Trial reportBlood2015
Bone marrow skeletal stem/progenitor cell defects in dyskeratosis congenita and telomere biology disorders.
Trial report in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Bone mesenchymal stem cell therapy for ovariectomized osteoporotic rats: a systematic review and meta-analysis.BMC musculoskeletal disorders · 2019Pooled it
- Novel lineage depletion preserves autologous blood stem cells for gene therapy of Fanconi anemia complementation group A.Haematologica · 2018Trial
- N-Terminal Variant p.Ala2Val in X-Linked Dyskeratosis Congenita Gene (DKC1) Disrupts Its Post-Translational Modification and Nucleolar Localization.Molecular genetics & genomic medicine · 2026Article
- Late-onset dyskeratosis congenita due to a TERC (n.269G > C) variant-first reported case from Indonesia: a case report.Journal of medical case reports · 2026Article
- Avascular Necrosis and Minimal Trauma Fractures in Telomere Biology Disorders.Clinical genetics · 2026Article
- Premature ageing of lung alveoli and bone marrow cells from Terc deficient mice with different telomere lengths.Scientific reports · 2025Article
- POT1a deficiency in mesenchymal niches perturbs B-lymphopoiesis.Communications biology · 2023Article
- Many Functions of Telomerase Components: Certainties, Doubts, and Inconsistencies.International journal of molecular sciences · 2022Review
- Molecular insight of dyskeratosis congenita: Defects in telomere length homeostasis.Journal of clinical and translational research · 2022Review
- Network inference with Granger causality ensembles on single-cell transcriptomics.Cell reports · 2022Article
- New progress in the study of germline susceptibility genes of myeloid neoplasms.Oncology letters · 2021Review
- Article
- Inhibition of the Prostaglandin EP-1 Receptor in Periosteum Progenitor Cells Enhances Osteoblast Differentiation and Fracture Repair.Annals of biomedical engineering · 2020Article
- MYC drives overexpression of telomerase RNA (hTR/TERC) in prostate cancer.The Journal of pathology · 2018Article
- The Telomerase Complex Directly Controls Hematopoietic Stem Cell Differentiation and Senescence in an Induced Pluripotent Stem Cell Model of Telomeropathy.Frontiers in genetics · 2018Article
- CD146+ skeletal stem cells from growth plate exhibit specific chondrogenic differentiation capacity in vitro.Molecular medicine reports · 2017Article
- Shorter Remission Telomere Length Predicts Delayed Neutrophil Recovery After Acute Myeloid Leukemia Therapy: A Report From the Children's Oncology Group.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2016Article
- The molecular genetics of the telomere biology disorders.RNA biology · 2016Review
- The shelterin complex and hematopoiesis.The Journal of clinical investigation · 2016Review
- Mammalian telomeres and their partnership with lamins.Nucleus (Austin, Tex.) · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
Abstract
Dyskeratosis congenita (DC) is an inherited multisystem disorder, characterized by oral leukoplakia, nail dystrophy, and abnormal skin pigmentation, as well as high rates of bone marrow (BM) failure, solid tumors, and other medical problems such as osteopenia. DC and telomere biology disorders (collectively referred to as TBD here) are caused by germline mutations in telomere biology genes leading to very short telomeres and limited proliferative potential of hematopoietic stem cells. We found that skeletal stem cells (SSCs) within the BM stromal cell population (BMSCs, also known as BM-derived mesenchymal stem cells), may contribute to the hematologic phenotype. TBD-BMSCs exhibited reduced clonogenicity, spontaneous differentiation into adipocytes and fibrotic cells, and increased senescence in vitro. Upon in vivo transplantation into mice, TBD-BMSCs failed to form bone or support hematopoiesis, unlike normal BMSCs. TERC reduction (a TBD-associated gene) in normal BMSCs by small interfering TERC-RNA (siTERC-RNA) recapitulated the TBD-BMSC phenotype by reducing proliferation and secondary colony-forming efficiency, and by accelerating senescence in vitro. Microarray profiles of control and siTERC-BMSCs showed decreased hematopoietic factors at the messenger RNA level and decreased secretion of factors at the protein level. These findings are consistent with defects in SSCs/BMSCs contributing to BM failure in TBD.
Indexed as
Identifiers
What OpenQuestion holds
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.