Evidence map›Paper›PMID 21706325›Full record

ReviewJournal of cancer research and clinical oncology2011

TRAIL and guardian angel of genome integrity: ATM boards TRAIL blazer.

Ammad Ahmad Farooqi, Salman Waseem, Muhammad Sajjad Ashraf, Muhammed Javed Iqbal, Shahzad Bhatti

Abstract readReview
In one paragraph

Review in Journal of cancer research and clinical oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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.

Ammad Ahmad FarooqiInstitute of Molecular Biology and Biotechnology (IMBB), The University of Lahore, Lahore, Pakistan. ammadahmad638@yahoo.com
Salman Waseem
Muhammad Sajjad Ashraf
Muhammed Javed Iqbal
Shahzad Bhatti

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is a multifaceted progressive multistep disorder that arises because of accumulation of genetic and epigenetic abnormalities, which escort to the transformation of normal cells into malignant derivatives. Despite tremendous strides have been made in the understanding of prostate cancer biology, yet approaches towards cancer-targeted therapy still face confrontations in standardization. This review brings to attention, the regulators in complex genetic backgrounds to enlighten our understanding of transformation and metastasis in human systems. Recent evidence gives a clue that prostate cancer may be linked to deregulated DNA damage repair processes, as various combinations of targeted deletions in genes controlling cell-cycle checkpoints; apoptosis and DNA repair result in prostate cancer progression and aggressiveness. An insight of the orchestration between DNA damage-based molecular responses and TRAIL provides an understanding of the mechanisms that cause apoptosis and may provide rationale for the development of novel therapeutic strategies.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsCarcinomaCell Cycle ProteinsDNA-Binding ProteinsDNA RepairEpigenesis, GeneticGenomic InstabilityHumansMaleModels, BiologicalProstatic NeoplasmsProtein BindingProtein Serine-Threonine KinasesSignal TransductionTNF-Related Apoptosis-Inducing LigandAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA-Binding ProteinsProtein Serine-Threonine KinasesTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTumor Suppressor Proteins

Identifiers

PMID21706325
PMCPMC11828323

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.