Evidence map›Paper›PMID 14597413›Full record

ArticleExperimental cell research2003

Unique tissue-specific level of DNA nucleotide excision repair in primary human mammary epithelial cultures.

Jean J Latimer, Tariq Nazir, Lisa C Flowers, Michael J Forlenza, Kelly Beaudry-Rodgers, Crystal M Kelly, Julie A Conte, Kenneth Shestak, Amal Kanbour-Shakir, Stephen G Grant

Open access · greenAbstract readComparative Study
In one paragraph

Article in Experimental cell research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Nucleotide excision repair deficiency is intrinsic in sporadic stage I breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Analysis of DNA repair using transfection-based host cell reactivation.Methods in molecular biology (Clifton, N.J.) · 2005
    Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Jean J LatimerDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA 15213, USA. latimerj@pitt.edu
Tariq Nazir
Lisa C Flowers
Michael J Forlenza
Kelly Beaudry-Rodgers
Crystal M Kelly
Julie A Conte
Kenneth Shestak
Amal Kanbour-Shakir
Stephen G Grant
University of Pittsburgh · USMagee-Womens Research Institute · US

Funding

DNA REPAIR AND BREAST CANCERR29CA071894 · NCI · MAGEE-WOMEN'S RES INST AND FOUNDATION · PI LATIMER, JEAN J · 1997 to 2001
$212k
NCI NIH HHS CA 71894-01A1NCI NIH HHS R29 CA071894
6 · The paper itself

Abstract

DNA repair is essential for the maintenance of genomic integrity and stability. Nucleotide excision repair (NER) is a major pathway responsible for remediation of damage caused by UV light, bulky adducts, and cross-linking agents. We now show that NER capacity is differentially expressed in human tissues. We established primary cultures of peripheral blood lymphocytes (PBLs: N = 33) and foreskin fibroblasts (FF: N = 6), as well as adult breast tissue (N = 22) using a unique culture system, and measured their NER capacity using the unscheduled DNA synthesis (UDS) functional assay. Relative to FF, primary cultures of breast cells exhibited only 24.6 +/- 2.1% of NER capacity and PBLs only 8.9 +/- 1.2%. Cells from the breast therefore have a unique and distinctive DNA repair capacity. The NER capacities of all three cell types had similar coefficients of variation in the range of 10%-15%, which should be taken into account when running controls for this contextual assay. Unlike previous studies and speculation in the field, we found that NER was not affected by cell morphology, donor age, or proliferation as measured by the S phase index. While the NER capacity of the transformed lymphoblastoid cell line TK6 was within the range of our PBL samples, the breast tumor-derived MDA MB-231 cell line was four-fold higher than normal breast tissue. These studies show that analysis of baseline DNA repair in normal human cell types is critical as a basis for evaluation of the effects of "mutator" genes as etiological factors in the development of cancer.

Indexed as

AdultAge FactorsBreast NeoplasmsCarcinomaCell DivisionCell Line, TumorCells, CulturedCell SizeCell Transformation, NeoplasticDNADNA DamageDNA RepairEpithelial CellsFemaleFibroblastsGene Expression Regulation, NeoplasticDNA

Identifiers

PMID14597413
PMCPMC4729389
OpenAlexW1969600377

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.