Evidence map›Paper›PMID 25506060›Full record

ArticleEBioMedicine2014

A PREVIOUSLY UNKNOWN UNIQUE CHALLENGE FOR INHIBITORS OF SYK ATP-BINDING SITE: ROLE OF SYK AS A CELL CYCLE CHECKPOINT REGULATOR.

Fatih M Uckun, Hong Ma, Zahide Ozer, Patricia Goodman, Jian Zhang, Sanjive Qazi

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Syk-dependent homologous recombination activation promotes cancer resistance to DNA targeted therapy.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2024
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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

6 authors at 5 institutions in 2 countries.

Fatih M UckunChildren's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, CA 90027 ; Department of Pediatrics, University of Southern California Keck School of Medicine, Los Angeles, CA 90027, USA.
Hong MaChildren's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, CA 90027 ; Molecular Oncology Program, Parker Hughes Institute, St. Paul, MN 55113, USA; USA.
Zahide OzerChildren's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, CA 90027 ; Molecular Oncology Program, Parker Hughes Institute, St. Paul, MN 55113, USA; USA.
Patricia GoodmanMolecular Oncology Program, Parker Hughes Institute, St. Paul, MN 55113, USA; USA ; Department of Veterinary and Biomedical Science, University of Minnesota, St. Paul, MN 55108.
Jian ZhangMedicinal Bioinformatics Center, Shanghai Jiatong University.
Sanjive QaziChildren's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, CA 90027 ; Molecular Oncology Program, Parker Hughes Institute, St. Paul, MN 55113, USA; USA ; Department of Biology and Bioinformatics Program, Gustavus Adolphus College, 800 W College Avenue, St. Peter, MN 56082, USA.
Children's Hospital of Los Angeles · USGustavus Adolphus College · USParker Hughes Cancer Center · USShanghai Jiao Tong University · CNUniversity of Minnesota · US

Funding

USC/NORRIS COMPREHENSIVE CANCER CENTER (CORE) SUPPORTP30CA014089 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Fumito Ito · 1985 to 2026
$181.4M
Targeting SYK Kinase in B-Lineage ALL with CD19-Specific C-61 NanoparticlesU01CA151837 · NCI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI UCKUN, FATIH M · 2010 to 2014
$2.3M
Targeting SYK Tyrosine Kinase to Overcome Radiation Resistance in ALLR01CA154471 · NCI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI UCKUN, FATIH M · 2011 to 2015
$1.6M
NCI NIH HHS P30 CA014089NCI NIH HHS R01 CA154471NCI NIH HHS U01 CA151837
6 · The paper itself

Abstract

The identification of SYK as a molecular target in B-lineage leukemia/lymphoma cells prompted the development of SYK inhibitors as a new class of anti-cancer drug candidates. Here we report that induction of the SYK gene expression in human cells causes a significant down-regulation of evolutionarily conserved genes associated with mitosis and cell cycle progression providing unprecedented evidence that SYK is a master regulator of cell cycle regulatory checkpoint genes in human cells. We further show that SYK regulates the G

Indexed as

Cell cyclecheckpoint controlgenomnic instabilityphosphatasetyrosine kinase

Identifiers

PMID25506060
PMCPMC4259291
OpenAlexW2005894094

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.