Evidence map›Paper›PMID 24398858›Full record

ReviewCancer metastasis reviews2014

Histone H2A.Z deregulation in prostate cancer. Cause or effect?

Deanna Dryhurst, Juan Ausió

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer metastasis reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 38 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Deanna DryhurstDepartment of Biochemistry and Microbiology, University of Victoria, Petch building, 258a, Victoria, British Columbia, Canada, V8W 3P6.
Juan Ausió
University of Victoria · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Genetic and epigenetic changes are at the root of all cancers. The epigenetic component involves alterations of the post-synthetic modifications of DNA (methylation) and histones (histone posttranslational modifications, PTMs) as well as of those of their molecular "writers," "readers," and "erasers." Noncoding RNAs (ncRNA) can also play a role. Here, we focus on the involvement of histone alterations in cancer, in particular that of the histone variant H2A.Z in the etiology of prostate cancer. The structural mechanisms putatively responsible for the contribution of H2A.Z to oncogenic gene expression programs are first described, followed by what is currently known about the involvement of this histone variant in the regulation of androgen receptor regulated gene expression. The implications of this and their relevance to oncogene deregulation in different stages of prostate cancer, including the progression toward androgen independence, are discussed. This review underscores the increasing awareness of the epigenetic contribution of histone variants to oncogenic progression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsDisease ProgressionEpigenesis, GeneticHistonesHumansMaleProstatic NeoplasmsReceptors, AndrogenHistonesReceptors, Androgen

Identifiers

PMID24398858
PMCPMC4113680
OpenAlexW2015445150

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.