Evidence map›Paper›PMID 24424114›Full record

ArticleCancer biology & therapy2014

Crosstalk between ERK, AKT, and cell survival.

Paul Dent

Abstract readComment
In one paragraph

Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
–field-weighted citation impact
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

62 citing papers in PubMed.

  1. Article
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  5. Novel affibody molecules targeting the AXL extracellular structural domain for molecular imaging and targeted therapy of gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
    Article
  6. Osteocyte connexin hemichannels and prostaglandin EProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Review
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  17. Article
  18. Review
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2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Paul DentDepartment of Biochemistry; Massey Cancer Center; Virginia Commonwealth University; Richmond, VA USA.

Funding

SIGNALING PATHWAYS REGULATING EPITHELIAL CELL SURVIVALR01DK052825 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI DENT, PAUL · 1999 to 2013
$3.3M
NIDDK NIH HHS R01 DK052825NIDDK NIH HHS R01 DK52825
6 · The paper itself

Abstract

It is historically well known that signaling by the PI3K-AKT and MEK1/2-ERK1/2 pathways in a cell type-dependent fashion can collaborate to maintain cell viability. (1)(-) (3) Signaling pathways can also crosstalk with each other wherein one pathway can signal to either enhance or suppress signaling by another. (4) Signaling by the ERK1/2 pathway can also stimulate release of growth factors which can feed back onto tumor cells to re-energize signaling pathways. (5) The studies described by Toulany et al. add to this knowledge base by examining the relationship between PI3K-AKT and MEK1/2-ERK1/2 pathway signaling, EGF receptor signaling, K-RAS function, and tumor cell survival. (6.)

Indexed as

Phosphoinositide-3 Kinase InhibitorsHumansMitogen-Activated Protein Kinase 1Oncogene Protein v-aktProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsKRAS protein, humanMAPK1 protein, humanMitogen-Activated Protein Kinase 1Oncogene Protein v-aktPhosphoinositide-3 Kinase InhibitorsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsEGFRerlotinibHNSCCK-RASMAPK/ERKNSCLCPI-103PI3K/Akt

Identifiers

PMID24424114
PMCPMC3974823

What OpenQuestion holds

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LicenceCC BY-NC
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.