Evidence map›Paper›PMID 24616570›Full record

ReviewWorld journal of gastroenterology2014

Telomeres, telomerase and colorectal cancer.

Roberta Bertorelle, Enrica Rampazzo, Salvatore Pucciarelli, Donato Nitti, Anita De Rossi

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Menin in Cancer.Genes · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. The Antagonistic and Synergistic Role of FePharmaceuticals (Basel, Switzerland) · 2024
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Novel Diagnostic Biomarkers in Colorectal Cancer.International journal of molecular sciences · 2022
    Review
  20. Article
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 at 1 institution in 1 country.

Roberta BertorelleRoberta Bertorelle, Enrica Rampazzo, Anita De Rossi, Department of Surgery, Oncology and Gastroenterology, Section of Oncology and Immunology, University of Padova, IOV-IRCCS, 35128 Padova, Italy.
Enrica RampazzoRoberta Bertorelle, Enrica Rampazzo, Anita De Rossi, Department of Surgery, Oncology and Gastroenterology, Section of Oncology and Immunology, University of Padova, IOV-IRCCS, 35128 Padova, Italy.
Salvatore PucciarelliRoberta Bertorelle, Enrica Rampazzo, Anita De Rossi, Department of Surgery, Oncology and Gastroenterology, Section of Oncology and Immunology, University of Padova, IOV-IRCCS, 35128 Padova, Italy.
Donato NittiRoberta Bertorelle, Enrica Rampazzo, Anita De Rossi, Department of Surgery, Oncology and Gastroenterology, Section of Oncology and Immunology, University of Padova, IOV-IRCCS, 35128 Padova, Italy.
Anita De RossiRoberta Bertorelle, Enrica Rampazzo, Anita De Rossi, Department of Surgery, Oncology and Gastroenterology, Section of Oncology and Immunology, University of Padova, IOV-IRCCS, 35128 Padova, Italy.
University of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the third most common cancer worldwide and, despite improved treatments, is still an important cause of cancer-related deaths. CRC encompasses a complex of diseases arising from a multi-step process of genetic and epigenetic events. Besides heterogeneity in the molecular and biological features of CRC, chromosomal instability is a hallmark of cancer and cancer cells may also circumvent replicative senescence and acquire the ability to sustain unlimited proliferation. Telomere/telomerase interplay is an important mechanism involved in both genomic stability and cellular replicative potential, and its dysfunction plays a key role in the oncogenetic process. The erosion of telomeres, mainly because of cell proliferation, may be accelerated by specific alterations in the genes involved in CRC, such as APC and MSH2. Although there is general agreement that the shortening of telomeres plays a role in the early steps of CRC carcinogenesis by promoting chromosomal instability, the prognostic role of telomere length in CRC is still under debate. The activation of telomerase reverse transcriptase (TERT), the catalytic component of the telomerase complex, allows cancer cells to grow indefinitely by maintaining the length of the telomeres, thus favouring tumour formation/progression. Several studies indicate that TERT increases with disease progression, and most studies suggest that telomerase is a useful prognostic factor. Plasma TERT mRNA may also be a promising marker for the minimally invasive monitoring of disease progression and response to therapy.

Indexed as

Biomarkers, TumorCell ProliferationCell Transformation, NeoplasticCellular SenescenceChromosomal InstabilityChromosomesColorectal NeoplasmsDisease ProgressionDNAEpigenesis, GeneticHumansPrognosisTelomeraseTelomereTreatment OutcomeBiomarkers, TumorDNATelomeraseColorectal cancerPrognostic markerTelomeraseTelomerase reverse transcriptaseTelomere

Identifiers

PMID24616570
PMCPMC3934464
OpenAlexW1993934102

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.