Evidence map›Paper›PMID 18239083›Full record

ReviewBlood2008

Telomere maintenance and human bone marrow failure.

Rodrigo T Calado, Neal S Young

2 registry-linked trialsOpen access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
13.3field-weighted citation impact, top 1% 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.

NCT01441037 phase1 / phase2completednot on this mapstarted 2011, after this paper: background citation

Male Hormones for Telomere Related Diseases

TypeinterventionalSponsorNational Heart, Lung, and Blood Institute (NHLBI)Ran2011 to 2016Enrolled27ConditionsAplastic AnemiaArmsDanazol
NCT02055456 phase1 / phase2completednot on this mapstarted 2014, after this paper: background citation

Male Hormones for Telomere Related Diseases

TypeinterventionalSponsorUniversity of Sao PauloRan2014 to 2017Enrolled20ConditionsAplastic Anemia, Bone Marrow Failure Syndromes, Idiopathic Pulmonary Fibrosis, Telomere ShorteningArmsNandrolone Decanoate
3 · Its place in the literature

Who cites it

94 citing papers in PubMed, 217 citations in OpenAlex.

  1. Trial
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  7. Alemtuzumab treatment of intermediate-1 myelodysplasia patients is associated with sustained improvement in blood counts and cytogenetic remissions.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2010
    Trial
  8. Review
  9. Review
  10. Review
  11. Article
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  13. Aging, Cancer, and Inflammation: The Telomerase Connection.International journal of molecular sciences · 2024
    Review
  14. Telomerase-Mediated Anti-Ageing Interventions.Sub-cellular biochemistry · 2024
    Review
  15. Lung transplant recipients with telomere-mediated pulmonary fibrosis have increased risk for hematologic complications.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023
    Article
  16. Article
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  20. Review

34 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Rodrigo T CaladoHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. calador@nhlbi.nih.gov
Neal S Young
National Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Pathogenesis And Treatment Of Aplastic AnemiaZIAHL002315 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI YOUNG, NEAL S · 2009 to 2025
$60.1M
PATHOGENESIS AND TREATMENT OF APLASTIC ANEMIAZ01HL002315 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI YOUNG, NEAL S · 1985 to 2008
$9.5M
Intramural NIH HHS
6 · The paper itself

Abstract

Acquired and congenital aplastic anemias recently have been linked molecularly and pathophysiologically by abnormal telomere maintenance. Telomeres are repeated nucleotide sequences that cap the ends of chromosomes and protect them from damage. Telomeres are eroded with cell division, but in hematopoietic stem cells, maintenance of their length is mediated by telomerase. Accelerated telomere shortening is virtually universal in dyskeratosis congenita, caused by mutations in genes encoding components of telomerase or telomere-binding protein (TERT, TERC, DKC1, NOP10, or TINF2). About one-third of patients with acquired aplastic anemia also have short telomeres, which in some cases associate with TERT or TERC mutations. These mutations cause low telomerase activity, accelerated telomere shortening, and diminished proliferative capacity of hematopoietic progenitors. As in other genetic diseases, additional environmental, genetic, and epigenetic modifiers must contribute to telomere erosion and ultimately to disease phenotype. Short telomeres also may cause genomic instability and malignant progression in these marrow failure syndromes. Identification of short telomeres has potential clinical implications: it may be useful in dyskeratosis congenita diagnosis, in suggesting mutations in patients with acquired aplastic anemia, and for selection of suitable hematopoietic stem cell family donors for transplantation in telomerase-deficient patients.

Indexed as

Bone Marrow DiseasesHumansMultiprotein ComplexesMutationTelomeraseTelomereTelomere-Binding ProteinsMultiprotein ComplexesTelomeraseTelomere-Binding Proteins

Identifiers

PMID18239083
PMCPMC2343587
OpenAlexW2118999711

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.