Evidence map›Paper›PMID 15993550›Full record

ArticleInternational journal of radiation oncology, biology, physics2005

Adenoviral-E2F-1 radiosensitizes p53wild-type and p53null human prostate cancer cells.

Khanh H Nguyen, Paul Hachem, Li-Yan Khor, Naji Salem, Kelly K Hunt, Peter R Calkins, Alan Pollack

Abstract read
In one paragraph

Article in International journal of radiation oncology, biology, physics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Hydroalcoholic extract ofFrontiers in pharmacology · 2023
    Article
  2. Review
  3. Article
  4. Article
  5. Adenovirus E2F1 overexpression sensitizes LNCaP and PC3 prostate tumor cells to radiation in vivo.International journal of radiation oncology, biology, physics · 2011
    Article
  6. Article
  7. Article
  8. Article
  9. 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

7 authors at 4 institutions in 2 countries.

Khanh H NguyenDepartment of Radiation Oncology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Paul Hachem
Li-Yan Khor
Naji Salem
Kelly K Hunt
Peter R Calkins
Alan Pollack
Fox Chase Cancer Center · USBaylor College of Medicine · USInstitut Paoli-Calmettes · FRThe University of Texas MD Anderson Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
NCI NIH HHS CA-006927NCI NIH HHS P30 CA006927
6 · The paper itself

Abstract

purposeE2F-1 is a transcription factor that enhances the radiosensitivity of various cell lines by inducing apoptosis. However, there are conflicting data concerning whether this enhancement is mediated via p53 dependent pathways. Additionally, the role of E2F-1 in the response of human prostate cancer to radiation has not been well characterized. In this study, we investigated the effect of Adenoviral-E2F-1 (Ad-E2F-1) on the radiosensitivity of p53wild-type (LNCaP) and p53null (PC3) prostate cancer cell lines. METHODS AND MATERIALS: LNCaP and PC3 cells were transduced with Ad-E2F-1, Adenoviral-Luciferase (Ad-Luc) control vector, or Adenoviral-p53 (Ad-p53). Expression of E2F-1 and p53 was examined by Western blot analysis. Annexin V and caspase 3 + 7 assays were performed to estimate the levels of apoptosis. Clonogenic survival assays were used to determine overall cell death. Statistical significance was determined by analysis of variance, using the Bonferroni method to correct for multiple comparisons.

resultsWestern blot analysis confirmed the efficacy of transductions with Ad-E2F-1 and Ad-p53. Ad-E2F-1 transduction significantly enhanced apoptosis and decreased clonogenic survival in both cell lines. These effects were compounded by the addition of RT. Although E2F-1-mediated radiosensitization was independent of p53 status, this effect was more pronounced in p53wild-type LNCaP cells. When PC3 cells were treated with Ad-p53 in combination with RT and Ad-E2F-1, there was at least an additive reduction in clonogenic survival.

conclusionsOur results suggest that Ad-E2F-1 significantly enhances the response of p53wild-type and p53null prostate cancer cells to radiation therapy, although radiosensitization is more pronounced in the presence of p53. Ad-E2F-1 may be a useful adjunct to radiation therapy in the treatment of prostate cancer.

Indexed as

Genes, p53AdenoviridaeApoptosisCell Cycle ProteinsCell Line, TumorDNA-Binding ProteinsE2F1 Transcription FactorE2F Transcription FactorsHumansMaleProstatic NeoplasmsProto-Oncogene Proteins p21(ras)Radiation-Sensitizing AgentsRadiation ToleranceTranscription FactorsTransduction, GeneticCell Cycle ProteinsDNA-Binding ProteinsE2F1 protein, humanE2F1 Transcription FactorE2F Transcription FactorsHRAS protein, humanProto-Oncogene Proteins p21(ras)Radiation-Sensitizing AgentsTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID15993550
PMCPMC4347813
OpenAlexW2049509123

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.