Evidence map›Paper›PMID 30654820›Full record

ReviewJournal of experimental & clinical cancer research : CR2019

Emerging roles of telomeric chromatin alterations in cancer.

Stefano Cacchione, Annamaria Biroccio, Angela Rizzo

Open access · goldAbstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2019. 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
4.0field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. TERRA G-quadruplex stabilization as a new therapeutic strategy for multiple myeloma.Journal of experimental & clinical cancer research : CR · 2023
    Article
  6. Article
  7. Review
  8. Article
  9. Telomere Targeting Approaches in Cancer: Beyond Length Maintenance.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. A Truncating Germline Mutation ofThyroid : official journal of the American Thyroid Association · 2020
    Article
  17. Review
  18. Article
  19. Article
  20. Telomerase and Telomeres Biology in Thyroid Cancer.International journal of molecular sciences · 2019
    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

3 authors at 3 institutions in 3 countries.

Stefano CacchioneDepartment of Biology and Biotechnology "Charles Darwin", Sapienza University of Roma, Piazzale Aldo Moro 5, 00185, Rome, Italy. stefano.cacchione@uniroma1.it.
Annamaria BiroccioOncogenomic and Epigenetic Unit, IRCCS-Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144, Rome, Italy.
Angela RizzoOncogenomic and Epigenetic Unit, IRCCS-Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144, Rome, Italy. angela.rizzo@ifo.gov.it.ORCID http://orcid.org/0000-0001-5421-3085
Istituti di Ricovero e Cura a Carattere Scientifico · ITNational Cancer Institute · MYSapienza University of Rome · IT

Funding

Associazione Italiana per la Ricerca sul Cancro (AIRC) 16910
6 · The paper itself

Abstract

Telomeres, the nucleoprotein structures that cap the ends of eukaryotic chromosomes, play important and multiple roles in tumorigenesis. Functional telomeres need the establishment of a protective chromatin structure based on the interplay between the specific complex named shelterin and a tight nucleosomal organization. Telomere shortening in duplicating somatic cells leads eventually to the destabilization of the telomere capping structure and to the activation of a DNA damage response (DDR) signaling. The final outcome of this process is cell replicative senescence, which constitute a protective barrier against unlimited proliferation. Cells that can bypass senescence checkpoint continue to divide until a second replicative checkpoint, crisis, characterized by chromosome fusions and rearrangements leading to massive cell death by apoptosis. During crisis telomere dysfunctions can either inhibit cell replication or favor tumorigenesis by the accumulation of chromosomal rearrangements and neoplastic mutations. The acquirement of a telomere maintenance mechanism allows fixing the aberrant phenotype, and gives the neoplastic cell unlimited replicative potential, one of the main hallmarks of cancer.Despite the crucial role that telomeres play in cancer development, little is known about the epigenetic alterations of telomeric chromatin that affect telomere protection and are associated with tumorigenesis. Here we discuss the current knowledge on the role of telomeric chromatin in neoplastic transformation, with a particular focus on H3.3 mutations in alternative lengthening of telomeres (ALT) cancers and sirtuin deacetylases dysfunctions.

Indexed as

Genetic VariationAnimalsCell Transformation, NeoplasticChromatinDNA DamageEpigenesis, GeneticHeterochromatinHumansNeoplasmsSirtuinsTelomereTelomere HomeostasisChromatinHeterochromatinSirtuinsALTCancerChromatinEpigeneticsHeterochromatinSirtuinsTelomere

Identifiers

PMID30654820
PMCPMC6337846
OpenAlexW2915411726

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.