Evidence map›Paper›PMID 36106109›Full record

ArticleFrontiers in oncology2022

Radiation induces ESCRT pathway dependent CD44v3

Gene Chatman Clark, James David Hampton, Jennifer E Koblinski, Bridget Quinn, Sitara Mahmoodi, Olga Metcalf, Chunqing Guo, Erica Peterson, Paul B Fisher, Nicholas P Farrell and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
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 2 institutions in 1 country.

Gene Chatman ClarkVirginia Commonwealth University, Richmond, VA, United States.
James David HamptonVirginia Commonwealth University, Richmond, VA, United States.
Jennifer E KoblinskiVirginia Commonwealth University, Richmond, VA, United States.
Bridget QuinnVirginia Commonwealth University, Richmond, VA, United States.
Sitara MahmoodiVirginia Commonwealth University, Richmond, VA, United States.
Olga MetcalfUniversity of Virginia, Charlottesville, VA, United States.
Chunqing GuoVirginia Commonwealth University, Richmond, VA, United States.
Erica PetersonVirginia Commonwealth University, Richmond, VA, United States.
Paul B FisherVirginia Commonwealth University, Richmond, VA, United States.
Nicholas P FarrellVirginia Commonwealth University, Richmond, VA, United States.
Xiang-Yang WangVirginia Commonwealth University, Richmond, VA, United States.
Ross B MikkelsenVirginia Commonwealth University, Richmond, VA, United States.
Virginia Commonwealth University · USUniversity of Virginia · US

Funding

Host-tumor interactions and cancer relapse after radiation therapyR01CA175033 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI WANG, XIANG-YANG SHAWN · 2014 to 2018
$1.6M
The impact of chronic stress on radiation induced cell death and the anti-tumor immune responseF30CA265127 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MACDONALD, CAMERON RIKER · 2021 to 2024
$169k
NCI NIH HHS R01 CA175033
6 · The paper itself

Abstract

Despite recent advances in radiotherapeutic strategies, acquired resistance remains a major obstacle, leading to tumor recurrence for many patients. Once thought to be a strictly cancer cell intrinsic property, it is becoming increasingly clear that treatment-resistance is driven in part by complex interactions between cancer cells and non-transformed cells of the tumor microenvironment. Herein, we report that radiotherapy induces the production of extracellular vesicles by breast cancer cells capable of stimulating tumor-supporting fibroblast activity, facilitating tumor survival and promoting cancer stem-like cell expansion. This pro-tumor activity was associated with fibroblast production of the paracrine signaling factor IL-6 and was dependent on the expression of the heparan sulfate proteoglycan CD44v3 on the vesicle surface. Enzymatic removal or pharmaceutical inhibition of its heparan sulfate side chains disrupted this tumor-fibroblast crosstalk. Additionally, we show that the radiation-induced production of CD44v3

Indexed as

cancer associated fibroblasts (CAF)cancer stem cell (CSC)CD44ESCRT pathwayextracurricular vesicles (EVs)heparan sulfate (HS)radioresistanceradiotherapy

Identifiers

PMID36106109
PMCPMC9465418
OpenAlexW4293427311

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.