Evidence map›Paper›PMID 35022962›Full record

ReviewCancer metastasis reviews2022

Of vascular defense, hemostasis, cancer, and platelet biology: an evolutionary perspective.

David G Menter, Vahid Afshar-Kharghan, John Paul Shen, Stephanie L Martch, Anirban Maitra, Scott Kopetz, Kenneth V Honn, Anil K Sood

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

7 citing papers in PubMed, 21 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

8 authors at 2 institutions in 1 country.

David G MenterDepartment of GI Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. dmenter@mdanderson.org.ORCID 0000-0003-2967-4095
Vahid Afshar-KharghanDivision of Internal Medicine, Benign Hematology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
John Paul ShenDepartment of GI Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Stephanie L MartchDepartment of GI Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Anirban MaitraDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Scott KopetzDepartment of GI Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Kenneth V HonnDepartment of Pathology, Bioactive Lipids Research Program, Wayne State University, 5101 Cass Ave. 430 Chemistry, Detroit, MI, 48202, USA.
Anil K SoodDepartment of Gynecologic Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
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 DIANE BODURKA · 1985 to 2026
$290.8M
The RAS and P13K Pathways in Pancreatic AdenocarcinomaP01CA117969 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KALLURI, RAGHU · 2006 to 2025
$41.7M
Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
Project 3: Inhibiting Oxidative Phosphorylation in Pancreatic CancerP50CA221707 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KOPETZ, SCOTT · 2019 to 2023
$11.0M
U.T. M. D. Anderson Cancer Center SPORE in Ovarian CancerP50CA217685 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SOOD, ANIL K · 2017 to 2021
$7.9M
Harnessing the power of exosomes for non-coding RNA deliveryR35CA209904 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SOOD, ANIL K · 2017 to 2023
$5.0M
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
Longitudinal therapeutic monitoring of colorectal cancer patients using exosome-based liquid biopsiesR01CA218230 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KOPETZ, SCOTT, MAITRA, ANIRBAN · 2018 to 2022
$3.3M
Genetics of Graft-versus-Host DiseaseR01CA231141 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI AFSHAR-KHARGHAN, VAHID, GORLOVA, OLGA · 2018 to 2022
$1.6M
NCI NIH HHS 3P30CA016672NCI NIH HHS P01CA117969NCI NIH HHS P50 CA098258NCI NIH HHS P50CA217685NCI NIH HHS P50CA221707NCI NIH HHS R01 CA177909NCI NIH HHS R01CA177909NCI NIH HHS R01CA218230NCI NIH HHS R01 CA231141NCI NIH HHS R01CA231141NCI NIH HHS R35 CA209904
6 · The paper itself

Abstract

We have established considerable expertise in studying the role of platelets in cancer biology. From this expertise, we were keen to recognize the numerous venous-, arterial-, microvascular-, and macrovascular thrombotic events and immunologic disorders are caused by severe, acute-respiratory-syndrome coronavirus 2 (SARS-CoV-2) infections. With this offering, we explore the evolutionary connections that place platelets at the center of hemostasis, immunity, and adaptive phylogeny. Coevolutionary changes have also occurred in vertebrate viruses and their vertebrate hosts that reflect their respective evolutionary interactions. As mammals adapted from aquatic to terrestrial life and the heavy blood loss associated with placentalization-based live birth, platelets evolved phylogenetically from thrombocytes toward higher megakaryocyte-blebbing-based production rates and the lack of nuclei. With no nuclei and robust RNA synthesis, this adaptation may have influenced viral replication to become less efficient after virus particles are engulfed. Human platelets express numerous receptors that bind viral particles, which developed from archetypal origins to initiate aggregation and exocytic-release of thrombo-, immuno-, angiogenic-, growth-, and repair-stimulatory granule contents. Whether by direct, evolutionary, selective pressure, or not, these responses may help to contain virus spread, attract immune cells for eradication, and stimulate angiogenesis, growth, and wound repair after viral damage. Because mammalian and marsupial platelets became smaller and more plate-like their biophysical properties improved in function, which facilitated distribution near vessel walls in fluid-shear fields. This adaptation increased the probability that platelets could then interact with and engulf shedding virus particles. Platelets also generate circulating microvesicles that increase membrane surface-area encounters and mark viral targets. In order to match virus-production rates, billions of platelets are generated and turned over per day to continually provide active defenses and adaptation to suppress the spectrum of evolving threats like SARS-CoV-2.

Indexed as

COVID-19NeoplasmsAnimalsBiologyBlood PlateletsHemostasisHumansMammalsSARS-CoV-2C–C chemokine receptors (CCR 1,3And 4)CoagulationCorona virus disease 2019 (COVID-19)PlateletSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Toll-like receptor (TLR)

Identifiers

PMID35022962
PMCPMC8754476
OpenAlexW4205425356

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.