Evidence map›Paper›PMID 29093807›Full record

ReviewTherapeutic advances in hematology2017

Biological and clinical implications of telomere dysfunction in myeloid malignancies.

Ashwin Kishtagari, Justin Watts

Open access · bronzeAbstract readReview
In one paragraph

Review in Therapeutic advances in hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Short Dysfunctional Telomere Is Highly Predictive of Dismal Outcome in MDS but Not in AML Patients.International journal of hematology-oncology and stem cell research · 2020
    Article
  8. 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.

Ashwin KishtagariDepartment of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland, OH, USA.
Justin WattsDivision of Hematology, Department of Medicine, University of Miami, Miller School of Medicine, Sylvester Comprehensive Cancer Center, 1475 NW 12th Avenue, Miami, FL 33136-1002, USA.
University of Miami · US

Funding

Miami Clinical and Translational Science InstituteKL2TR000461 · NCATS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SACCO, RALPH L. · 2012 to 2016
$2.1M
NCATS NIH HHS KL2 TR000461
6 · The paper itself

Abstract

Telomeres at the ends of linear chromosomes protect the genome. Telomeres shorten with each round of cell division, placing a finite limit on cell growth. Telomere attrition is associated with cell senescence and apoptosis. Telomerase, a specialized ribonucleoprotein complex, maintains telomeres homeostasis through repeat addition of telomere sequences to the 3' telomeric overhang. Telomere biology is closely related to cancer and normal aging. Upregulation of telomerase or activation of the alternative pathway of telomere lengthening is a hallmark of cancer cells, making telomerase an attractive target for cancer therapeutics. In this review, we will discuss telomere biology and the prognostic implications of telomere length in acute myeloid leukemia, and review exciting new investigational approaches using telomerase inhibitors in acute myeloid leukemia and other myeloid malignancies.

Indexed as

acute myeloid leukemiamyeloid malignanciestelomerasetelomerase inhibitorstelomere lengthtelomeres

Identifiers

PMID29093807
PMCPMC5652659
OpenAlexW2762448249

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.