Evidence map›Paper›PMID 32051529›Full record

ArticleLeukemia2020

SRSF1 mediates cytokine-induced impaired imatinib sensitivity in chronic myeloid leukemia.

Joanna R Sinnakannu, Kian Leong Lee, Shanshan Cheng, Jia Li, Mengge Yu, Siew Peng Tan, Clara Chong Hui Ong, Huihua Li, Hein Than, Olga Anczuków-Camarda and 7 more

Open access · greenAbstract read
In one paragraph

Article in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Targeting O-GlcNAcylated METTL3 impedes MDS/AML progression via diminishing SRSF1 mMolecular therapy : the journal of the American Society of Gene Therapy · 2025
    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

17 authors at 6 institutions in 2 countries.

Joanna R SinnakannuCancer and Stem Cell Biology Programme, Duke-NUS Medical School, Singapore, Singapore.
Kian Leong LeeCancer and Stem Cell Biology Programme, Duke-NUS Medical School, Singapore, Singapore.
Shanshan ChengCancer and Stem Cell Biology Programme, Duke-NUS Medical School, Singapore, Singapore.
Jia LiCancer Science Institute of Singapore, Singapore, Singapore.
Mengge YuCancer and Stem Cell Biology Programme, Duke-NUS Medical School, Singapore, Singapore.
Siew Peng TanCancer and Stem Cell Biology Programme, Duke-NUS Medical School, Singapore, Singapore.
Clara Chong Hui OngDepartment of Anatomical Pathology, Singapore General Hospital, Singapore, Singapore.
Huihua LiHealth Services Research Unit, Singapore General Hospital, Singapore, Singapore.
Hein ThanDepartment of Haematology, Singapore General Hospital, Singapore, Singapore.
Olga Anczuków-CamardaThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Adrian R KrainerCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Xavier RocaSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
Steven G RozenCancer and Stem Cell Biology Programme, Duke-NUS Medical School, Singapore, Singapore.
Jabed IqbalDepartment of Anatomical Pathology, Singapore General Hospital, Singapore, Singapore.
Henry YangCancer Science Institute of Singapore, Singapore, Singapore.
Charles ChuahCancer and Stem Cell Biology Programme, Duke-NUS Medical School, Singapore, Singapore.
Sin Tiong OngCancer and Stem Cell Biology Programme, Duke-NUS Medical School, Singapore, Singapore. sintiong.ong@duke-nus.edu.sg.
Duke-NUS Medical School · SGSingapore General Hospital · SGNational University Cancer Institute, Singapore · SGCold Spring Harbor Laboratory · USJackson Laboratory · USNanyang Technological University · SG

Funding

VIRAL TRANSACTIVATIONP01CA013106 · NCI · COLD SPRING HARBOR LABORATORY · PI Camila dos Santos · 1985 to 2026
$116.8M
NCI NIH HHS P01 CA013106
6 · The paper itself

Abstract

Patients with chronic myeloid leukemia (CML) who are treated with tyrosine kinase inhibitors (TKIs) experience significant heterogeneity regarding depth and speed of responses. Factors intrinsic and extrinsic to CML cells contribute to response heterogeneity and TKI resistance. Among extrinsic factors, cytokine-mediated TKI resistance has been demonstrated in CML progenitors, but the underlying mechanisms remain obscure. Using RNA-sequencing, we identified differentially expressed splicing factors in primary CD34

Indexed as

Biomarkers, TumorBone MarrowCytokinesDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplastic Stem CellsPrognosisProtein Kinase InhibitorsSerine-Arginine Splicing FactorsTumor Cells, CulturedBiomarkers, TumorCytokinesImatinib MesylateProtein Kinase InhibitorsSerine-Arginine Splicing FactorsSRSF1 protein, human

Identifiers

PMID32051529
PMCPMC7682023
OpenAlexW3006473636

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.