Evidence map›Paper›PMID 19182515›Full record

ReviewCell cycle (Georgetown, Tex.)2009

Paths of FGFR-driven tumorigenesis.

Victor D Acevedo, Michael Ittmann, David M Spencer

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02307500 (An Open-label Phase II Study of Regorafenib in Patients With Metastatic Solid Tumors Who Have Progressed After Standard Therapy - RESOUND), which is not on this map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
7.3field-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.

NCT02307500 phase2completednot on this mapstarted 2014, after this paper: background citation

An Open-label Phase II Study of Regorafenib in Patients With Metastatic Solid Tumors Who Have Progressed After Standard Therapy - RESOUND

TypeinterventionalSponsorIstituto Clinico HumanitasRan2014 to 2020Enrolled82ConditionsPancreas Cancer, Ovarian Cancer, Melanoma, SarcomaArmsRegorafenib
3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Breast Cancer Progression by the FGF/FGFR Axis: A Metabolic Perspective.Journal of mammary gland biology and neoplasia · 2025
    Review
  4. Review
  5. A Promising Paradigm Shift in Cancer Treatment with FGFR Inhibitors.Anti-cancer agents in medicinal chemistry · 2025
    Review
  6. Article
  7. Characterization of Alternative Splicing in High-Risk Wilms' Tumors.International journal of molecular sciences · 2024
    Article
  8. Emerging molecular therapies in the treatment of bladder cancer.Exploration of targeted anti-tumor therapy · 2024
    Review
  9. Review
  10. Angiogenic signaling pathways and anti-angiogenic therapy for cancer.Signal transduction and targeted therapy · 2023
    Review
  11. Review
  12. Article
  13. A novel small molecule RK-019 inhibitsFrontiers in pharmacology · 2022
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

13 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

3 authors at 1 institution in 1 country.

Victor D AcevedoProgram in Cell and Molecular Biology, Department of Immunology, Baylor College of Medicine, Houston, Texas 77030, USA.
Michael Ittmann
David M Spencer
Russian State Agrarian Correspondence University · RU

Funding

Initiative for Maximizing Student Development (IMSD) ProgramR25GM056929 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI PEREIRA, FRED A · 1998 to 2023
$12.4M
TRANSGENIC MOUSE MODELS OF PROSTATE CANCERU01CA084296 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GREENBERG, NORMAN MICHAEL · 1999 to 2008
$7.6M
Role of FGFR axis in Prostate Cancer Tumor ProgressionF31GM069044 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI ACEVEDO, VICTOR D · 2003 to 2006
$119k
NCI NIH HHS U01 CA084296NCI NIH HHS U01-CA84296NIGMS NIH HHS F31 GM069044NIGMS NIH HHS F31-GM069044NIGMS NIH HHS R25 GM056929
6 · The paper itself

Abstract

Fibroblast growth factor receptors (FGFRs) comprise a subfamily of receptor tyrosine kinases (RTKs) that are master regulators of a broad spectrum of cellular and developmental processes, including apoptosis, proliferation, migration and angiogenesis. Due to their broad impact, FGFRs and other RTKs are highly regulated and normally only basally active. Deregulation of FGFR signaling by activating mutations or ligand/receptor overexpression could allow these receptors to become constitutively active, leading to cancer development, including both hematopoietic and solid tumors, such as breast, bladder and prostate carcinomas. In this review, we focus on potential modes of FGFR-mediated tumorigenesis, in particular, the role of FGFR1 during prostate cancer progression.

Indexed as

Prostatic NeoplasmsAnimalsCell CommunicationDisease ProgressionEpithelial CellsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleNeovascularization, PathologicProtein IsoformsProtein-Tyrosine KinasesReceptors, AndrogenReceptors, Fibroblast Growth FactorSignal TransductionStromal CellsProtein IsoformsProtein-Tyrosine KinasesReceptors, AndrogenReceptors, Fibroblast Growth Factor

Identifiers

PMID19182515
PMCPMC7441526
OpenAlexW1982887112

What OpenQuestion holds

Textmetadata
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Read underepoch 390

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.