Evidence map›Paper›PMID 23576558›Full record

ArticleCancer research2013

FGFR1 is essential for prostate cancer progression and metastasis.

Feng Yang, Yongyou Zhang, Steven J Ressler, Michael M Ittmann, Gustavo E Ayala, Truong D Dang, Fen Wang, David R Rowley

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 109 citations in OpenAlex.

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  12. Impact of cell plasticity on prostate tumor heterogeneity and therapeutic response.American journal of clinical and experimental urology · 2024
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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

8 authors at 3 institutions in 1 country.

Feng YangDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA. fyang@bcm.edu
Yongyou Zhang
Steven J Ressler
Michael M Ittmann
Gustavo E Ayala
Truong D Dang
Fen Wang
David R Rowley
Baylor College of Medicine · USTexas A&M University · USThe University of Texas Health Science Center at Houston · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
STEROID RECEPTORS SUPERFAMILY MEMBERS--THEIR ROLE IN PROSTATE CANCERP50CA058204 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ITTMANN, MICHAEL M. · 1992 to 2007
$21.3M
TRANSGENIC MOUSE MODELS OF PROSTATE CANCERU01CA084296 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GREENBERG, NORMAN MICHAEL · 1999 to 2008
$7.6M
MESENCHYMAL DERIVED GROWTH FACTORS IN PROSTATIC CANCERR01CA058093 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ROWLEY, DAVID R · 1992 to 2013
$3.3M
Receptor-specific signaling of FGFR in the prostateR01CA096824 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI WANG, FEN · 2003 to 2013
$2.5M
Interleukin-8 Induced Biology in Benign Prostatic HyperplasiaR01DK083293 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI ROWLEY, DAVID R · 2010 to 2013
$1.3M
STROMAL GROWTH FACTORS IN BENIGN PROSTATIC HYPERPLASIAR01DK045909 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI ROWLEY, DAVID R · 1992 to 2003
$1.0M
NCI NIH HHS P30 CA125123NCI NIH HHS P30CA125123NCI NIH HHS P50 CA058204NCI NIH HHS P50-CA58204NCI NIH HHS R01 CA058093NCI NIH HHS R01-CA058093NCI NIH HHS R01 CA096824NCI NIH HHS R01-CA096824NCI NIH HHS U01 CA084296NCI NIH HHS U01-CA84296NIDDK NIH HHS R01 DK045909NIDDK NIH HHS R01-DK045909NIDDK NIH HHS R01 DK083293
6 · The paper itself

Abstract

The fibroblast growth factor receptor 1 (FGFR1) is ectopically expressed in prostate carcinoma cells, but its functional contributions are undefined. In this study, we report the evaluation of a tissue-specific conditional deletion mutant generated in an ARR2PBi(Pbsn)-Cre/TRAMP/fgfr1(loxP/loxP) transgenic mouse model of prostate cancer. Mice lacking fgfr1, in prostate cells developed smaller tumors that also included distinct cancer foci still expressing fgfr1 indicating focal escape from gene excision. Tumors with confirmed fgfr1 deletion exhibited increased foci of early, well-differentiated cancer and phyllodes-type tumors, and tumors that escaped fgfr1 deletion primarily exhibited a poorly differentiated phenotype. Consistent with these phenotypes, mice carrying the fgfr1 null allele survived significantly longer than those without fgfr1 deletion. Most interestingly, all metastases were primarily negative for the fgfr1 null allele, exhibited high FGFR1 expression, and a neuroendocrine phenotype regardless of fgfr1 status in the primary tumors. Together, these results suggest a critical and permissive role of ectopic FGFR1 signaling in prostate tumorigenesis and particularly in mechanisms of metastasis.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsDisease ProgressionIn Situ HybridizationMaleMiceMice, Inbred C57BLMice, Inbred ICRMice, KnockoutMice, TransgenicNeoplasm MetastasisProstateProstatic NeoplasmsReceptor, Fibroblast Growth Factor, Type 1Survival AnalysisReceptor, Fibroblast Growth Factor, Type 1

Identifiers

PMID23576558
PMCPMC3686853
OpenAlexW2113332865

What OpenQuestion holds

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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.