Evidence map›Paper›PMID 37558703›Full record

ArticleScientific reports2023

Characterizing the role of Phlda3 in the development of acute toxicity and malignant transformation of hematopoietic cells induced by total-body irradiation in mice.

Stephanie Hasapis, Isibel Caraballo, Timothy J Sears, Kennedy D Brock, John B Cart, Everett J Moding, Chang-Lung Lee

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

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Iodine-125 plesiotherapy for murine tumor treatment.Radiation oncology (London, England) · 2025
    Article
  4. Review
  5. Article
  6. Review
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

7 authors at 3 institutions in 1 country.

Stephanie HasapisDepartment of Radiation Oncology, Duke University School of Medicine, Duke University Medical Center, Box 3813, Durham, NC, 27708, USA.
Isibel CaraballoDepartment of Radiation Oncology, Duke University School of Medicine, Duke University Medical Center, Box 3813, Durham, NC, 27708, USA.
Timothy J SearsDepartment of Radiation Oncology, Stanford Cancer Institute, Stanford University, 875 Blake Wilbur Drive, Stanford, CA, 94305-5847, USA.
Kennedy D BrockDepartment of Radiation Oncology, Duke University School of Medicine, Duke University Medical Center, Box 3813, Durham, NC, 27708, USA.
John B CartDepartment of Radiation Oncology, Duke University School of Medicine, Duke University Medical Center, Box 3813, Durham, NC, 27708, USA.
Everett J ModingDepartment of Radiation Oncology, Stanford Cancer Institute, Stanford University, 875 Blake Wilbur Drive, Stanford, CA, 94305-5847, USA. emoding@stanford.edu.
Chang-Lung LeeDepartment of Radiation Oncology, Duke University School of Medicine, Duke University Medical Center, Box 3813, Durham, NC, 27708, USA. chang-lung.lee@duke.edu.
Duke Medical Center · USStanford University · USDuke University · US

Funding

Somatostatin analogues as countermeasures against intestinal radiation toxicityU19AI067798 · NIAID · DUKE UNIVERSITY · PI CHAO, NELSON J. · 2005 to 2024
$82.1M
Ionizing radiation promotes clonal expansion of premalignant cells in the thymusR00CA212198 · NCI · DUKE UNIVERSITY · PI LEE, CHANG-LUNG · 2018 to 2020
$747k
Dissecting mechanism(s) by which ionizing radiation promotes clonal expansion of premalignant cells in the thymusK99CA212198 · NCI · DUKE UNIVERSITY · PI LEE, CHANG-LUNG · 2016 to 2017
$229k
Minimizing the risk of therapy-related myeloid neoplasms by inhibiting genotoxic stress-induced expansion of leukemia-initiating cells with p53 mutationsR03CA249562 · NCI · DUKE UNIVERSITY · PI LEE, CHANG-LUNG · 2021 to 2022
$161k
NCI NIH HHS K99 CA212198NCI NIH HHS R00 CA212198NCI NIH HHS R03 CA249562NIAID NIH HHS U19 AI067798
6 · The paper itself

Abstract

The tumor suppressor p53 is a transcriptional factor that plays a crucial role in controlling acute toxicity and long-term malignant transformation of hematopoietic cells induced by genotoxic stress such as ionizing radiation. Among all transcriptional targets of p53, one gene that is robustly induced by radiation is the pleckstrin homology domain-only protein Phlda3. However, the role that Phlda3 plays in regulating the response of hematopoietic cells to radiation is unknown. Here, using isogenic cell lines and genetically engineered mouse models, we showed that radiation induces Phlda3 in human leukemia cells and mouse normal hematopoietic cells in a p53-dependent manner. However, deletion of the Phlda3 gene did not ameliorate radiation-induced acute hematologic toxicity. In addition, distinct from mice that lose p53, loss of Phlda3 did not alter the latency and incidence of radiation-induced thymic lymphoma in mice. Remarkably, whole-exome sequencing data showed that lymphomas in irradiated Phlda3

Indexed as

LymphomaNuclear ProteinsThymus NeoplasmsAnimalsCell LineCell Transformation, NeoplasticHumansMiceTumor Suppressor Protein p53Nuclear ProteinsTSSC3 proteinTumor Suppressor Protein p53

Identifiers

PMID37558703
PMCPMC10412554
OpenAlexW4385700428

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.