Evidence map›Paper›PMID 19275762›Full record

ReviewCurrent cancer drug targets2009

Targeted therapy for advanced prostate cancer: inhibition of the PI3K/Akt/mTOR pathway.

Todd M Morgan, Theodore D Koreckij, Eva Corey

Open access · bronzeAbstract readReview
In one paragraph

Review in Current cancer drug targets, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed
6.3field-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

153 citing papers in PubMed, 278 citations in OpenAlex.

  1. Review
  2. Article
  3. Preclinical Evaluation of aACS pharmacology & translational science · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Silencing APLNR enhances the radiosensitivity of prostate cancer by modulating the PI3K/AKT/mTOR signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  12. Article
  13. Article
  14. The Prognostic and Therapeutic Potential of Fragile X Mental Retardation 1 (International journal of molecular sciences · 2024
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Pyrogallol fromInternational journal of molecular sciences · 2023
    Article
  20. Review

93 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.

Todd M MorganDepartment of Urology, University of Washington School of Medicine, Seattle, WA 98195, USA.
Theodore D Koreckij
Eva Corey
University of Washington · US

Funding

TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI John Kyung Lee · 2002 to 2026
$58.1M
Transmembrane Proteases and Prostate CarcinogenesisP01CA085859 · NCI · UNIVERSITY OF WASHINGTON · PI VESSELLA, ROBERT LOUIS · 2002 to 2013
$21.2M
Roles of Nemo-like kinase in CaP and its effects on androgen receptor signalingR01CA125395 · NCI · UNIVERSITY OF WASHINGTON · PI COREY, EVA · 2007 to 2010
$948k
NCI NIH HHS 5R01 CA 125395-02NCI NIH HHS P01 CA085859NCI NIH HHS P01 CA 85859-01A1NCI NIH HHS P50 CA 097186NCI NIH HHS P50 CA097186NCI NIH HHS R01 CA125395
6 · The paper itself

Abstract

A large number of novel therapeutics is currently undergoing clinical evaluation for the treatment of prostate cancer, and small molecule signal transduction inhibitors are a promising class of agents. These inhibitors have recently become a standard therapy in renal cell carcinoma and offer significant promise in prostate cancer. Through an understanding of the key pathways involved in prostate cancer progression, a rational drug design can be aimed at the molecules critical to cellular signaling. This may enable administration of selective therapies based on the expression of molecular targets, more appropriately individualizing treatment for prostate cancer patients. One pathway with a prominent role in prostate cancer is the PI3K/Akt/mTOR pathway. Current estimates suggest that PI3K/Akt/mTOR signaling is upregulated in 30-50% of prostate cancers, often through loss of PTEN. Molecular changes in the PI3K/Akt/mTOR signaling pathway have been demonstrated to differentiate benign from malignant prostatic epithelium and are associated with increasing tumor stage, grade, and risk of biochemical recurrence. Multiple inhibitors of this pathway have been developed and are being assessed in the laboratory and in clinical trials, with much attention focusing on mTOR inhibition. Current clinical trials in prostate cancer are assessing efficacy of mTOR inhibitors in combination with multiple targeted or traditional chemotherapies, including bevacizumab, gefitinib, and docetaxel. Completion of these trials will provide substantial information regarding the importance of this pathway in prostate cancer and the clinical implications of its targeted inhibition. In this article we review the data surrounding PI3K/Akt/mTOR inhibition in prostate cancer and their clinical implications.

Indexed as

Phosphoinositide-3 Kinase InhibitorsAndrogen Receptor AntagonistsAnimalsAntineoplastic AgentsHumansMaleOncogene Protein v-aktPhosphatidylinositol 3-KinasesProstatic NeoplasmsProtein KinasesSignal TransductionTOR Serine-Threonine KinasesAndrogen Receptor AntagonistsAntineoplastic AgentsMTOR protein, humanOncogene Protein v-aktPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein KinasesTOR Serine-Threonine Kinases

Identifiers

PMID19275762
PMCPMC2921605
OpenAlexW2115806147

What OpenQuestion holds

Textmetadata
LicenceTDM
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.