ReviewCurrent hematologic malignancy reports2026
Clonal Signatures of Telomere Biology Disorders.
Review in Current hematologic malignancy reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewIn inherited bone marrow failure syndromes (IBMFS), clonal hematopoiesis (CH) has been increasingly recognized as a molecular fingerprint of the underlying pathophysiology. A specific clonal profile has been reported in telomere biology disorders (TBDs), an IBMFS caused by pathogenic germline variants (PGV) in genes related to telomere maintenance and characterized by short/dysfunctional telomeres and increased risk of cancer. This review summarizes current data on specific somatic mutational profiles seen in TBDs and their associations with clinical features and cancer risk. RECENT
findingsRecent studies have reported a specific CH landscape in TBDs that is associated with patients’ age, genotype, and phenotype. CH often involves the affected germline gene, with reversion or compensation of the PGV, or mutations in PPM1D, TERT promoter, or POT1—none of which are associated with increased risk of cancer. In contrast, a distinct group of recurrent CH that modulates TP53 pathway has been associated with cancer development in TBDs. These differing patterns of CH in TBDs have important implications for patients’ diagnosis, risk stratification, and surveillance. Characterization of clonal profiles across TBDs cohorts has helped identify potential molecular markers that can aid in diagnosis and guide future adapted surveillance and early intervention strategies. Although opportunities exist to incorporate CH into clinical care of patients with TBDs, multicenter longitudinal studies are still needed for validation and to allow for wide-scale adoption of CH into clinical care protocols.
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.