Evidence map›Paper›PMID 27940576›Full record

ArticleCancer research2017

Aspirin Suppresses Growth in PI3K-Mutant Breast Cancer by Activating AMPK and Inhibiting mTORC1 Signaling.

Whitney S Henry, Tyler Laszewski, Tiffany Tsang, Francisco Beca, Andrew H Beck, Sandra S McAllister, Alex Toker

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
5.6field-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

75 citing papers in PubMed, 125 citations in OpenAlex.

  1. Trial
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  9. Aspirin Attenuates Liver Fibrosis via Autophagy Induction.Journal of cellular and molecular medicine · 2025
    Article
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  11. Review
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  19. Role of EGFR and FASN in breast cancer progression.Journal of cell communication and signaling · 2023
    Review
  20. Article

15 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

7 authors at 2 institutions in 1 country.

Whitney S HenryDepartment of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts.
Tyler LaszewskiHematology Division, Brigham and Women's Hospital, Boston, Massachusetts.
Tiffany TsangDepartment of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts.
Francisco BecaDepartment of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts.
Andrew H BeckDepartment of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts.
Sandra S McAllisterHarvard Medical School, Boston, Massachusetts.
Alex TokerDepartment of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts. atoker@bidmc.harvard.edu.
Harvard University · USBroad Institute · US

Funding

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
Understanding How Breast Cancers Activate and Respond to the Systemic EnvironmentR01CA166284 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI MCALLISTER, SANDRA S · 2012 to 2018
$2.2M
Howard Hughes Medical InstituteNCI NIH HHS R01 CA166284NCI NIH HHS R01 CA177910
6 · The paper itself

Abstract

Despite the high incidence of oncogenic mutations in PIK3CA, the gene encoding the catalytic subunit of PI3K, PI3K inhibitors have yielded little clinical benefit for breast cancer patients. Recent epidemiologic studies have suggested a therapeutic benefit from aspirin intake in cancers harboring oncogenic PIK3CA Here, we show that mutant PIK3CA-expressing breast cancer cells have greater sensitivity to aspirin-mediated growth suppression than their wild-type counterparts. Aspirin decreased viability and anchorage-independent growth of mutant PIK3CA breast cancer cells independently of its effects on COX-2 and NF-κB. We ascribed the effects of aspirin to AMP-activated protein kinase (AMPK) activation, mTORC1 inhibition, and autophagy induction. In vivo, oncogenic PIK3CA-driven mouse mammary tumors treated daily with aspirin resulted in decreased tumor growth kinetics, whereas combination therapy of aspirin and a PI3K inhibitor further attenuated tumor growth. Our study supports the evaluation of aspirin and PI3K pathway inhibitors as a combination therapy for targeting breast cancer. Cancer Res; 77(3); 790-801. ©2016 AACR.

Indexed as

AMP-Activated Protein KinasesAnimalsAnti-Inflammatory Agents, Non-SteroidalAspirinBreast NeoplasmsCell Line, TumorCell ProliferationClass I Phosphatidylinositol 3-KinasesFemaleGene Knockdown TechniquesHumansImmunoblottingMechanistic Target of Rapamycin Complex 1MiceMice, Inbred NODMice, TransgenicAMP-Activated Protein KinasesAnti-Inflammatory Agents, Non-SteroidalAspirinClass I Phosphatidylinositol 3-KinasesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesPhosphatidylinositol 3-KinasesPIK3CA protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID27940576
PMCPMC5290090
OpenAlexW2559934684

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.