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Triple Negative Breast Cancers Have a Reduced Expression of DNA Repair Genes

Ribeiro, Enilze
•
Ganzinelli, Monica
•
Andreis, Daniele
altro
Damia, Giovanna
2013
  • journal article

Periodico
PLOS ONE
Abstract
DNA repair is a key determinant in the cellular response to therapy and tumor repair status could play an important role in tailoring patient therapy. Our goal was to evaluate the mRNA of 13 genes involved in different DNA repair pathways (base excision, nucleotide excision, homologous recombination, and Fanconi anemia) in paraffin embedded samples of triple negative breast cancer (TNBC) compared to luminal A breast cancer (LABC). Most of the genes involved in nucleotide excision repair and Fanconi Anemia pathways, and CHK1 gene were significantly less expressed in TNBC than in LABC. PARP1 levels were higher in TNBC than in LABC. In univariate analysis high level of FANCA correlated with an increased overall survival and event free survival in TNBC; however multivariate analyses using Cox regression did not confirm FANCA as independent prognostic factor. These data support the evidence that TNBCs compared to LABCs harbour DNA repair defects.
DOI
10.1371/journal.pone.0066243
WOS
WOS:000321223000012
Archivio
http://hdl.handle.net/11368/2857760
info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84879376177
http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0066243&representation=PDF
Diritti
open access
license:digital rights management non definito
FVG url
https://arts.units.it/bitstream/11368/2857760/1/journal.pone.0066243.pdf
Soggetti
  • Adult

  • Aged

  • Aged, 80 and over

  • DNA Repair

  • Fanconi Anemia

  • Female

  • Homologous Recombinat...

  • Human

  • Middle Aged

  • RNA, Messenger

  • Receptors, Estrogen

  • Triple Negative Breas...

  • Down-Regulation

  • Gene Expression Regul...

  • Agricultural and Biol...

  • Biochemistry, Genetic...

  • Medicine (all)

Scopus© citazioni
28
Data di acquisizione
Jun 7, 2022
Vedi dettagli
Web of Science© citazioni
31
Data di acquisizione
Mar 21, 2024
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