Evidence map›Paper›PMID 15856014›Full record

ArticleOncogene2005

A single acute exposure to a chemotherapeutic agent induces hyper-recombination in distantly descendant cells and in their neighbors.

Rebecca E Rugo, Karen H Almeida, Carrie A Hendricks, Vidya S Jonnalagadda, Bevin P Engelward

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. 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
0.5field-weighted citation impact, top 38% 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, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Bystander effects and radiotherapy.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2015
    Review
  7. Article
  8. Article
  9. Article
  10. Mitochondrial mutagenesis induced by tumor-specific radiation bystander effects.Journal of molecular medicine (Berlin, Germany) · 2010
    Article
  11. Article
  12. Review
  13. Article
  14. Review
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

5 authors at 1 institution in 1 country.

Rebecca E RugoBiological Engineering Division, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Karen H Almeida
Carrie A Hendricks
Vidya S Jonnalagadda
Bevin P Engelward
Massachusetts Institute of Technology · US

Funding

TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LEVINE, STUART S · 1985 to 2020
$25.6M
"Mechanisms of Damage-Induced Homologous Recombination"R01CA079827 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ENGELWARD, BEVIN P. · 1999 to 2011
$1.9M
FLUORESCENCE DETECTION OF GENETIC INSTABILITY IN MICER33CA084740 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ENGELWARD, BEVIN P. · 2001 to 2003
$1.2M
FLUORESCENCE DETECTION OF GENETIC INSTABILITY IN MICER21CA084740 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ENGELWARD, BEVIN P. · 2000 to 2000
$155k
NCI NIH HHS CA84740NCI NIH HHS R01 CA079827NCI NIH HHS R21 CA084740NIEHS NIH HHS P30 ES002109NIEHS NIH HHS P30-ES02109
6 · The paper itself

Abstract

Homologous recombination can induce tumorigenic sequence rearrangements. Here, we show that persistent hyper-recombination can be induced following exposure to a bifunctional alkylating agent, mitomycin C (MMC), and that the progeny of exposed cells induce a hyper-recombination phenotype in unexposed neighboring cells. Residual damage cannot be the cause of delayed recombination events, since recombination is observed after drug and template damage are diluted over a million-fold. Furthermore, not only do progeny of MMC-exposed cells induce recombination in unexposed cells (bystanders), but these bystanders can in turn induce recombination in their unexposed neighbors. Thus, a signal to induce homologous recombination can be passed from cell to cell. Although the underlying molecular mechanism is not yet known, these studies reveal that cells suffer consequences of damage long after exposure, and that can signal unexposed neighboring cells to respond similarly. Thus, a single acute exposure to a chemotherapeutic agent can cause long-term changes in genomic stability. If the results of these studies of mouse embryonic stem (ES) cells are generally applicable to many cell types, these results suggest that a relatively small number of cells could potentially induce a tissue-wide increase in the risk of de novo homologous recombination events.

Indexed as

AnimalsAntineoplastic AgentsBystander EffectCell CommunicationMiceMitomycinRecombination, GeneticStem CellsAntineoplastic AgentsMitomycin

Identifiers

PMID15856014
OpenAlexW1992845765

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.