Evidence map›Paper›PMID 23608884›Full record

ArticleLeukemia2014

Loss of p53 and altered miR15-a/16-1MCL-1 pathway in CLL: insights from TCL1-Tg:p53(-/-) mouse model and primary human leukemia cells.

J Liu, G Chen, L Feng, W Zhang, H Pelicano, F Wang, M A Ogasawara, W Lu, H M Amin, C M Croce and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Complete miRNA-15/16 loss in mice promotes hematopoietic progenitor expansion and a myeloid-biased hyperproliferative state.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Small RNAs, Big Diseases.International journal of molecular sciences · 2020
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. A Looking-Glass of Non-coding RNAs in oral cancer.International journal of molecular sciences · 2017
    Review
  18. Article
  19. Article
  20. 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

12 authors at 3 institutions in 1 country.

J Liu1] Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX, USA.
G ChenDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
L FengDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
W Zhang1] Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
H PelicanoDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
F Wang1] Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, China.
M A Ogasawara1] Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX, USA.
W LuDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
H M AminDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
C M CroceDepartment of Molecular Virology, Immunology and Medical Genetics, The Ohio State University Medical Center, Columbus, OH, USA.
M J KeatingDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
P Huang1] Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX, USA [3] State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, China.
The University of Texas MD Anderson Cancer Center · USUniversity of Houston · USThe Ohio State University Wexner Medical Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Kathrin Milbury · 1985 to 2026
$290.8M
Tissue CoreP01CA081534 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RASSENTI, LAURA Z · 2000 to 2016
$59.5M
Superoxide, ROS, and novel targets for cancer therapyR01CA085563 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUANG, PENG · 2001 to 2016
$3.1M
p53 in Cellular Response to ROS-Mediated DNA DamageR01CA100428 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUANG, PENG · 2003 to 2012
$2.7M
TOWARD AN UNDERSTANDING OF CLL PROGRESSIONR01CA151319 · NCI · OHIO STATE UNIVERSITY · PI CROCE, CARLO M · 2011 to 2015
$1.5M
NCI NIH HHS CA016672NCI NIH HHS CA085563NCI NIH HHS CA100428NCI NIH HHS P01 CA081534NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA085563NCI NIH HHS R01 CA100428NCI NIH HHS R01 CA151319
6 · The paper itself

Abstract

Chronic lymphocytic leukemia (CLL) patients with deletion of chromosome 17p, where the p53 gene is located, often develop more aggressive disease with poor clinical outcomes. To investigate the underlying mechanisms for the highly malignant phenotype of 17p- CLL and to facilitate in vivo evaluation of potential drugs against CLL with p53 deletion, we have generated a mouse model with TCL1-Tg:p53(-/-) genotype. These mice develop B-cell leukemia at an early age with an early appearance of CD5+ / IgM+ B cells in the peritoneal cavity and spleen, and exhibit an aggressive path of disease development and drug resistance phenotype similar to human CLL with 17p deletion. The TCL1-Tg:p53(-/-) leukemia cells exhibit higher survival capacity and are more drug resistant than the leukemia cells from TCL1-Tg:p53wt mice. Analysis of microRNA expression reveals that p53 deletion resulted in a decrease of miR-15a and miR-16-1, leading to an elevated expression of Mcl-1. Primary leukemia cells from CLL patients with 17p deletion also show a decrease in miR-15a/miR-16-1 and an increase in Mcl-1. Our study suggests that the p53/miR15a/16-1/Mcl-1 axis may be an important pathway that regulates Mcl-1 expression and contributes to drug resistance and aggressive phenotype in CLL cells with loss of p53.

Indexed as

Disease Models, AnimalGenes, p53AnimalsCell Line, TumorHumansMiceMice, TransgenicMicroRNAsMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene ProteinsMCL1 protein, humanMicroRNAsMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene ProteinsTCL1A protein, human

Identifiers

PMID23608884
PMCPMC3806892
OpenAlexW2025965695

What OpenQuestion holds

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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.