Evidence map›Paper›PMID 31794893›Full record

ArticleDNA repair2020

Loss of Setd4 delays radiation-induced thymic lymphoma in mice.

Xing Feng, Huimei Lu, Jingyin Yue, Neta Schneider, Jingmei Liu, Lisa K Denzin, Chang S Chan, Subhajyoti De, Zhiyuan Shen

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in DNA repair, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Deletion of Mouse Setd4 Promotes the Recovery of Hematopoietic Failure.International journal of radiation oncology, biology, physics · 2020
    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

9 authors at 2 institutions in 1 country.

Xing FengRutgers Cancer Institute of New Jersey, Department of Radiation Oncology, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ 08903, USA.
Huimei LuRutgers Cancer Institute of New Jersey, Department of Radiation Oncology, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ 08903, USA.
Jingyin YueRutgers Cancer Institute of New Jersey, Department of Radiation Oncology, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ 08903, USA.
Neta SchneiderRutgers Cancer Institute of New Jersey, Department of Radiation Oncology, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ 08903, USA.
Jingmei LiuRutgers Cancer Institute of New Jersey, Department of Radiation Oncology, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ 08903, USA.
Lisa K DenzinChild Health Institute of New Jersey, Rutgers Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ, USA.
Chang S ChanCenter for Systems and Computational Biology, Rutgers Cancer Institute of New Jersey, Rutgers the State University of New Jersey, New Brunswick, NJ 08901, USA.
Subhajyoti DeCenter for Systems and Computational Biology, Rutgers Cancer Institute of New Jersey, Rutgers the State University of New Jersey, New Brunswick, NJ 08901, USA.
Zhiyuan ShenRutgers Cancer Institute of New Jersey, Department of Radiation Oncology, Rutgers Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ 08903, USA. Electronic address: shenzh@cinj.rutgers.edu.
Rutgers, The State University of New Jersey · USRutgers Cancer Institute of New Jersey

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Tracie Saunders · 1997 to 2026
$94.5M
Molecular modulators of radiation-induced chromosome instability and hematopoietic damageR01CA195612 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI SHEN, ZHIYUAN · 2015 to 2025
$3.6M
Alternative Mechanisms to Inactivate p53 During OncogenesisR01CA156706 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI SHEN, ZHIYUAN · 2011 to 2015
$1.9M
Computational approaches for identifying epigenomic contexts of somatic mutationsR01GM129066 · NIGMS · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI DE, SUBHAJYOTI · 2019 to 2023
$1.7M
NCI NIH HHS P30 CA072720NCI NIH HHS R01 CA156706NCI NIH HHS R01 CA195612NIGMS NIH HHS R01 GM129066
6 · The paper itself

Abstract

Radiation-induced lymphomagenesis results from a clonogenic lymphoid cell proliferation due to genetic alterations and immunological dysregulation. Mouse models had been successfully used to identify risk and protective factors for radiation-induced DNA damage and carcinogenesis. The mammalian SETD4 is a poorly understood putative methyl-transferase. Here, we report that conditional Setd4 deletion in adult mice significantly extended the survival of radiation-induced T-lymphoma. However, in Tp53 deficient mice, Setd4 deletion did not delay the radiation-induced lymphomagenesis although it accelerated the spontaneous T-lymphomagenesis in non-irradiated mice. The T-lymphomas were largely clonogenic in both Setd4

Indexed as

Gene DeletionAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesDisease Models, AnimalLymphomaMethyltransferasesMiceNeoplasms, Radiation-InducedReceptors, Antigen, T-Cell, alpha-betaSequence Analysis, DNAThymus NeoplasmsTumor Suppressor Protein p53MethyltransferasesReceptors, Antigen, T-Cell, alpha-betaSetd4 protein, mouseTrp53 protein, mouseTumor Suppressor Protein p53Chromosome rearrangementGenomic instabilityRadiation carcinogenesisSetd4T-cell lymphoma

Identifiers

PMID31794893
PMCPMC6960333
OpenAlexW2991402378

What OpenQuestion 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 OpenQuestion graph.