Evidence map›Paper›PMID 24335962›Full record

ArticleCancer research2014

Targeting Akt3 signaling in triple-negative breast cancer.

Y Rebecca Chin, Taku Yoshida, Andriy Marusyk, Andrew H Beck, Kornelia Polyak, Alex Toker

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

95 citing papers in PubMed, 154 citations in OpenAlex.

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35 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

6 authors at 3 institutions in 1 country.

Y Rebecca ChinAuthors' Affiliations: Department of Pathology, Beth Israel Deaconess Medical Center; Department of Medicine, Harvard Medical School; Department of Medical Oncology, Dana-Farber Cancer Institute; and Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
Taku Yoshida
Andriy Marusyk
Andrew H Beck
Kornelia Polyak
Alex Toker
Beth Israel Deaconess Medical Center · USBrigham and Women's Hospital · USDana-Farber Cancer Institute · US

Funding

The Role of PlGF in Normal and Neoplastic AngiogenesisP01CA092644 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DVORAK, HAROLD FISHER · 2002 to 2013
$17.2M
Novel regulation of PI3K/Akt to direct targeted breast cancer therapiesR01CA177910 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2013 to 2023
$3.9M
TRAINING PROGRAM IN CANCER BIOLOGYT32CA081156 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI BALK, STEVEN P. · 2000 to 2011
$2.9M
Akt isoform-specific signaling in breast cancer metastasisR00CA157945 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CHIN, YUET MING REBECCA · 2014 to 2016
$711k
Akt isoform-specific signaling in breast cancer metastasisK99CA157945 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CHIN, YUET MING REBECCA · 2011 to 2012
$338k
NCI NIH HHS CA092644NCI NIH HHS K99 CA157945NCI NIH HHS K99CA157945NCI NIH HHS P01 CA092644NCI NIH HHS R00 CA157945NCI NIH HHS R01 CA177910NCI NIH HHS T32 CA081156NCI NIH HHS T32 CA081156-09
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is currently the only major breast tumor subtype without effective targeted therapy and, as a consequence, in general has a poor outcome. To identify new therapeutic targets in TNBC, we performed a short hairpin RNA (shRNA) screen for protein kinases commonly amplified and overexpressed in breast cancer. Using this approach, we identified AKT3 as a gene preferentially required for the growth of TNBCs. Downregulation of Akt3 significantly inhibits the growth of TNBC lines in three-dimensional (3D) spheroid cultures and in mouse xenograft models, whereas loss of Akt1 or Akt2 have more modest effects. Akt3 silencing markedly upregulates the p27 cell-cycle inhibitor and this is critical for the ability of Akt3 to inhibit spheroid growth. In contrast with Akt1, Akt3 silencing results in only a minor enhancement of migration and does not promote invasion. Depletion of Akt3 in TNBC sensitizes cells to the pan-Akt inhibitor GSK690693. These results imply that Akt3 has a specific function in TNBCs; thus, its therapeutic targeting may provide a new treatment option for this tumor subtype.

Indexed as

Signal TransductionAnimalsCell Line, TumorDisease Models, AnimalDrug Resistance, NeoplasmFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansMiceNeoplasm InvasivenessProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRNA IsoformsSpheroids, CellularTriple Negative Breast NeoplasmsAKT3 protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRNA Isoforms

Identifiers

PMID24335962
PMCPMC3946502
OpenAlexW2135630508

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.