Evidence map›Paper›PMID 22753496›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

JNK and PTEN cooperatively control the development of invasive adenocarcinoma of the prostate.

Anette Hübner, David J Mulholland, Claire L Standen, Maria Karasarides, Julie Cavanagh-Kyros, Tamera Barrett, Hongbo Chi, Dale L Greiner, Cathy Tournier, Charles L Sawyers and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
9.8field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 102 citations in OpenAlex.

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  8. HER2-driven breast cancer suppression by the JNK signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 6 institutions in 2 countries.

Anette HübnerUniversity of Massachusetts Medical School, Worcester, MA 01605, USA.
David J Mulholland
Claire L Standen
Maria Karasarides
Julie Cavanagh-Kyros
Tamera Barrett
Hongbo Chi
Dale L Greiner
Cathy Tournier
Charles L Sawyers
Richard A Flavell
Hong Wu
Roger J Davis
Howard Hughes Medical Institute · USUniversity of Massachusetts Chan Medical School · USInstitute for Molecular Medicine · USSt. Jude Children's Research Hospital · USUniversity of California, Los Angeles · USUniversity of Manchester · GB

Funding

Virology and Technology CoreP01AI046629 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WELSH, RAYMOND M · 1999 to 2014
$19.1M
PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
Mechanisms of Action of Pro-inflammatory CytokinesR01CA065861 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DAVIS, ROGER J. · 1995 to 2010
$2.8M
Study of cell-of-origin and cancer stem cells in prostatic adenocarcinomaR01CA121110 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WU, HONG · 2008 to 2012
$1.7M
PTEN and Prostate Cancer ProgressionR01CA107166 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WU, HONG · 2004 to 2008
$1.7M
Deciphering Beta-Catenin Contributions in Prostate CanceF32CA112988 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MULHOLLAND, DAVID · 2005 to 2008
$138k
Howard Hughes Medical InstituteNCI NIH HHS CA065861NCI NIH HHS CA107166NCI NIH HHS CA112988NCI NIH HHS CA121110NCI NIH HHS F32 CA112988NCI NIH HHS R01 CA065861NCI NIH HHS R01 CA107166NCI NIH HHS R01 CA121110NIAID NIH HHS AI046629NIAID NIH HHS P01 AI046629NIDDK NIH HHS DK032520NIDDK NIH HHS P30 DK032520
6 · The paper itself

Abstract

The c-Jun NH(2)-terminal kinase (JNK) signal transduction pathway is implicated in cancer, but the role of JNK in tumorigenesis is poorly understood. Here, we demonstrate that the JNK signaling pathway reduces the development of invasive adenocarcinoma in the phosphatase and tensin homolog (Pten) conditional deletion model of prostate cancer. Mice with JNK deficiency in the prostate epithelium (ΔJnk ΔPten mice) develop androgen-independent metastatic prostate cancer more rapidly than control (ΔPten) mice. Similarly, prevention of JNK activation in the prostate epithelium (ΔMkk4 ΔMkk7 ΔPten mice) causes rapid development of invasive adenocarcinoma. We found that JNK signaling defects cause an androgen-independent expansion of the immature progenitor cell population in the primary tumor. The JNK-deficient progenitor cells display increased proliferation and tumorigenic potential compared with progenitor cells from control prostate tumors. These data demonstrate that the JNK and PTEN signaling pathways can cooperate to regulate the progression of prostate neoplasia to invasive adenocarcinoma.

Indexed as

AdenocarcinomaAnimalsCell Transformation, NeoplasticHistological TechniquesJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Signaling SystemMiceMice, TransgenicMicroscopy, FluorescenceProstatic NeoplasmsPTEN PhosphohydrolaseJNK Mitogen-Activated Protein KinasesPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID22753496
PMCPMC3409732
OpenAlexW1994637653

What OpenQuestion holds

Textmetadata
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.