Evidence map›Paper›PMID 25132269›Full record

ReviewOncogene2015

DNA damage response and prostate cancer: defects, regulation and therapeutic implications.

S Karanika, T Karantanos, L Li, P G Corn, T C Thompson

Open access · bronzeAbstract readReview
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Targeting Prostate Cancer, the 'Tousled Way'.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Article
  18. Review
  19. Detection ofBiomedicines · 2022
    Article
  20. 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

5 authors at 1 institution in 1 country.

S KaranikaDepartment of Genitourinary Medical Oncology Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
T KarantanosDepartment of Genitourinary Medical Oncology Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
L LiDepartment of Genitourinary Medical Oncology Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
P G CornDepartment of Genitourinary Medical Oncology Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
T C ThompsonDepartment of Genitourinary Medical Oncology Research, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting Tumor Microenvironment-Induced Therapy Resistance in Prostate Cancer Bone MetastasisP50CA140388 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOGOTHETIS, CHRISTOPHER J., THOMPSON, TIMOTHY CHARLES · 2009 to 2022
$23.4M
NCI NIH HHS 5 P30 CA016672NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA140388
6 · The paper itself

Abstract

DNA damage response (DDR) includes the activation of numerous cellular activities that prevent duplication of DNA lesions and maintain genomic integrity, which is critical for the survival of normal and cancer cells. Specific genes involved in the DDR such as BRCA1/2 and P53 are mutated during prostate cancer progression, while various oncogenic signaling such as Akt and c-Myc are activated, enhancing the replication stress and increasing the genomic instability of cancer cells. These events may render prostate cancer cells particularly sensitive to inhibition of specific DDR pathways, such as PARP in homologous recombination DNA repair and Chk1 in cell cycle checkpoint and DNA repair, creating opportunities for synthetic lethality or synergistic cytotoxicity. Recent reports highlight the critical role of androgen receptor (AR) as a regulator of DDR genes, providing a rationale for combining DNA-damaging agents or targeted DDR inhibitors with hormonal manipulation or AR inhibition as treatment for aggressive disease. The aims of this review are to discuss specific DDR defects in prostate cancer that occur during disease progression, to summarize recent advances in understanding the regulation of DDR in prostate cancer, and to present potential therapeutic opportunities through combinational targeting of the intact components of DDR signaling pathways.

Indexed as

AnimalsCell Cycle CheckpointsDNA DamageDNA, NeoplasmDNA RepairDNA ReplicationGene Expression Regulation, NeoplasticGenomic InstabilityHumansMaleProstatic NeoplasmsReceptors, AndrogenAR protein, humanDNA, NeoplasmReceptors, Androgen

Identifiers

PMID25132269
PMCPMC4333141
OpenAlexW2095514878

What OpenQuestion holds

Textmetadata
LicenceTDM
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.