Evidence map›Paper›PMID 21411864›Full record

ReviewOncotarget2011

Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR inhibitors: rationale and importance to inhibiting these pathways in human health.

William H Chappell, Linda S Steelman, Jacquelyn M Long, Ruth C Kempf, Stephen L Abrams, Richard A Franklin, Jörg Bäsecke, Franca Stivala, Marco Donia, Paolo Fagone and 16 more

Open access · hybridAbstract readReview
In one paragraph

Review in Oncotarget, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 325 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
325citing papers in PubMed, 1 pooled it
26.0field-weighted citation impact, top 1% 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

325 citing papers in PubMed, 1 synthesis or guideline pooled it, 575 citations in OpenAlex.

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  15. The role of SPRED1 mutation in melanoma.European journal of medical research · 2025
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265 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

26 authors at 12 institutions in 5 countries.

William H ChappellDepartment of Microbiology and Immunology, Brody School of Medicine at East Carolina University, USA.
Linda S Steelman
Jacquelyn M Long
Ruth C Kempf
Stephen L Abrams
Richard A Franklin
Jörg Bäsecke
Franca Stivala
Marco Donia
Paolo Fagone
Graziella Malaponte
Maria C Mazzarino
Ferdinando Nicoletti
Massimo Libra
Danijela Maksimovic-Ivanic
Sanja Mijatovic
Giuseppe Montalto
Melchiorre Cervello
Piotr Laidler
Michele Milella
Agostino Tafuri
Antonio Bonati
Camilla Evangelisti
Lucio Cocco
Alberto M Martelli
James A McCubrey
University of Catania · ITEast Carolina University · USGreenville College · USUniversity of Belgrade · RSUniversity of Bologna · ITIstituto Ortopedico Rizzoli · ITJagiellonian University · PLNational Research Council · ITSapienza University of Rome · ITUniversity of Göttingen · DEUniversity of Palermo · ITUniversity of Parma · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Integral components of these pathways, Ras, B-Raf, PI3K, and PTEN are also activated/inactivated by mutations. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of these pathways can contribute to chemotherapeutic drug resistance, proliferation of cancer initiating cells (CICs) and premature aging. This review will evaluate more recently described potential uses of MEK, PI3K, Akt and mTOR inhibitors in the proliferation of malignant cells, suppression of CICs, cellular senescence and prevention of aging. Ras/Raf/MEK/ERK and Ras/PI3K/PTEN/Akt/mTOR pathways play key roles in the regulation of normal and malignant cell growth. Inhibitors targeting these pathways have many potential uses from suppression of cancer, proliferative diseases as well as aging.

Indexed as

Cell Line, TumorCell Transformation, NeoplasticExtracellular Signal-Regulated MAP KinasesHumansMAP Kinase Signaling SystemMitogen-Activated Protein Kinase KinasesNeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN Phosphohydrolaseraf Kinasesras ProteinsTOR Serine-Threonine KinasesExtracellular Signal-Regulated MAP KinasesMitogen-Activated Protein Kinase KinasesMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanraf Kinasesras ProteinsTOR Serine-Threonine Kinases

Identifiers

PMID21411864
PMCPMC3260807
OpenAlexW1752845679

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.