Evidence map›Paper›PMID 25833940›Full record

ReviewCold Spring Harbor perspectives in medicine2015

Signal transduction in cancer.

Richard Sever, Joan S Brugge

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 426 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
426citing papers in PubMed, 3 pooled it
–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

426 citing papers in PubMed, 3 syntheses or guidelines pooled it, 983 citations in OpenAlex.

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366 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 2 institutions in 1 country.

Richard SeverCold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724.
Joan S BruggeHarvard Medical School, Department of Cell Biology, Boston, Massachusetts 02115.
Cold Spring Harbor Laboratory · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is driven by genetic and epigenetic alterations that allow cells to overproliferate and escape mechanisms that normally control their survival and migration. Many of these alterations map to signaling pathways that control cell growth and division, cell death, cell fate, and cell motility, and can be placed in the context of distortions of wider signaling networks that fuel cancer progression, such as changes in the tumor microenvironment, angiogenesis, and inflammation. Mutations that convert cellular proto-oncogenes to oncogenes can cause hyperactivation of these signaling pathways, whereas inactivation of tumor suppressors eliminates critical negative regulators of signaling. An examination of the PI3K-Akt and Ras-ERK pathways illustrates how such alterations dysregulate signaling in cancer and produce many of the characteristic features of tumor cells.

Indexed as

MAP Kinase Signaling SystemOncogenesCell MovementCell PolarityCell ProliferationGenomic InstabilityHumansMutationNeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTumor MicroenvironmentPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID25833940
PMCPMC4382731
OpenAlexW2108215899

What Socratic 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 Socratic graph.