Linked Life Data

7829222

Source:http://linkedlifedata.com/resource/pubmed/id/7829222

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-2-17
pubmed:abstractText
Response to chemotherapeutic agents in malignant tumors depends on many factors, most of which are as yet unknown. We investigated the correlation between the activation of different oncogenes and protein-kinase-C (PKC) modulation, and the cytotoxicity of some of the most widely used anti-cancer drugs. We transformed the murine keratinocyte cell line PAM 212, with different oncogenes (v-H-ras, v-myc and adenovirus E1a) and a mutant p53 suppressor gene (mp53). The cytotoxic effect of cisplatin (CDDP), doxorubicin (DOX) and vincristine (VCR), together with the concomitant action of modulators of PKC, TPA and staurosporine were evaluated by the crystal-violet method, thymidine incorporation and flow cytometry. We report that (a) the oncogene v-H-ras induces resistance to CDDP (> 50%), DOX (> 25%) and VCR (> 20%); (b) the E1a oncogene induces only resistance to VCR (> 40%) and marked sensitivity to CDDP and DOX; (c) the mp53 oncogene induces more resistance to VCR and insignificant resistance to the other drugs; and (d) activation of PKC by TPA increases the resistance to VCR and DOX in cells transformed by the v-H-ras, while it significantly increases the lethality with CDDP of the E1a-transformed cells. Staurosporine increases the cytoxicity of all the drugs, especially in the E1a-transformed keratinocytes. In the flow-cytometry analysis, the percentage of BUdR incorporation was related to sensitivity to anti-cancer drugs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0020-7136
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
235-43
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Modulation of cellular chemoresistance in keratinocytes by activation of different oncogenes.
pubmed:affiliation
Department of Pathology, Clínica Puerta de Hierro, Universidad Autónoma de Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't