Evidence map›Paper›PMID 24860738›Full record

ArticleProteomes2013

Exosomal Proteome Profiling: A Potential Multi-Marker Cellular Phenotyping Tool to Characterize Hypoxia-Induced Radiation Resistance in Breast Cancer.

Stefani N Thomas, Zhongping Liao, David Clark, Yangyi Chen, Ramin Samadani, Li Mao, David K Ann, Janet E Baulch, Paul Shapiro, Austin J Yang

Open access · goldAbstract read
In one paragraph

Article in Proteomes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
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  6. Extracellular Vesicles in Cancer Drug Resistance: Roles, Mechanisms, and Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Review
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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

10 authors at 6 institutions in 1 country.

Stefani N ThomasDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; sthoma92@jhmi.edu.
Zhongping LiaoEli Lilly and Company, Indianapolis, IN 46285, USA; zliao001@umaryland.edu.
David ClarkGreenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA; djclark81@gmail.com (D.C.); yangyic@gmail.com (Y.C.); pshapiro@rx.umaryland.edu (P.S.) ; Division of Oncology, University of Maryland School of Dentistry, Baltimore, MD 21201, USA.
Yangyi ChenGreenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA; djclark81@gmail.com (D.C.); yangyic@gmail.com (Y.C.); pshapiro@rx.umaryland.edu (P.S.).
Ramin SamadaniDepartment of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD 21201, USA; rsama002@umaryland.edu.
Li MaoOncology and Diagnostic Sciences, University of Maryland School of Dentistry, Baltimore, MD 21201, USA; LMao@umaryland.edu.
David K AnnDepartment of Molecular Pharmacology, Beckman Research Institute, City of Hope, Duarte, CA 91010, USA; dann@coh.org ; Irell and Manella Graduate School of Biological Sciences, Beckman Research Institute, City of Hope, Duarte, CA 91010, USA.
Janet E BaulchDepartment of Radiation Oncology, University of California, Irvine, CA 92697, USA; jbaulch@uci.edu.
Paul ShapiroGreenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA; djclark81@gmail.com (D.C.); yangyic@gmail.com (Y.C.); pshapiro@rx.umaryland.edu (P.S.) ; Department of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD 21201, USA; rsama002@umaryland.edu.
Austin J YangGreenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA; djclark81@gmail.com (D.C.); yangyic@gmail.com (Y.C.); pshapiro@rx.umaryland.edu (P.S.) ; Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
University of Maryland, Baltimore · USCity of Hope · USEli Lilly (United States) · USJohns Hopkins Medicine · USU-M Rogel Cancer CenterUniversity of California, Irvine · US

Funding

Proteome Characterization Center: A Genoproteomics Pipeline for Cance ResearchU24CA160036 · NCI · JOHNS HOPKINS UNIVERSITY · PI CHAN, DANIEL WANYUI, ZHANG, HUI · 2011 to 2016
$10.7M
Proteomics of age-related neurodegenerationR01AG025323 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI YANG, AUSTIN · 2004 to 2008
$1.5M
The tau code of Alzheimer's diseaseR21NS077441 · NINDS · OHIO STATE UNIVERSITY · PI KURET, JEFF, YANG, AUSTIN · 2012 to 2013
$427k
NCI NIH HHS U24 CA160036NIA NIH HHS R01 AG025323NINDS NIH HHS R21 NS077441
6 · The paper itself

Abstract

Radiation and drug resistance are significant challenges in the treatment of locally advanced, recurrent and metastatic breast cancer that contribute to mortality. Clinically, radiotherapy requires oxygen to generate cytotoxic free radicals that cause DNA damage and allow that damage to become fixed in the genome rather than repaired. However, approximately 40% of all breast cancers have hypoxic tumor microenvironments that render cancer cells significantly more resistant to irradiation. Hypoxic stimuli trigger changes in the cell death/survival pathway that lead to increased cellular radiation resistance. As a result, the development of noninvasive strategies to assess tumor hypoxia in breast cancer has recently received considerable attention. Exosomes are secreted nanovesicles that have roles in paracrine signaling during breast tumor progression, including tumor-stromal interactions, activation of proliferative pathways and immunosuppression. The recent development of protocols to isolate and purify exosomes, as well as advances in mass spectrometry-based proteomics have facilitated the comprehensive analysis of exosome content and function. Using these tools, studies have demonstrated that the proteome profiles of tumor-derived exosomes are indicative of the oxygenation status of patient tumors. They have also demonstrated that exosome signaling pathways are potentially targetable drivers of hypoxia-dependent intercellular signaling during tumorigenesis. This article provides an overview of how proteomic tools can be effectively used to characterize exosomes and elucidate fundamental signaling pathways and survival mechanisms underlying hypoxia-mediated radiation resistance in breast cancer.

Indexed as

breast cancerexosomeshypoxiaproteomicsradiationtumor microenvironment

Identifiers

PMID24860738
PMCPMC4029595
OpenAlexW2125915625

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.