Evidence map›Paper›PMID 22307624›Full record

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

Oncogene-specific activation of tyrosine kinase networks during prostate cancer progression.

Justin M Drake, Nicholas A Graham, Tanya Stoyanova, Amir Sedghi, Andrew S Goldstein, Houjian Cai, Daniel A Smith, Hong Zhang, Evangelia Komisopoulou, Jiaoti Huang and 2 more

Abstract 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 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
–field-weighted citation impact
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

96 citing papers in PubMed.

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  10. Impact of cell plasticity on prostate tumor heterogeneity and therapeutic response.American journal of clinical and experimental urology · 2024
    Review
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  12. Article
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  20. MEK inhibitor sensitivity in BRAF fusion-driven prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article

36 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

12 authors.

Justin M DrakeDepartment of Microbiology, Immunology, and Molecular Genetics, Crump Institute for Molecular Imaging, Institute for Molecular Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Nicholas A Graham
Tanya Stoyanova
Amir Sedghi
Andrew S Goldstein
Houjian Cai
Daniel A Smith
Hong Zhang
Evangelia Komisopoulou
Jiaoti Huang
Thomas G Graeber
Owen N Witte

Funding

TUMOR CELL SURFACES AND CHROMOSOMEST32CA009056 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Gay M Crooks, David A. Nathanson · 1985 to 2026
$10.5M
Biopsy Tracking and MRI Fusion to Enhance Imaging of Cancer Within the ProstateR01CA158627 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARKS, LEONARD STEPHEN · 2011 to 2013
$1.4M
Howard Hughes Medical InstituteNCI NIH HHS 1R01CA158627-01NCI NIH HHS PC101008NCI NIH HHS PC101928NCI NIH HHS R01 CA158627NCI NIH HHS T32 CA009056
6 · The paper itself

Abstract

Dominant mutations or DNA amplification of tyrosine kinases are rare among the oncogenic alterations implicated in prostate cancer. We demonstrate that castration-resistant prostate cancer (CRPC) in men exhibits increased tyrosine phosphorylation, raising the question of whether enhanced tyrosine kinase activity is observed in prostate cancer in the absence of specific tyrosine kinase mutation or DNA amplification. We generated a mouse model of prostate cancer progression using commonly perturbed non-tyrosine kinase oncogenes and pathways and detected a significant up-regulation of tyrosine phosphorylation at the carcinoma stage. Phosphotyrosine peptide enrichment and quantitative mass spectrometry identified oncogene-specific tyrosine kinase signatures, including activation of EGFR, ephrin type-A receptor 2 (EPHA2), and JAK2. Kinase:substrate relationship analysis of the phosphopeptides also revealed ABL1 and SRC tyrosine kinase activation. The observation of elevated tyrosine kinase signaling in advanced prostate cancer and identification of specific tyrosine kinase pathways from genetically defined tumor models point to unique therapeutic approaches using tyrosine kinase inhibitors for advanced prostate cancer.

Indexed as

OncogenesAnimalsEnzyme ActivationMaleMass SpectrometryMicePhosphorylationProstatic NeoplasmsProtein-Tyrosine KinasesProteomicsTyrosineUp-RegulationProtein-Tyrosine KinasesTyrosine

Identifiers

PMID22307624
PMCPMC3277127

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.