Evidence map›Paper›PMID 26164533›Full record

ReviewRedox biology2015

NO to cancer: The complex and multifaceted role of nitric oxide and the epigenetic nitric oxide donor, RRx-001.

Jan Scicinski, Bryan Oronsky, Shoucheng Ning, Susan Knox, Donna Peehl, Michelle M Kim, Peter Langecker, Gary Fanger

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
7.7field-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

45 citing papers in PubMed, 114 citations in OpenAlex.

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  13. S-Nitrosylation in Tumor Microenvironment.International journal of molecular sciences · 2021
    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

8 authors at 2 institutions in 1 country.

Jan ScicinskiEpicentRx, Inc., 800 W El Camino Real, Suite 180, Mountain View, CA 94040, United States. Electronic address: jscicinski@epicentrx.com.
Bryan OronskyEpicentRx, Inc., 800 W El Camino Real, Suite 180, Mountain View, CA 94040, United States.
Shoucheng NingDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, United States.
Susan KnoxDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, United States.
Donna PeehlDepartment of Urology, Stanford University, Stanford, CA, United States.
Michelle M KimUniversity of Michigan, Radiation Oncology, Ann Arbor, MI, United States.
Peter LangeckerLos Gatos Pharmaceuticals, Los Gatos, CA, United States.
Gary FangerEpicentRx, Inc., 800 W El Camino Real, Suite 180, Mountain View, CA 94040, United States.
Stanford University · USUniversity of Michigan–Ann Arbor · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endogenous mediator of vasodilation, nitric oxide (NO), has been shown to be a potent radiosensitizer. However, the underlying mode of action for its role as a radiosensitizer - while not entirely understood - is believed to arise from increased tumor blood flow, effects on cellular respiration, on cell signaling, and on the production of reactive oxygen and nitrogen species (RONS), that can act as radiosensitizers in their own right. NO activity is surprisingly long-lived and more potent in comparison to oxygen. Reports of the effects of NO with radiation have often been contradictory leading to confusion about the true radiosensitizing nature of NO. Whether increasing or decreasing tumor blood flow, acting as radiosensitizer or radioprotector, the effects of NO have been controversial. Key to understanding the role of NO as a radiosensitizer is to recognize the importance of biological context. With a very short half-life and potent activity, the local effects of NO need to be carefully considered and understood when using NO as a radiosensitizer. The systemic effects of NO donors can cause extensive side effects, and also affect the local tumor microenvironment, both directly and indirectly. To minimize systemic effects and maximize effects on tumors, agents that deliver NO on demand selectively to tumors using hypoxia as a trigger may be of greater interest as radiosensitizers. Herein we discuss the multiple effects of NO and focus on the clinical molecule RRx-001, a hypoxia-activated NO donor currently being investigated as a radiosensitizer in the clinic.

Indexed as

AnimalsAntineoplastic AgentsAzetidinesEpigenesis, GeneticGamma RaysHemoglobinsHumansHypoxiaMiceModels, MolecularNeoplasmsNitric OxideNitric Oxide DonorsNitric Oxide Synthase Type IINitro CompoundsOxidation-ReductionAntineoplastic AgentsAzetidinesdeoxyhemoglobinHemoglobinsNitric OxideNitric Oxide DonorsNitric Oxide Synthase Type IINitro CompoundsOxygenRadiation-Sensitizing AgentsRRx-001CancerHypoxiaNitric oxideRadiosensitizationRadiotherapy

Identifiers

PMID26164533
PMCPMC4529402
OpenAlexW770767527

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.