Evidence map›Paper›PMID 24331662›Full record

ArticleInternational journal of radiation oncology, biology, physics2014

A critical role of the PTEN/PDGF signaling network for the regulation of radiosensitivity in adenocarcinoma of the prostate.

Michael Christensen, Abdo J Najy, Michael Snyder, Lisa S Movilla, Hyeong-Reh Choi Kim

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in International journal of radiation oncology, biology, physics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03296124 (Prognostic Value of Androgen Receptor Expression and Mutations Within Oncogenes and Tumor Suppressor Genes in Patients Treated for High Risk Prostate Cancer With Proton Therapy), which is not on this map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 23% 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.

NCT03296124 withdrawnnot on this mapstarted 2017, after this paper: background citation

Prognostic Value of Androgen Receptor Expression and Mutations Within Oncogenes and Tumor Suppressor Genes in Patients Treated for High Risk Prostate Cancer With Proton Therapy

TypeobservationalSponsorUniversity of FloridaRan2017 to 2020Enrolled0ConditionsProstate Cancer
3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Silencing APLNR enhances the radiosensitivity of prostate cancer by modulating the PI3K/AKT/mTOR signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  2. Review
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  5. Article
  6. Observational
  7. Review
  8. OverexpressingOncotarget · 2018
    Article
  9. Review
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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

5 authors at 2 institutions in 1 country.

Michael ChristensenDepartment of Radiation Oncology, Wayne State University School of Medicine, Barbara Ann Karmanos Cancer Center, Detroit, Michigan. Electronic address: mechristense@uwalumni.com.
Abdo J NajyDepartment of Pathology, Wayne State University School of Medicine, Barbara Ann Karmanos Cancer Center, Detroit, Michigan.
Michael SnyderDepartment of Radiation Oncology, Wayne State University School of Medicine, Barbara Ann Karmanos Cancer Center, Detroit, Michigan.
Lisa S MovillaDepartment of Radiation Oncology, Wayne State University School of Medicine, Barbara Ann Karmanos Cancer Center, Detroit, Michigan.
Hyeong-Reh Choi KimDepartment of Pathology, Wayne State University School of Medicine, Barbara Ann Karmanos Cancer Center, Detroit, Michigan.
The Barbara Ann Karmanos Cancer Institute · USWayne State University · US

Funding

PDGF D AND PROSTATE CANCER BONE METASTASISR01CA123362 · NCI · WAYNE STATE UNIVERSITY · PI KIM, HYEONG-REH CHOI · 2010 to 2020
$3.1M
ELUCIDATING THE FUNCTION OF MATRIPTASE-ACTIVATED PDGF D IN BONE METASTATIC PROSTAF32CA142038 · NCI · WAYNE STATE UNIVERSITY · PI NAJY, ABDO JAMAL · 2010 to 2012
$160k
NCI NIH HHS F32 CA142038NCI NIH HHS F32-CA 142038NCI NIH HHS R01 CA123362NCI NIH HHS R01CA123362
6 · The paper itself

Abstract

purposeLoss or mutation of the phosphate and tensin homologue (PTEN) is a common genetic abnormality in prostate cancer (PCa) and induces platelet-derived growth factor D (PDGF D) signaling. We examined the role of the PTEN/PDGF axis on radioresponse using a murine PTEN null prostate epithelial cell model. METHODS AND MATERIALS: PTEN wild-type (PTEN+/+) and PTEN knockout (PTEN-/-) murine prostate epithelial cell lines were used to examine the relationship between the PTEN status and radiosensitivity and also to modulate the PDGF D expression levels. PTEN-/- cells were transduced with a small hairpin RNA (shRNA) lentiviral vector containing either scrambled nucleotides (SCRM) or sequences targeted to PDGF D (shPDGF D). Tumorigenesis and morphogenesis of these cell lines were evaluated in vivo via subcutaneous injection of male nude mice and in vitro using Matrigel 3-dimensional (3D) culture. Effects of irradiation on clonogenic survival, cell migration, and invasion were measured with respect to the PTEN status and the PDGF D expression level. In addition, apoptosis and cell cycle redistribution were examined as potential mechanisms for differences seen.

resultsPTEN-/- cells were highly tumorigenic in animals and effectively formed foci in 3D culture. Importantly, loss of PDGF D in these cell lines drastically diminished these phenotypes. Furthermore, PTEN-/- cells demonstrated increased clonogenic survival in vitro compared to PTEN+/+, and attenuation of PDGF D significantly reversed this radioresistant phenotype. PTEN-/- cells displayed greater migratory and invasive potential at baseline as well as after irradiation. Both the basal and radiation-induced migratory and invasive phenotypes in PTEN-/- cells required PDGF D expression. Interestingly, these differences were independent of apoptosis and cell cycle redistribution, as they showed no significant difference.

conclusionsWe propose that PDGF D represents a potentially promising target for PCa treatment resistance in the absence of PTEN function, and warrants further laboratory evaluation and clinical study.

Indexed as

Cell Transformation, NeoplasticAdenocarcinomaAnimalsApoptosisCell CycleCell Line, TumorCell MovementCell SurvivalLymphokinesMaleMiceMice, NudeMice, SCIDNeoplasm InvasivenessNeoplasm ProteinsPhenotypeLymphokinesNeoplasm ProteinsPDGFD protein, humanPlatelet-Derived Growth FactorPTEN PhosphohydrolasePTEN protein, humanReceptor, Platelet-Derived Growth Factor beta

Identifiers

PMID24331662
PMCPMC4920083
OpenAlexW1968952135

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Registered trials

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.