|
|
| Research article summary (published 27 Nov 1996): |
Enhanced XPA mRNA levels in cisplatin-resistant human ovarian cancer are not associated with XPA mutations or gene amplification.
Full Abstract
Enhanced expression of the nucleotide excision repair gene XPA is associated with resistance to cisplatin treatment in human ovarian cancer. Understanding the cause of enhanced XPA expression will provide new molecular targets for therapy directed at overcoming chemoresistance. Enhanced gene expression in cancer cells is often caused by mutations or gene amplification. Molecular analyses of the XPA genes in human ovarian cancers indicate that gene mutation and amplification are not the cause of enhanced XPA mRNA levels in ovarian cancers overexpressing XPA. Altered nucleotide excision repair (NER) gene regulation in chemoresistant tumors is discussed.
Author information
Author/s: States, J C (JC); Reed, E (E);
Affiliation: Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI, USA.cstates(-atsign-)cmb.biosci.wayne.edu
Journal and publication information
Publication Type: Journal Article
Journal: Cancer letters (Cancer Lett), published in IRELAND. (Language: eng)
Reference: 1996-Nov; vol 108 (issue 2) : pp 233-7
Dates: Created 1997/01/09; Completed 1997/01/09; Revised 2005/11/17;
PMID: 8973600, status: MEDLINE (last retrieved date: 2/18/2009)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
External Links for this article
(including full text providers, if available):
Click Electronic Full-text Provider Links to see options for finding the electronic full text links to this article. Note there may be a subscription or fee required for access to the full text. See our FAQ for information on finding FREE full text articles.
This article may also be located in paper journal collections available in many libraries. Use the Journal and Publication Information above to find the full article.
MeSH headings (categories)
This article was linked to the MeSH Headings (categories) shown below.
Note: Bold headings indicate primary MeSH headings or qualifiers.
Associated Chemicals: Antineoplastic Agents (0) ; DNA-Binding Proteins (0) ; Neoplasm Proteins (0) ; RNA, Messenger (0) ; Tumor Suppressor Protein p53 (0) ; XPA protein, human (0) ; Xeroderma Pigmentosum Group A Protein (0) ; Cisplatin (15663-27-1)Related articles
These are the most related articles currently in our database:
- Int-2, an autocrine and/or ultra-short-range effector in transgenic mammary tissue transplants.
Jun 1992 - Role of protein phosphorylation in activation of interferon-stimulated gene factors.
23 Mar 1992 - A Drosophila CREB/ATF transcriptional activator binds to both fat body- and liver-specific regulatory elements.
28 Feb 1992 - Inhibition of specific pathways of myeloid cell differentiation by an activated Hox-2.4 homeobox gene.
29 Sep 1992 - Genomic structure, evolutionary conservation and aniridia mutations in the human PAX6 gene.
30 Oct 1992 - Elevation of large-T antigen production by sodium butyrate treatment of SV40-transformed WI-38 fibroblasts.
29 Apr 1992 - Amino acid substitutions in the DNA-binding domain of the human androgen receptor are a frequent cause of receptor-binding positive androgen resistance.
28 Feb 1992 - Murine helix-loop-helix transcriptional activator proteins binding to the E-box motif of the Akv murine leukemia virus enhancer identified by cDNA cloning.
30 Jul 1992 - Inhibition of the activation of heat shock factor in vivo and in vitro by flavonoids.
30 Jul 1992 - Adipogenesis in a myeloid supporting bone marrow stromal cell line.
30 Aug 1992
Related Article Map
Legend:
- FREE Full text Article.
- Abstract only.
- Title only. More help.
See a larger map of 100+ related articles.