Evidence map›Paper›PMID 25655194›Full record

ArticleLeukemia2015

The role of Lin28b in myeloid and mast cell differentiation and mast cell malignancy.

L D Wang, T N Rao, R G Rowe, P T Nguyen, J L Sullivan, D S Pearson, S Doulatov, L Wu, R C Lindsley, H Zhu and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Regulation of HSC development and function by Lin28b.Frontiers in cell and developmental biology · 2025
    Review
  4. Article
  5. Article
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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

13 authors at 4 institutions in 1 country.

L D Wang1] Department of Pathology, Joslin Diabetes Center, Boston, MA, USA [2] Harvard Stem Cell Institute, Cambridge, MA, USA [3] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA [4] Stem Cell Transplantation Program, Division of Pediatric Hematology/Oncology, Dana-Farber/Boston Children's Center for Cancer and Blood Disorders, Boston, MA, USA [5] Department of Medicine, Boston Children's Hospital, Boston, MA, USA.
T N Rao1] Department of Pathology, Joslin Diabetes Center, Boston, MA, USA [2] Harvard Stem Cell Institute, Cambridge, MA, USA [3] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
R G Rowe1] Harvard Stem Cell Institute, Cambridge, MA, USA [2] Stem Cell Transplantation Program, Division of Pediatric Hematology/Oncology, Dana-Farber/Boston Children's Center for Cancer and Blood Disorders, Boston, MA, USA [3] Department of Medicine, Boston Children's Hospital, Boston, MA, USA [4] Manton Center for Orphan Disease Research, Boston, MA, USA [5] Howard Hughes Medical Institute, Boston, MA, USA.
P T Nguyen1] Department of Pathology, Joslin Diabetes Center, Boston, MA, USA [2] Harvard Stem Cell Institute, Cambridge, MA, USA [3] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
J L Sullivan1] Department of Pathology, Joslin Diabetes Center, Boston, MA, USA [2] Harvard Stem Cell Institute, Cambridge, MA, USA [3] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
D S Pearson1] Harvard Stem Cell Institute, Cambridge, MA, USA [2] Stem Cell Transplantation Program, Division of Pediatric Hematology/Oncology, Dana-Farber/Boston Children's Center for Cancer and Blood Disorders, Boston, MA, USA [3] Department of Medicine, Boston Children's Hospital, Boston, MA, USA [4] Manton Center for Orphan Disease Research, Boston, MA, USA [5] Howard Hughes Medical Institute, Boston, MA, USA [6] Medical Scientist Training Program, Harvard Medical School, Boston, MA, USA.
S Doulatov1] Harvard Stem Cell Institute, Cambridge, MA, USA [2] Stem Cell Transplantation Program, Division of Pediatric Hematology/Oncology, Dana-Farber/Boston Children's Center for Cancer and Blood Disorders, Boston, MA, USA [3] Department of Medicine, Boston Children's Hospital, Boston, MA, USA [4] Manton Center for Orphan Disease Research, Boston, MA, USA [5] Howard Hughes Medical Institute, Boston, MA, USA.
L Wu1] Department of Pediatrics and Internal Medicine, Children's Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA [2] Organ Transplant Center, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
R C Lindsley1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA [2] Division of Hematology, Brigham and Women's Hospital, Boston, MA, USA.
H ZhuDepartment of Pediatrics and Internal Medicine, Children's Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
D J DeAngeloDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
G Q Daley1] Harvard Stem Cell Institute, Cambridge, MA, USA [2] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA [3] Stem Cell Transplantation Program, Division of Pediatric Hematology/Oncology, Dana-Farber/Boston Children's Center for Cancer and Blood Disorders, Boston, MA, USA [4] Department of Medicine, Boston Children's Hospital, Boston, MA, USA [5] Manton Center for Orphan Disease Research, Boston, MA, USA [6] Howard Hughes Medical Institute, Boston, MA, USA [7] Medical Scientist Training Program, Harvard Medical School, Boston, MA, USA [8] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.
A J Wagers1] Department of Pathology, Joslin Diabetes Center, Boston, MA, USA [2] Harvard Stem Cell Institute, Cambridge, MA, USA [3] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA [4] Howard Hughes Medical Institute, Boston, MA, USA.
Harvard Stem Cell Institute · USJoslin Diabetes Center · USDana-Farber Cancer Institute · USThe University of Texas Southwestern Medical Center · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
Physician Scientist Training in Cancer ResearchT32CA009172 · NCI · DANA-FARBER CANCER INSTITUTE · PI Jennifer R Brown, James A. DeCaprio · 1985 to 2026
$17.1M
Control of HSC proliferation and migration by the transcription factor EGR1R01HL088582 · NHLBI · JOSLIN DIABETES CENTER · PI WAGERS, AMY JO · 2009 to 2013
$2.2M
Understanding the role of the lin28 paralogs and branching morphogenesisR01GM107536 · NIGMS · BOSTON CHILDREN'S HOSPITAL · PI DALEY, GEORGE Q · 2014 to 2017
$1.9M
Reactivation of embryonic growth programs in liver cancerR01CA190525 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI ZHU, HAO · 2015 to 2019
$1.8M
Metabolic roles for Lin28-let-7 miRNA pathway in sarcoma tumorigenesisK08CA157727 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI ZHU, HAO · 2011 to 2015
$807k
NCI NIH HHS K08 CA157727NCI NIH HHS K08-CA157727NCI NIH HHS R01 CA190525NCI NIH HHS T32 CA009172NHLBI NIH HHS R01 HL088582NHLBI NIH HHS R01-HL088582NIDDK NIH HHS P30 DK036836NIDDK NIH HHS P30DK036836NIGMS NIH HHS R01 GM107536NIGMS NIH HHS R01-GM107536NIGMS NIH HHS T32 GM007753Wellcome Trust
6 · The paper itself

Abstract

Mast cells (MCs) are critical components of the innate immune system and important for host defense, allergy, autoimmunity, tissue regeneration and tumor progression. Dysregulated MC development leads to systemic mastocytosis (SM), a clinically variable but often devastating family of hematologic disorders. Here we report that induced expression of Lin28, a heterochronic gene and pluripotency factor implicated in driving a fetal hematopoietic program, caused MC accumulation in adult mice in target organs such as the skin and peritoneal cavity. In vitro assays revealed a skewing of myeloid commitment in LIN28B-expressing hematopoietic progenitors, with increased levels of LIN28B in common myeloid and basophil-MC progenitors altering gene expression patterns to favor cell fate choices that enhanced MC specification. In addition, LIN28B-induced MCs appeared phenotypically and functionally immature, and in vitro assays suggested a slowing of MC terminal differentiation in the context of LIN28B upregulation. Finally, interrogation of human MC leukemia samples revealed upregulation of LIN28B in abnormal MCs from patients with SM. This work identifies Lin28 as a novel regulator of innate immune function and a new protein of interest in MC disease.

Indexed as

Cell DifferentiationAgedAged, 80 and overAnimalsBlotting, WesternBone Marrow TransplantationCells, CulturedDNA-Binding ProteinsFemaleFlow CytometryHematopoiesisHumansLeukemia, Mast-CellMaleMast CellsMastocytosis, SystemicDNA-Binding ProteinsLIN28B protein, humanLin28b protein, mouseRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID25655194
PMCPMC4456252
OpenAlexW2032699820

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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.