Evidence map›Paper›PMID 21646685›Full record

ReviewOncotarget2011

Elevated PI3K signaling drives multiple breast cancer subtypes.

Jessica R Adams, Nathan F Schachter, Jeff C Liu, Eldad Zacksenhaus, Sean E Egan

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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 52 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Jessica R AdamsProgram in Developmental and Stem Cell Biology, The Hospital for Sick Children, 101 College St., East Tower.
Nathan F Schachter
Jeff C Liu
Eldad Zacksenhaus
Sean E Egan
SickKids Foundation · CAUniversity Health Network · CAHospital for Sick Children · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most human breast tumors have mutations that elevate signaling through a key metabolic pathway that is induced by insulin and a number of growth factors. This pathway serves to activate an enzyme known as phosphatidylinositol 3' kinase (PI3K) as well as to regulate proteins that signal in response to lipid products of PI3K. The specific mutations that activate this pathway in breast cancer can occur in genes coding for tyrosine kinase receptors, adaptor proteins linked to PI3K, catalytic and regulatory subunits of PI3K, serine/threonine kinases that function downstream of PI3K, and also phosphatidylinositol 3' phosphatase tumor suppressors that function to antagonize this pathway. While each genetic change results in net elevation of PI3K pathway signaling, and all major breast cancer subtypes show pathway activation, the specific mutation(s) involved in any one tumor may play an important role in defining tumor subtype, prognosis and even sensitivity to therapy. Here, we describe mouse models of breast cancer with elevated PI3K signaling, and how they may be used to guide development of novel therapeutics.

Indexed as

AnimalsBreast NeoplasmsCarcinomaFemaleHumansMiceModels, BiologicalPhosphatidylinositol 3-KinasesSignal TransductionTumor Cells, CulturedUp-RegulationPhosphatidylinositol 3-Kinases

Identifiers

PMID21646685
PMCPMC3248195
OpenAlexW1918395140

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.