Evidence map›Paper›PMID 25606064›Full record

ArticleHereditary cancer in clinical practice2015

PARP inhibitors.

Maheen Anwar, Hafiz Muhammad Aslam, Shahzad Anwar

Abstract read
In one paragraph

Article in Hereditary cancer in clinical practice, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
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  10. Article
  11. Effects of NADBiomolecules · 2020
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Reverse the Resistance to PARP Inhibitors.International journal of biological sciences · 2017
    Review
  18. Review
  19. Article
  20. Dimethylfumarate inhibits melanoma cell proliferation via p21 and p53 induction and bcl-2 and cyclin B1 downregulation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

3 authors.

Maheen AnwarDow Medical College, Dow University of Health Sciences, Karachi, Pakistan.
Hafiz Muhammad AslamDow Medical College, Dow University of Health Sciences, Karachi, Pakistan.
Shahzad AnwarFinal year student of Dow Medical College, Dow University of Health Sciences, Karachi, Pakistan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poly (ADP-ribose) polymerases, abbreviated as PARPs, are a group of familiar proteins that play a central role in DNA repair employing the base excision repair (BER) pathway. There about 17 proteins in this family out of which the primary nuclear PARPs are PARP-1, PARP-2, PARP-3, and tankyrases 1 and 2 (PARP-5a and -5b) .The PARP family members are known to engage in a wide range of cellular activities, for example, DNA repair, transcription, cellular signaling, cell cycle regulation and mitosis amongst others. The chief functional units of PARP-1 are an amino terminal DNA binding domain (DBD), a central auto modification domain (AMD), and a carboxyl-terminal catalytic domain (CD). PARP inhibitors are currently undergoing clinical trials as targeted treatment modalities of breast, uterine, colorectal and ovarian cancer. This review summarizes current insights into the mechanism of action of PARP inhibitors, its recent clinical trials, and potential next steps in the evaluation of this promising class of anti-cancer drugs.

Indexed as

NicotinamidePoly (ADP-ribose) polymerasesRucaparib

Identifiers

PMID25606064
PMCPMC4300021

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.