Evidence map›Paper›PMID 21644828›Full record

ReviewFuture medicinal chemistry2011

Towards novel radiosensitizing agents: the role of cytosolic PLA2α in combined modality cancer therapy.

Jeffrey M Craft, Dennis Hallahan

Abstract readReview
In one paragraph

Review in Future medicinal chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Calcium-dependent phospholipase A2 modulates infection-induced diaphragm dysfunction.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  2. Article
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

2 authors.

Jeffrey M CraftDepartment of Radiation Oncology, Washington University, 4511 Forest Park, St Louis, MO 63130, USA.
Dennis Hallahan

Funding

Lysophospholipids in Radiation Induced Signal Transduction in Malignant GliomasR01CA140220 · NCI · WASHINGTON UNIVERSITY · PI HALLAHAN, DENNIS E · 2010 to 2014
$1.7M
NCI NIH HHS R01 CA140220
6 · The paper itself

Abstract

The radioresistant nature of some tumors serves as an obstacle to curative therapy for several poor-prognosis malignancies. The radiosensitivity of a cancer is dependent not only on the intrinsic ability of tumor cells to recover from radiation-induced damage, but also the ability of stromal elements (e.g., vasculature) in the tumor microenvironment to survive and continue proliferating in the face of ionizing radiation. In this regard, it is important to understand the initial events activating radiation-induced signal transduction pathways. Among these events is the activation of cytosolic phospholipase A2 α and the subsequent production of the lipid second messengers. These events occur within minutes following exposure to ionizing radiation, and have been shown to enhance cell viability through a number of prosurvival signaling pathways. Furthermore, inhibition of cytosolic phospholipase A2 α has now been shown to reduce the viability of endothelial cells in culture after exposure to ionizing radiation, as well as slowing the growth of tumors in animal models of cancer.

Indexed as

Combined Modality TherapyGroup IV Phospholipases A2HumansLysophospholipase DNeoplasmsPhosphoric Diester HydrolasesRadiation, IonizingRadiation-Sensitizing AgentsGroup IV Phospholipases A2Lysophospholipase DPhosphoric Diester HydrolasesRadiation-Sensitizing Agents

Identifiers

PMID21644828
PMCPMC3443401

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.