Evidence map›Paper›PMID 28270692›Full record

ArticleLeukemia2017

Imetelstat, a telomerase inhibitor, differentially affects normal and malignant megakaryopoiesis.

G Mosoyan, T Kraus, F Ye, K Eng, J D Crispino, R Hoffman, C Iancu-Rubin

Abstract read
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-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

25 citing papers in PubMed, 48 citations in OpenAlex.

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  5. Clinical applications of oligonucleotides for cancer therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  6. Telomere Reprogramming and Cellular Metabolism: Is There a Link?International journal of molecular sciences · 2024
    Review
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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

7 authors at 3 institutions in 1 country.

G MosoyanThe Tisch Cancer Institute, Division of Hematology and Medical Oncology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY USA.
T KrausCenter for Therapeutic Antibody Development, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
F YeDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
K EngOncoMed Pharmaceuticals, Redwood City, CA, USA.
J D CrispinoDepartment of Medicine-Hematology/Oncology, Northwestern University Feinberg School of Medicine, Evanston, IL, USA.
R HoffmanThe Tisch Cancer Institute, Division of Hematology and Medical Oncology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY USA.
C Iancu-RubinThe Tisch Cancer Institute, Division of Hematology and Medical Oncology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY USA.
Icahn School of Medicine at Mount Sinai · USNorthwestern University · USOncoMed (United States) · US

Funding

THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Deanna L Benson · 2015 to 2026
$35.4M
NCI NIH HHS P30 CA196521
6 · The paper itself

Abstract

Imetelstat (GRN163L) is a specific telomerase inhibitor that has demonstrated clinical activity in patients with myeloproliferative neoplasms (MPN) and in patients with solid tumors. The antitumor effects were associated with the development of thrombocytopenia, one of the common side effects observed in patients treated with imetelstat. The events underlying these adverse effects are not apparent. In this report, we investigated the potential mechanisms that account for imetelstat's beneficial effects in MPN patients and the manner by which imetelstat treatment leads to a reduction in platelet numbers. Using a well-established system of ex vivo megakaryopoiesis, we demonstrated that imetelestat treatment affects normal megakaryocyte (MK) development by exclusively delaying maturation of MK precursor cells. By contrast, additional stages along MPN MK development were affected by imetelstat resulting in reduced numbers of assayable colony-forming unit MK and impaired MK maturation. In addition, treatment with imetelstat inhibited the secretion of fibrogenic growth factors by malignant but not by normal MK. Our results indicate that the delay observed in normal MK maturation may account for imetelstat-induced thrombocytopenia, while the more global effects of imetelstat on several stages along the hierarchy of MPN megakaryopoiesis may be responsible for the favorable clinical outcomes reported in MPN patients.

Indexed as

Enzyme InhibitorsHumansIndolesMegakaryocytesNiacinamideOligonucleotidesPolyploidyTelomeraseEnzyme InhibitorsimetelstatIndolesNiacinamideOligonucleotidesTelomerase

Identifiers

PMID28270692
PMCPMC5985670
OpenAlexW2593674614

What OpenQuestion holds

Textmetadata
LicenceTDM
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.