Antisense,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Neoplasm
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0006-4971
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
86
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1148-58
|
| pubmed:dateRevised |
2007-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:7620167-Antineoplastic Agents,
pubmed-meshheading:7620167-Apoptosis,
pubmed-meshheading:7620167-Base Sequence,
pubmed-meshheading:7620167-Cell Cycle,
pubmed-meshheading:7620167-Chronic Disease,
pubmed-meshheading:7620167-DNA Damage,
pubmed-meshheading:7620167-DNA Nucleotidylexotransferase,
pubmed-meshheading:7620167-DNA Repair,
pubmed-meshheading:7620167-Drug Resistance,
pubmed-meshheading:7620167-Fusion Proteins, bcr-abl,
pubmed-meshheading:7620167-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:7620167-Humans,
pubmed-meshheading:7620167-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:7620167-Molecular Sequence Data,
pubmed-meshheading:7620167-Oligonucleotides, Antisense,
pubmed-meshheading:7620167-RNA, Messenger,
pubmed-meshheading:7620167-RNA, Neoplasm,
pubmed-meshheading:7620167-Radiation, Ionizing,
pubmed-meshheading:7620167-Tumor Cells, Cultured
|
| pubmed:year |
1995
|
| pubmed:articleTitle |
BCR-ABL-mediated inhibition of apoptosis with delay of G2/M transition after DNA damage: a mechanism of resistance to multiple anticancer agents.
|
| pubmed:affiliation |
Johns Hopkins Oncology Center, Baltimore, MD 21287, USA.
|
| pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|