Evidence map›Paper›PMID 24696047›Full record

ReviewCancer metastasis reviews2014

Platelets and cancer: a casual or causal relationship: revisited.

David G Menter, Stephanie C Tucker, Scott Kopetz, Anil K Sood, John D Crissman, Kenneth V Honn

Open access · greenAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
171citing papers in PubMed, 6 pooled it
7.9field-weighted citation impact, top 2% 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

171 citing papers in PubMed, 6 syntheses or guidelines pooled it, 311 citations in OpenAlex.

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111 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 2 institutions in 1 country.

David G MenterGastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77054, USA.
Stephanie C Tucker
Scott Kopetz
Anil K Sood
John D Crissman
Kenneth V Honn
The University of Texas MD Anderson Cancer Center · USWayne State University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS MD ANDERSON SPORE IN OVARIAN CANCERP50CA083639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BAST, ROBERT C · 1999 to 2015
$33.0M
Targeting CDK4 in TGS-B Inactivated Gastrointestinal CancersP01CA130821 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MISHRA, LOPA · 2008 to 2013
$6.9M
Platelets promote growth of ovarian cancerR01CA177909 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI AFSHAR-KHARGHAN, VAHID, SOOD, ANIL K · 2013 to 2023
$4.1M
NCI NIH HHS CA177909NCI NIH HHS P01 CA130821NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA083639NCI NIH HHS R01 CA177909
6 · The paper itself

Abstract

Human platelets arise as subcellular fragments of megakaryocytes in bone marrow. The physiologic demand, presence of disease such as cancer, or drug effects can regulate the production circulating platelets. Platelet biology is essential to hemostasis, vascular integrity, angiogenesis, inflammation, innate immunity, wound healing, and cancer biology. The most critical biological platelet response is serving as "First Responders" during the wounding process. The exposure of extracellular matrix proteins and intracellular components occurs after wounding. Numerous platelet receptors recognize matrix proteins that trigger platelet activation, adhesion, aggregation, and stabilization. Once activated, platelets change shape and degranulate to release growth factors and bioactive lipids into the blood stream. This cyclic process recruits and aggregates platelets along with thrombogenesis. This process facilitates wound closure or can recognize circulating pathologic bodies. Cancer cell entry into the blood stream triggers platelet-mediated recognition and is amplified by cell surface receptors, cellular products, extracellular factors, and immune cells. In some cases, these interactions suppress immune recognition and elimination of cancer cells or promote arrest at the endothelium, or entrapment in the microvasculature, and survival. This supports survival and spread of cancer cells and the establishment of secondary lesions to serve as important targets for prevention and therapy.

Indexed as

AnimalsBlood PlateletsCell CommunicationHemostasisHumansModels, BiologicalNeoplasmsPlatelet ActivationPrognosis

Identifiers

PMID24696047
PMCPMC4186918
OpenAlexW2079629625

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.