Evidence map›Paper›PMID 23603750›Full record

ReviewCellular signalling2013

Cell survival and metastasis regulation by Akt signaling in colorectal cancer.

Ekta Agarwal, Michael G Brattain, Sanjib Chowdhury

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
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.

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

81 citing papers in PubMed, 164 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Review
  8. Role of EGFR and FASN in breast cancer progression.Journal of cell communication and signaling · 2023
    Review
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21 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.

Ekta AgarwalDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Michael G Brattain
Sanjib Chowdhury
University of Nebraska Medical Center · US

Funding

HETEROGENEITY OF HUMAN COLONIC CARCINOMAR01CA034432 · NCI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI BRATTAIN, MICHAEL G · 1985 to 2013
$3.8M
Cell Survival Determinants of Metastasis in IGF1R-Dependent CRCR01CA054807 · NCI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI BLACK, JENNIFER D. · 1991 to 2016
$3.7M
MECHANISM OF ACTION OF DIFFERENTIATION AGENTSR37CA038173 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BRATTAIN, MICHAEL G · 2001 to 2008
$3.1M
AUTOCRINE TGF BETA AND CELL DEATHR01CA072001 · NCI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI BRATTAIN, MICHAEL G · 1997 to 2011
$2.8M
MECHANISM OF ACTION OF DIFFERENTIATION AGENTSR01CA038173 · NCI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI BRATTAIN, MICHAEL G · 1986 to 2014
$1.8M
NCI NIH HHS 2R01 CA054807-21NCI NIH HHS 5R01 CA034432-26NCI NIH HHS 5R01 CA038173-25NCI NIH HHS 5 R01 CA072001-14NCI NIH HHS R01 CA034432NCI NIH HHS R01 CA038173NCI NIH HHS R01 CA054807NCI NIH HHS R01 CA072001NCI NIH HHS R37 CA038173
6 · The paper itself

Abstract

Dissemination of cancer cells to distant organ sites is the leading cause of death due to treatment failure in different types of cancer. Mehlen and Puisieux have reviewed the importance of the development of inappropriate cell survival signaling for various steps in the metastatic process and have noted the particular importance of aberrant cell survival to successful colonization at the metastatic site. Therefore, the understanding of mechanisms that govern cell survival fate of these metastatic cells could lead to the understanding of a new paradigm for the control of metastatic potential and could provide the basis for developing novel strategies for the treatment of metastases. Numerous studies have documented the widespread role of Akt in cell survival and metastasis in colorectal cancer, as well as many other types of cancer. Akt acts as a key signaling node that bridges the link between oncogenic receptors to many essential pro-survival cellular functions, and is perhaps the most commonly activated signaling pathway in human cancer. In recent years, Akt2 and Akt3 have emerged as significant contributors to malignancy alongside the well-characterized Akt1 isoform, with distinct non-overlapping functions. This review is aimed at gaining a better understanding of the Akt-driven cell survival mechanisms that contribute to cancer progression and metastasis and the pharmacological inhibitors in clinical trials designed to counter the Akt-driven cell survival responses in cancer.

Indexed as

Neoplasm MetastasisAntineoplastic AgentsCell SurvivalColorectal NeoplasmsHumansPhosphatidylinositol 3-KinasesProtein IsoformsProto-Oncogene Proteins c-aktSignal TransductionTransforming Growth Factor betaAntineoplastic AgentsPhosphatidylinositol 3-KinasesProtein IsoformsProto-Oncogene Proteins c-aktTransforming Growth Factor beta

Identifiers

PMID23603750
PMCPMC3686084
OpenAlexW2012319099

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.