Evidence map›Paper›PMID 30670536›Full record

ArticleBlood advances2019

Aspirin inhibits platelets from reprogramming breast tumor cells and promoting metastasis.

Kelly E Johnson, Julia R Ceglowski, Harvey G Roweth, Jodi A Forward, Mason D Tippy, Saleh El-Husayni, Rajesh Kulenthirarajan, Michael W Malloy, Kellie R Machlus, Wendy Y Chen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 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

12 authors at 3 institutions in 1 country.

Kelly E JohnsonDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Julia R CeglowskiDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Harvey G RowethDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Jodi A ForwardDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Mason D TippyDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Saleh El-HusayniDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Rajesh KulenthirarajanDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Michael W MalloyDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Kellie R MachlusDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Wendy Y ChenDana-Farber Cancer Institute, Boston MA; and.
Joseph E ItalianoDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Elisabeth M BattinelliDivision of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA.
Brigham and Women's Hospital · USHarvard University · USDana-Farber Cancer Institute · US

Funding

How does malignancy subvert platelet and megakaryocytic biology?R01CA200748 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI BATTINELLI, ELISABETH M, ITALIANO, JOSEPH E · 2017 to 2021
$2.7M
National Cancer Institute R01 CA200748NCI NIH HHS R01 CA200748
6 · The paper itself

Abstract

It is now recognized that compounds released from tumor cells can activate platelets, causing the release of platelet-derived factors into the tumor microenvironment. Several of these factors have been shown to directly promote neovascularization and metastasis, yet how the feedback between platelet releasate and the tumor cell affects metastatic phenotype remains largely unstudied. Here, we identify that breast tumor cells secrete high levels of interleukin 8 (IL-8, CXCL8) in response to platelet releasate, which promotes their invasive capacity. Furthermore, we found that platelets activate the Akt pathway in breast tumor cells, and inhibition of this pathway eliminated IL-8 production. We therefore hypothesized inhibiting platelets with aspirin could reverse the prometastatic effects of platelets on tumor cell signaling. Platelets treated with aspirin did not activate the Akt pathway, resulting in reduced IL-8 secretion and impaired tumor cell invasion. Of note, patients with breast cancer receiving aspirin had lower circulating IL-8, and their platelets did not increase tumor cell invasion compared with patients not receiving aspirin. Our data suggest platelets support breast tumor metastasis by inducing tumor cells to secrete IL-8. Our data further support that aspirin acts as an anticancer agent by disrupting the communication between platelets and breast tumor cells.

Indexed as

AspirinBlood PlateletsBreast NeoplasmsCell Line, TumorCytokinesFemaleHumansNeoplasm MetastasisNeoplasm StagingNeovascularization, PathologicPlatelet Aggregation InhibitorsProto-Oncogene Proteins c-aktSignal TransductionAspirinCytokinesPlatelet Aggregation InhibitorsProto-Oncogene Proteins c-akt

Identifiers

PMID30670536
PMCPMC6341186
OpenAlexW2912067439

What OpenQuestion 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 OpenQuestion graph.