Evidence map›Paper›PMID 24686169›Full record

ArticleCancer research2014

NF-κB gene signature predicts prostate cancer progression.

Renjie Jin, Yajun Yi, Fiona E Yull, Timothy S Blackwell, Peter E Clark, Tatsuki Koyama, Joseph A Smith, Robert J Matusik

Abstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Review
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  10. Article
  11. Microorganisms · 2024
    Article
  12. Review
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  15. Prostate Cancer Stem Cells: Biology and Treatment Implications.International journal of molecular sciences · 2023
    Review
  16. Review
  17. Article
  18. Article
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  20. Article

23 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

Renjie JinAuthors' Affiliations: Department of Urologic Surgery and Vanderbilt Prostate Cancer Center; Division of Genetic Medicine, Department of Medicine; Departments of Cancer Biology and Medicine; and Division of Cancer Biostatistics, Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee.
Yajun YiAuthors' Affiliations: Department of Urologic Surgery and Vanderbilt Prostate Cancer Center; Division of Genetic Medicine, Department of Medicine; Departments of Cancer Biology and Medicine; and Division of Cancer Biostatistics, Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee.
Fiona E YullAuthors' Affiliations: Department of Urologic Surgery and Vanderbilt Prostate Cancer Center; Division of Genetic Medicine, Department of Medicine; Departments of Cancer Biology and Medicine; and Division of Cancer Biostatistics, Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee.
Timothy S BlackwellAuthors' Affiliations: Department of Urologic Surgery and Vanderbilt Prostate Cancer Center; Division of Genetic Medicine, Department of Medicine; Departments of Cancer Biology and Medicine; and Division of Cancer Biostatistics, Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee.
Peter E ClarkAuthors' Affiliations: Department of Urologic Surgery and Vanderbilt Prostate Cancer Center; Division of Genetic Medicine, Department of Medicine; Departments of Cancer Biology and Medicine; and Division of Cancer Biostatistics, Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee.
Tatsuki KoyamaAuthors' Affiliations: Department of Urologic Surgery and Vanderbilt Prostate Cancer Center; Division of Genetic Medicine, Department of Medicine; Departments of Cancer Biology and Medicine; and Division of Cancer Biostatistics, Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee.
Joseph A SmithAuthors' Affiliations: Department of Urologic Surgery and Vanderbilt Prostate Cancer Center; Division of Genetic Medicine, Department of Medicine; Departments of Cancer Biology and Medicine; and Division of Cancer Biostatistics, Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee.
Robert J MatusikAuthors' Affiliations: Department of Urologic Surgery and Vanderbilt Prostate Cancer Center; Division of Genetic Medicine, Department of Medicine; Departments of Cancer Biology and Medicine; and Division of Cancer Biostatistics, Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TennesseeAuthors' Affiliations: Department of Urologic Surgery and Vanderbilt Prostate Cancer Center; Division of Genetic Medicine, Department of Medicine; Departments of Cancer Biology and Medicine; and Division of Cancer Biostatistics, Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee robert.matusik@vanderbilt.edu.
Vanderbilt University Medical Center · US

Funding

TRANSGENIC MOUSE MODEL FOR PROSTATE CANCERR01CA076142 · NCI · VANDERBILT UNIVERSITY · PI MATUSIK, ROBERT J. · 1998 to 2012
$4.8M
Epithelial NF-KappaB signaling in Mammary TumorigenesisR01CA113734 · NCI · VANDERBILT UNIVERSITY · PI YULL, FIONA E · 2007 to 2011
$1.4M
NCI NIH HHS 4R01 CA076142-15NCI NIH HHS R01 CA076142NCI NIH HHS R01 CA113734NCI NIH HHS R01-CA113734
6 · The paper itself

Abstract

In many patients with prostate cancer, the cancer will be recurrent and eventually progress to lethal metastatic disease after primary treatment, such as surgery or radiation therapy. Therefore, it would be beneficial to better predict which patients with early-stage prostate cancer would progress or recur after primary definitive treatment. In addition, many studies indicate that activation of NF-κB signaling correlates with prostate cancer progression; however, the precise underlying mechanism is not fully understood. Our studies show that activation of NF-κB signaling via deletion of one allele of its inhibitor, IκBα, did not induce prostatic tumorigenesis in our mouse model. However, activation of NF-κB signaling did increase the rate of tumor progression in the Hi-Myc mouse prostate cancer model when compared with Hi-Myc alone. Using the nonmalignant NF-κB-activated androgen-depleted mouse prostate, a NF-κB-activated recurrence predictor 21 (NARP21) gene signature was generated. The NARP21 signature successfully predicted disease-specific survival and distant metastases-free survival in patients with prostate cancer. This transgenic mouse model-derived gene signature provides a useful and unique molecular profile for human prostate cancer prognosis, which could be used on a prostatic biopsy to predict indolent versus aggressive behavior of the cancer after surgery.

Indexed as

AnimalsCarcinogenesisCell Line, TumorDisease Models, AnimalDisease ProgressionGene Expression ProfilingGene Regulatory NetworksHumansI-kappa B ProteinsMaleMiceMice, TransgenicNeoplasm MetastasisNF-kappa BNF-KappaB Inhibitor alphaProstatic NeoplasmsI-kappa B ProteinsNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanNfkbia protein, mouse

Identifiers

PMID24686169
PMCPMC4024337
OpenAlexW2015009117

What OpenQuestion holds

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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.