Evidence map›Paper›PMID 27768860›Full record

ReviewBiochimica et biophysica acta2016

Means to the ends: The role of telomeres and telomere processing machinery in metastasis.

Nathaniel J Robinson, William P Schiemann

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2016. 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 18% 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, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Molecular mechanisms of aging and anti-aging strategies.Cell communication and signaling : CCS · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Emerging roles of telomeric chromatin alterations in cancer.Journal of experimental & clinical cancer research : CR · 2019
    Review
  18. Article
  19. 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

2 authors at 1 institution in 1 country.

Nathaniel J RobinsonDepartment of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
William P SchiemannCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH 44106, USA. Electronic address: william.schiemann@case.edu.
Case Western Reserve University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
NRSA Training CoreTL1TR002549 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI HARDING, CLIFFORD V · 2018 to 2022
$2.9M
Integrin-Mediated Regulation of TGF-Beta Signaling and TumorigenesisR01CA129359 · NCI · UNIVERSITY OF COLORADO DENVER · PI SCHIEMANN, WILLIAM · 2007 to 2016
$2.9M
Clinical and Translational Science Collaborative of ClevelandTL1TR000441 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI KONSTAN, MICHAEL W. · 2012 to 2016
$2.8M
Image-guided EMT inhibition for treating metastatic breast cancerR01CA194518 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI LU, ZHENG-RONG, SCHIEMANN, WILLIAM · 2015 to 2019
$2.4M
c-Abl-mediated Suppression of Breast Cancer Development and MetastasisR01CA177069 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI SCHIEMANN, WILLIAM · 2013 to 2018
$1.7M
NCATS NIH HHS TL1 TR000441NCATS NIH HHS TL1 TR002549NCI NIH HHS R01 CA129359NCI NIH HHS R01 CA177069NCI NIH HHS R01 CA194518NIGMS NIH HHS T32 GM007250
6 · The paper itself

Abstract

Despite significant clinical advancements, cancer remains a leading cause of mortality throughout the world due largely to the process of metastasis and the dissemination of cancer cells from their primary tumor of origin to distant secondary sites. The clinical burden imposed by metastasis is further compounded by a paucity of information regarding the factors that mediate metastatic progression. Linear chromosomes are capped by structures known as telomeres, which dictate cellular lifespan in humans by shortening progressively during successive cell divisions. Although telomere shortening occurs in nearly all somatic cells, telomeres may be elongated via two seemingly disjoint pathways: (i) telomerase-mediated extension, and (ii) homologous recombination-based alternative lengthening of telomeres (ALT). Both telomerase and ALT are activated in various human cancers, with more recent evidence implicating both pathways as potential mediators of metastasis. Here we review the known roles of telomere homeostasis in metastasis and posit a mechanism whereby metastatic activity is determined by a dynamic fluctuation between ALT and telomerase, as opposed to the mere activation of a generic telomere elongation program. Additionally, the pleiotropic nature of the telomere processing machinery makes it an attractive therapeutic target for metastasis, and as such, we also explore the therapeutic implications of our proposed mechanism.

Indexed as

Neoplasm MetastasisAnimalsHomologous RecombinationHumansTelomeraseTelomereTelomere HomeostasisTelomeraseAlternative lengthening of telomeresDNA damageDNA repairEpithelial-mesenchymal transitionMetastasisSignal transductionTelomere homeostasisTelomeres

Identifiers

PMID27768860
PMCPMC5138103
OpenAlexW2534640110

What OpenQuestion holds

Textmetadata
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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.