Linked Life Data

14695163

Source:http://linkedlifedata.com/resource/pubmed/id/14695163

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
24
pubmed:dateCreated
2003-12-25
pubmed:abstractText
Advances in our understanding of the mechanisms by which tumor cells detect drug-induced DNA damage leading to apoptotic death have aided in the design of novel, potentially more selective strategies for cancer treatment. Several of these strategies use proapoptotic factors and have shown promise in sensitizing tumor cells to the cytotoxic actions of traditional cancer chemotherapeutic drugs. Although antiapoptotic factors are generally regarded as poor prognostic factors for successful cancer chemotherapy, strategies that use antiapoptotic factors in combination with suicide or other gene therapies can also be considered. The introduction of antiapoptotic factors that act downstream of drug-induced mitochondrial transition delays, but does not block, the ultimate cytotoxic response to cancer chemotherapeutic drugs that activate a mitochondrial pathway of cell death. Recent studies using the cytochrome P-450 prodrug cyclophosphamide exemplify how the antiapoptotic, caspase-inhibitory baculovirus protein p35 can be combined with P-450 gene-directed enzyme prodrug therapy to prolong localized, intratumoral production of cytotoxic drug metabolites without inducing tumor cell drug resistance. This model may be adapted to other gene therapies, including those that target death receptor pathways, to maximize the production of soluble, bystander cytotoxic factors and prodrug metabolites and thereby amplify the therapeutic response.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8563-72
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Harnessing apoptosis for improved anticancer gene therapy.
pubmed:affiliation
Division of Cell and Molecular Biology, Department of Biology, Boston University, Boston, Massachusetts 02215, USA. djw@bu.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review