Evidence map›Paper›PMID 32276199›Full record

ReviewCurrent opinion in genetics & development2020

Cancer and myeloid clonal evolution in the short telomere syndromes.

Kristen E Schratz, Mary Armanios

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in genetics & development, 2020. 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
2.9field-weighted citation impact, top 8% 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, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Clonal evolution in inherited marrow failure syndromes predicts disease progression.Hematology. American Society of Hematology. Education Program · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Telomere-mediated lung disease.Physiological reviews · 2022
    Review
  16. Review
  17. The Role of Telomeres in Human Disease.Annual review of genomics and human genetics · 2022
    Review
  18. Review
  19. Article
  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

2 authors at 1 institution in 1 country.

Kristen E SchratzDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States; Telomere Center, Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States.
Mary ArmaniosDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States; Telomere Center, Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States; Department of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States; Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States. Electronic address: marmani1@jhmi.edu.
Johns Hopkins University · US

Funding

TRAINING PROGRAM IN HEMATOLOGYT32HL007525 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ROBERT A BRODSKY · 1985 to 2026
$6.2M
Mechanisms of Telomere-Induced EmphysemaR01HL119476 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ARMANIOS, MARY Y · 2014 to 2023
$4.5M
Cancer Genetics of Short Telomere SyndromesR01CA225027 · NCI · JOHNS HOPKINS UNIVERSITY · PI ARMANIOS, MARY Y · 2018 to 2022
$2.4M
NCI NIH HHS R01 CA225027NHLBI NIH HHS R01 HL119476NHLBI NIH HHS T32 HL007525
6 · The paper itself

Abstract

The short telomere syndromes are considered the most common premature aging disorders. Although studies in genetically modified cells and animal models have suggested telomere dysfunction may promote genome instability, only a minority of humans with inherited loss-of-function mutations in telomerase and related genes develop cancer. Solid tumors are overall rare, and the vast majority of cancers are bone marrow-derived with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) comprising three-quarter of cases. In contrast to young short telomere syndrome patients who develop aplastic anemia, MDS and AML are usually diagnosed in adults who have milder short telomere defects. Here, we dissect the mechanisms by which these two bone marrow failure states, aplastic anemia and MDS-AML, evolve in the setting of varying degrees of telomere shortening. We discuss the implications of these observations for patient care as well as for understanding the genetics and biology of age-related myeloid clonal evolution.

Indexed as

Clonal EvolutionGenomic InstabilityTelomereCell Transformation, NeoplasticHumansLeukemia, Myeloid, AcuteMutationMyelodysplastic SyndromesTelomeraseTelomeraseTERT protein, human

Identifiers

PMID32276199
PMCPMC8122241
OpenAlexW3015861729

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.