Evidence map›Paper›PMID 28675175›Full record

ReviewNature reviews. Urology2017

Telomeres and telomerase in prostate cancer development and therapy.

Mindy Kim Graham, Alan Meeker

Abstract readReview
In one paragraph

Review in Nature reviews. Urology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 126 citations in OpenAlex.

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  20. Role of telomere length in human carcinogenesis (Review).International journal of oncology · 2023
    Review

6 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Mindy Kim GrahamJohns Hopkins University School of Medicine, Pathology, Oncology, Urology, 1503 Jefferson Street, Bond Street Annex, Room B300, Baltimore, Maryland 21231, USA.
Alan MeekerJohns Hopkins University School of Medicine, Pathology, Oncology, Urology, 1503 Jefferson Street, Bond Street Annex, Room B300, Baltimore, Maryland 21231, USA.
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
TRAINING IN AREAS FUNDAMENTAL TO CANCER RESEARCHT32CA009110 · NCI · JOHNS HOPKINS UNIVERSITY · PI MATUNIS, MICHAEL J., WEERARATNA, ASHANI T · 1985 to 2025
$13.1M
Determining the Roles of ATRX and DAXX Abnormalities in Cancer Telomere BiologyR01CA172380 · NCI · JOHNS HOPKINS UNIVERSITY · PI MEEKER, ALAN KEITH · 2013 to 2017
$1.7M
Establishing in vitro carcinoma models of the Alternative Lengthening of Telomeres pathway to elucidate molecular mechanisms and identify therapeutic vulnerabilitiesF32CA213742 · NCI · JOHNS HOPKINS UNIVERSITY · PI GRAHAM, MINDY KIM · 2017 to 2018
$118k
NCI NIH HHS F32 CA213742NCI NIH HHS P30 CA006973NCI NIH HHS R01 CA172380NCI NIH HHS T32 CA009110
6 · The paper itself

Abstract

Aberrations in telomere biology are among the earliest events in prostate cancer tumorigenesis and continue during tumour progression. Substantial telomere shortening occurs in prostate cancer cells and high-grade prostatic intraepithelial neoplasia. Not all mechanisms of telomere shortening are understood, but oxidative stress from local inflammation might accelerate prostatic telomere loss. Critically short telomeres can drive the accumulation of tumour-promoting genomic alterations; however, continued telomere erosion is unsustainable and must be mitigated to ensure cancer cell survival and unlimited replication potential. Prostate cancers predominantly maintain telomeres by activating telomerase, but alternative mechanisms of telomere extension can occur in metastatic disease. Telomerase activity and telomere length assessment might be useful in prostate cancer diagnosis and prognosis. Telomere shortening in normal stromal cells has been associated with prostate cancer, whereas variable telomere lengths in prostate cancer cells and telomere shortening in cancer-associated stromal cells correlated with lethal disease. Single-agent telomerase-targeted treatments for solid cancers were ineffective in clinical trials but have not been investigated in prostate cancer and might be useful in combination with established regimens. Telomere-directed strategies have not been explored as extensively. Telomere deprotection strategies have the advantage of being effective in both telomerase-dependent and telomerase-independent cancers. Disruption of androgen receptor function in prostate cancer cells results in telomere dysfunction, indicating telomeres and telomerase as potential therapeutic targets in prostate cancer.

Indexed as

HumansMaleProstatic NeoplasmsTelomeraseTelomereTelomerase

Identifiers

PMID28675175
PMCPMC5626660
OpenAlexW2725721547

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.