Evidence map›Paper›PMID 22485197›Full record

ArticleAmerican journal of cancer research2012

Therapeutic implications of targeting the PI3Kinase/AKT/mTOR signaling module in melanoma therapy.

Ali R Jazirehi, Peter B Wenn, Mohsen Damavand

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Recent advances in drug delivery and targeting for the treatment of pancreatic cancer.Journal of controlled release : official journal of the Controlled Release Society · 2024
    Review
  5. Article
  6. Review
  7. Toward Development of a Diabetic Synovium Culture Model.Frontiers in bioengineering and biotechnology · 2022
    Article
  8. Review
  9. Costunolide suppresses melanoma growth via the AKT/mTOR pathwayAmerican journal of cancer research · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Observational
  15. Article
  16. Combination of celecoxib (CelebrexAmerican journal of clinical and experimental immunology · 2017
    Review
  17. Article
  18. Article
  19. Article
  20. Identification of genes associated with melanoma metastasis.The Kaohsiung journal of medical sciences · 2015
    Article
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.

Ali R JazirehiDepartment of Surgery, Division of Surgical Oncology, and the Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, University of California at Los Angeles Los Angeles, CA, USA. ajazirehi@mednet.ucla.edu
Peter B Wenn
Mohsen Damavand
University of California, Los Angeles · US

Funding

Resistance to apoptosis in clinical melanoma gene therapyR21CA149938 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JAZIREHI, ALI · 2011 to 2012
$577k
NCI NIH HHS R21 CA149938
6 · The paper itself

Abstract

The PI3Kinase/AKT/mTOR signaling module is implicated in various cellular functions including cell survival, growth and proliferation, glucose metabolism, apoptosis, migration, and angiogenesis. Increased expression of AKT and its up- and downstream regulators is linked to several types of cancer. Aberrant expression of AKT is observed in nearly 60% of melanomas culminating in apoptosis resistance via deactivation of apoptotic molecules Bad and Cas-pase-9. Through cross-talk with NF-κB, ERK1/2, JNK and p38MAPK signaling pathways, AKT induces a plethora of cellular effects often leading to tumor development and progression. Due to frequently observed resistance to other common cancer treatments such as chemotherapy, immunotherapy, and radiation, and the detrimental consequences of constitutive activation of the PI3Kinase/AKT/mTOR signaling module, targeted inhibition of the effectors and substrates involved in this module has become a viable and attractive option for molecular targeted therapy in melanoma. Pharmacological inhibitors of various components of this module, either alone or in combination with other agents, have shown significant decrease in proliferation, tumorigenesis, cell growth and survival of various tumors in phases I and II clinical trials. Some inhibitors have even received their Food and Drug Administration (FDA) approval. This review summarizes the current knowledge on this module, its cross-talk with other major cell survival pathways and its targeted inhibition for therapeutic purposes in melanoma.

Indexed as

AKTapoptosismelanomamTORPI3KinasePTENresistancesignal transductiontargeted therapy

Identifiers

PMID22485197
PMCPMC3304564
OpenAlexW154497552

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.