Evidence map›Paper›PMID 25117712›Full record

ArticleCancer cell2014

Lin28b is sufficient to drive liver cancer and necessary for its maintenance in murine models.

Liem H Nguyen, Daisy A Robinton, Marc T Seligson, Linwei Wu, Lin Li, Dinesh Rakheja, Sarah A Comerford, Saleh Ramezani, Xiankai Sun, Monisha S Parikh and 7 more

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

Article in Cancer cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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

130 citing papers in PubMed, 1 synthesis or guideline pooled it, 226 citations in OpenAlex.

  1. Pooled it
  2. Review
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  9. Review
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  19. Landscape of mFrontiers in pharmacology · 2024
    Review
  20. Article

70 more citing papers are in PubMed but not listed here.

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

17 authors at 6 institutions in 2 countries.

Liem H NguyenChildren's Research Institute, Departments of Pediatrics and Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Daisy A RobintonDivision of Pediatric Hematology/Oncology, Children's Hospital Boston, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Marc T SeligsonDivision of Pediatric Hematology/Oncology, Children's Hospital Boston, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Linwei WuChildren's Research Institute, Departments of Pediatrics and Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Organ Transplant Center, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510080, China.
Lin LiChildren's Research Institute, Departments of Pediatrics and Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Dinesh RakhejaDepartments of Pathology and Pediatrics, Children's Medical Center and University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Sarah A ComerfordDepartment of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Saleh RamezaniDepartment of Radiology and Advanced Imaging Research Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Xiankai SunDepartment of Radiology and Advanced Imaging Research Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Monisha S ParikhChildren's Research Institute, Departments of Pediatrics and Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Erin H YangChildren's Research Institute, Departments of Pediatrics and Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
John T PowersDivision of Pediatric Hematology/Oncology, Children's Hospital Boston, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Gen ShinodaDivision of Pediatric Hematology/Oncology, Children's Hospital Boston, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Samar P ShahDivision of Pediatric Hematology/Oncology, Children's Hospital Boston, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Robert E HammerDepartment of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
George Q DaleyDivision of Pediatric Hematology/Oncology, Children's Hospital Boston, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: george.daley@childrens.harvard.edu.
Hao ZhuChildren's Research Institute, Departments of Pediatrics and Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: hao.zhu@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USBoston Children's Hospital · USHarvard University · USChildren's Medical Center · USSouthwestern Medical Center · USSun Yat-sen University · CN

Funding

Understanding the role of the lin28 paralogs and branching morphogenesisR01GM107536 · NIGMS · BOSTON CHILDREN'S HOSPITAL · PI DALEY, GEORGE Q · 2014 to 2017
$1.9M
Metabolic roles for Lin28-let-7 miRNA pathway in sarcoma tumorigenesisK08CA157727 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI ZHU, HAO · 2011 to 2015
$807k
Howard Hughes Medical InstituteNCI NIH HHS 1K08CA157727-02NCI NIH HHS K08 CA157727NIGMS NIH HHS R01 GM107536
6 · The paper itself

Abstract

Lin28a/b are RNA-binding proteins that influence stem cell maintenance, metabolism, and oncogenesis. Poorly differentiated, aggressive cancers often overexpress Lin28, but its role in tumor initiation or maintenance has not been definitively addressed. We report that LIN28B overexpression is sufficient to initiate hepatoblastoma and hepatocellular carcinoma in murine models. We also detected Lin28b overexpression in MYC-driven hepatoblastomas, and liver-specific deletion of Lin28a/b reduced tumor burden, extended latency, and prolonged survival. Both intravenous siRNA against Lin28b and conditional Lin28b deletion reduced tumor burden and prolonged survival. Igf2bp proteins are upregulated, and Igf2bp3 is required in the context of LIN28B overexpression to promote growth. Therefore, multiple murine models demonstrate that Lin28b is both sufficient to initiate liver cancer and necessary for its maintenance.

Indexed as

AnimalsCarcinogenesisHepatoblastomaHumansLiver Neoplasms, ExperimentalMiceMice, TransgenicOncogenesProto-Oncogene Proteins c-mycRNA-Binding ProteinsTumor BurdenIGF2BP3 protein, humanLIN28B protein, humanMyc protein, mouseProto-Oncogene Proteins c-mycRNA-Binding Proteins

Identifiers

PMID25117712
PMCPMC4145706
OpenAlexW2033267718

What OpenQuestion holds

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Registered trials

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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.