Evidence map›Paper›PMID 23297823›Full record

ReviewCurrent cancer drug targets2013

Diverse mechanisms of AKT pathway activation in human malignancy.

Mitchell Cheung, Joseph R Testa

Abstract readReview
In one paragraph

Review in Current cancer drug targets, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
9.9field-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

96 citing papers in PubMed, 179 citations in OpenAlex.

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  11. Novel Mutations inCurrent issues in molecular biology · 2024
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36 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

2 authors at 1 institution in 1 country.

Mitchell CheungCancer Biology Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111-2497, USA.
Joseph R Testa
Fox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
Basis for Lymphomagenesis in Akt2 Transgenic MiceR01CA077429 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI TESTA, JOSEPH R. · 1998 to 2013
$4.7M
NCI NIH HHS CA06927NCI NIH HHS CA77429NCI NIH HHS P30 CA006927NCI NIH HHS R01 CA077429
6 · The paper itself

Abstract

AKT/PKB (Protein Kinase B) are central proteins mediating signals from receptor tyrosine kinases and phosphatidylinositol 3-kinase. AKT kinases are involved in a number of important cellular processes including cell proliferation and survival, cell size in response to nutrient availability, tumor invasion/metastasis, and angiogenesis.Various components of the AKT signaling pathway are encoded by tumor suppressor genes and oncogenes whose loss or activation, respectively, plays an important role in tumorigenesis. The growing body of evidence connecting deregulated AKT signaling with sporadic human cancers and inherited cancer predisposition syndromes is discussed. We also highlight new findings regarding the involvement of activating mutations of AKT1, AKT2, and AKT3 in somatic overgrowth disorders: Proteus syndrome, hypoglycemia with hypertrophy, and hemimegalencephaly, respectively. In addition, we review recent literature documenting the various ways the AKT signaling pathway is activated in human cancers and consequences for molecularly targeted therapies.

Indexed as

Models, BiologicalSignal TransductionAnimalsCell Transformation, NeoplasticDisease Models, AnimalEnzyme ActivationHumansMiceNeoplasm ProteinsNeoplasmsProto-Oncogene Proteins c-aktNeoplasm ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID23297823
PMCPMC3678724
OpenAlexW1979064162

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.