Evidence map›Paper›PMID 27007052›Full record

ArticleOncotarget2016

Differential regulation of the c-Myc/Lin28 axis discriminates subclasses of rearranged MLL leukemia.

Lili Chen, Yuqing Sun, Jingya Wang, Hui Jiang, Andrew G Muntean

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. MNT: a new target for AML.Blood neoplasia · 2025
    Article
  3. Article
  4. Review
  5. Correlation between expression of Lin28B and C-myc in patients with laryngeal squamous cell carcinoma and clinicopathological features and prognosis.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. RNA Regulators in Leukemia and Lymphoma.Cold Spring Harbor perspectives in medicine · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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

5 authors at 1 institution in 1 country.

Lili ChenDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA.
Yuqing SunDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA.
Jingya WangDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA.
Hui JiangDepartment of Biostatistics, School of Public Health,University of Michigan, Ann Arbor, MI, USA.
Andrew G MunteanDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · US

Funding

Post-translational regulation of MLL in leukemogenesisR00CA158136 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MUNTEAN, ANDREW GEORGE · 2012 to 2014
$670k
NCI NIH HHS R00 CA158136
6 · The paper itself

Abstract

MLL rearrangements occur in myeloid and lymphoid leukemias and are generally associated with a poor prognosis, however this varies depending on the fusion partner. We modeled acute myeloid leukemia (AML) in mice using various MLL fusion proteins (MLL-FPs) and observed significantly different survival outcomes. To better understand the differences between these leukemias, we examined the genome wide expression profiles of leukemic cells transformed with different MLL-FPs. RNA-sequencing and pathway analysis identified the c-Myc transcriptional program as one of the top distinguishing features. c-Myc protein levels were highly correlative with AML disease latency in mice. Functionally, overexpression of c-Myc resulted in a more aggressive proliferation rate in MLL-FP cell lines. While all MLL-FP transformed cells displayed sensitivity to BET inhibitors, high c-Myc expressing cells showed greater resistance to Brd4 inhibition. The Myc target Lin28B was also differentially expressed in MLL-FP cell lines in agreement with c-Myc expression. Examination of Lin28B miRNAs targets revealed that let-7g was significantly increased in leukemic cells associated with the longest disease latency and forced let-7g expression induced differentiation of leukemic blasts. Thus, differential regulation of the c-Myc/Lin28/let-7g program by different MLL-FPs is functionally related to disease latency and BET inhibitor resistance in MLL leukemias.

Indexed as

AnimalsCell Transformation, NeoplasticDrug Resistance, NeoplasmGene Expression Regulation, LeukemicGene RearrangementHistone-Lysine N-MethyltransferaseLeukemia, Myeloid, AcuteMiceMice, Inbred C57BLMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionProto-Oncogene Proteins c-mycRNA-Binding ProteinsHistone-Lysine N-MethyltransferaseKmt2a protein, mouseLin-28 protein, mouseMyc protein, mouseMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionProto-Oncogene Proteins c-mycRNA-Binding Proteinsacute myeloid leukemiac-Myclet-7Lin28MLL

Identifiers

PMID27007052
PMCPMC5041898
OpenAlexW2311505902

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.