Evidence map›Paper›PMID 24997151›Full record

ArticleHaematologica2014

The Sox4/Tcf7l1 axis promotes progression of BCR-ABL-positive acute lymphoblastic leukemia.

Haiqing Ma, Saradhi Mallampati, Yue Lu, Baohua Sun, Enze Wang, Xiaohong Leng, Yun Gong, Haifa Shen, C Cameron Yin, Dan Jones and 8 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. BioMed research international · 2021
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  19. Microarray-based identification of differentially expressed genes in extramammary Paget's disease.International journal of clinical and experimental medicine · 2015
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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

18 authors at 4 institutions in 2 countries.

Haiqing MaDepartment of Laboratory Medicine and the Center for Stem Cell and Developmental Biology, The University of Texas MD Anderson Cancer Center (MDACC), Houston, TX, USA Department of Oncology, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.
Saradhi MallampatiDepartment of Laboratory Medicine and the Center for Stem Cell and Developmental Biology, The University of Texas MD Anderson Cancer Center (MDACC), Houston, TX, USA.
Yue LuDepartment of Molecular Carcinogenesis, The University of Texas MDACC, Houston, TX, USA.
Baohua SunDepartment of Laboratory Medicine and the Center for Stem Cell and Developmental Biology, The University of Texas MD Anderson Cancer Center (MDACC), Houston, TX, USA.
Enze WangDepartment of Laboratory Medicine and the Center for Stem Cell and Developmental Biology, The University of Texas MD Anderson Cancer Center (MDACC), Houston, TX, USA.
Xiaohong LengDepartment of Translational Molecular Pathology, The University of Texas MDACC, Houston, TX, USA.
Yun GongDepartment of Pathology, The University of Texas MDACC, Houston, TX, USA.
Haifa ShenDepartment of Nanomedicine, Houston Methodist Research Institute, TX, and Department of Cell and Developmental Biology, Weill Cornell Medical College, New York, NY, USA.
C Cameron YinDepartment of Hematopathology, The University of Texas MDACC, Houston, TX, USA.
Dan JonesSchool of Health Sciences, The University of Texas MDACC, Houston, TX, USA.
Hesham M AminDepartment of Hematopathology, The University of Texas MDACC, Houston, TX, USA.
M James YouDepartment of Hematopathology, The University of Texas MDACC, Houston, TX, USA.
Patrick Zweidler-McKayDepartment of Pediatrics, The University of Texas MDACC, Houston, TX, USA.
Yupo MaDepartment of Pathology, Stony Brook University Medical Center, Stony Brook, NY, USA.
Hagop M KantarjianDepartment of Leukemia, The University of Texas MDACC, Houston, TX, USA.
Ralph B ArlinghausDepartment of Translational Molecular Pathology, The University of Texas MDACC, Houston, TX, USA.
Armand GlassmanDepartment of Microbiology and Immunology, The Medical University of South Carolina, Charleston, and Department of Pathology & Laboratory Medicine, The University of Texas Houston Health Science Center, Houston, TX, USA.
Xiaoping SunDepartment of Laboratory Medicine and the Center for Stem Cell and Developmental Biology, The University of Texas MD Anderson Cancer Center (MDACC), Houston, TX, USA xsun@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USThe University of Texas Health Science Center at Houston · USHouston Methodist · USStony Brook University Hospital · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
CHARACTERIZATION AND TARGETED THERAPY OF T-ALL DEFICIENT FOR PTEN AND INK4A/ARFR01CA164346 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YOU, M. JAMES · 2012 to 2015
$1.2M
NCI NIH HHS CA016672.NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA164346
6 · The paper itself

Abstract

The transcription factor Sox4 plays an indispensable role in the development of early progenitor B cells from hematopoietic stem cells. However, its role in B-cell acute lymphoblastic leukemia, a malignant counterpart of normal progenitor B cells, is not fully understood. Here we show that SOX4 is highly expressed in human acute lymphoblastic leukemia cells. To systematically study the function of Sox4 in acute lymphoblastic leukemia, we established a genetically defined mouse leukemia model by transforming progenitor B cells carrying a floxed Sox4 allele and inducing deletion of the allele by the self-excising Cre recombinase. This model allowed us to work with two groups of leukemic cells that had either one copy or both copies of Sox4 deleted. We found that depletion of Sox4 in transformed cells in vitro reduced cell growth in vitro and the progression of leukemia in vivo. Moreover, depletion of Sox4 in leukemic cells in vivo prolonged the survival of the mice, suggesting that it could be a potential target in acute lymphoblastic leukemia therapy. Our microarray and bioChIP studies revealed that Tcf7l1 was the key gene directly regulated by Sox4. Knockdown of Tcf7l1 reduced cell proliferation, just as did knockout of Sox4, and ectopic expression of Tcf7l1 could reverse the effect of Sox4 knockout on cell proliferation. These data suggest that Sox4 and Tcf7l1 form a functional axis that promotes the progression of BCR-ABL-positive acute lymphoblastic leukemia.

Indexed as

AnimalsCell Line, TumorCell Transformation, NeoplasticCluster AnalysisDisease ProgressionFusion Proteins, bcr-ablGene Expression ProfilingGene Expression Regulation, LeukemicHumansMiceMice, TransgenicPrecursor Cell Lymphoblastic Leukemia-LymphomaRNA InterferenceRNA, MessengerSOXC Transcription FactorsTranscription Factor 7-Like 1 ProteinFusion Proteins, bcr-ablRNA, MessengerSOXC Transcription FactorsTranscription Factor 7-Like 1 Protein

Identifiers

PMID24997151
PMCPMC4181255
OpenAlexW2076561248

What OpenQuestion holds

Textmetadata
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.