Evidence map›Paper›PMID 30005133›Full record

ArticleStem cells (Dayton, Ohio)2018

JAK2V617F Megakaryocytes Promote Hematopoietic Stem/Progenitor Cell Expansion in Mice Through Thrombopoietin/MPL Signaling.

Yu Zhang, Chi Hua Sarah Lin, Kenneth Kaushansky, Huichun Zhan

Open access · greenAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Hematopoietic Stem Cells and Their Niche in Bone Marrow.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Activation of JAK/STAT Signaling in Megakaryocytes Sustains MyeloproliferationClinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  20. Review
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

4 authors at 3 institutions in 2 countries.

Yu ZhangBiopharmaceutical R&D Center, Chinese Academy of Medical Sciences, Peking Union Medical College, Suzhou, People's Republic of China.
Chi Hua Sarah LinDepartment of Medicine, Division of Hematology-Oncology, Stony Brook Medicine, Stony Brook, New York, USA.
Kenneth KaushanskyOffice of the Sr. Vice President, Health Sciences, Stony Brook Medicine, Stony Brook, New York, USA.
Huichun ZhanDepartment of Medicine, Division of Hematology-Oncology, Stony Brook Medicine, Stony Brook, New York, USA.
Stony Brook Medicine · USChinese Academy of Medical Sciences & Peking Union Medical College · CNNorthport VA Medical Center · US

Funding

Molecular and Cellular Biology of Megakaryocytes in Normal and Neoplastic HematopoiesisR01HL134970 · NHLBI · STATE UNIVERSITY NEW YORK STONY BROOK · PI ZHAN, HUICHUN · 2017 to 2021
$1.8M
MicroRNA Deregulation in JAK2V617F-positive Chronic Myeloid NeoplasmsIK2BX001559 · VA · NORTHPORT VA MEDICAL CENTER · PI ZHAN, HUICHUN · 2012 to 2016
–
BLRD VA IK2 BX001559NHLBI NIH HHS R01 HL134970
6 · The paper itself

Abstract

The myeloproliferative neoplasms (MPNs) are stem cell disorders characterized by hematopoietic stem/progenitor cell (HSPC) expansion and overproduction of mature blood cells. The acquired kinase mutation JAK2V617F plays a central role in these disorders. The mechanisms responsible for HSPC expansion in MPNs are not fully understood, limiting the effectiveness of current treatments. One hallmark feature of the marrow in patients with MPNs is megakaryocyte (MK) hyperplasia. Previously, we reported that JAK2V617F-bearing MKs cause a murine myeloproliferative syndrome with HSPC expansion. Here we show that JAK2V617F MKs promote MPN stem cell function by inducing HSPC quiescence with increased repopulating capacity. In addition, we demonstrate that thrombopoietin and its receptor MPL are critical for the JAK2V617F-bearing MK-induced myeloproliferation, both by directly affecting the quantity and quality of MKs and by altering the MK-endothelial interaction and vascular niche function. Therefore, targeting HSPC niche-forming MKs and/or their interactions within the vascular niche could provide novel, more effective therapeutic strategies in patients with MPNs. Stem Cells 2018;36:1676-1684.

Indexed as

AnimalsCell ProliferationHematopoietic Stem CellsHumansJanus Kinase 2MegakaryocytesMiceMice, KnockoutMice, TransgenicMutationMyeloproliferative DisordersReceptors, ThrombopoietinSignal TransductionThrombopoietinJAK2 protein, humanJanus Kinase 2Mpl protein, mouseReceptors, ThrombopoietinThrombopoietinJAK2MegakaryocyteMPLMyeloproliferative neoplasmThrombopoietin

Identifiers

PMID30005133
PMCPMC6819142
OpenAlexW2883684302

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.