Evidence map›Paper›PMID 26477319›Full record

ArticleOncogene2016

Radiation promotes colorectal cancer initiation and progression by inducing senescence-associated inflammatory responses.

S B Kim, R G Bozeman, A Kaisani, W Kim, L Zhang, J A Richardson, W E Wright, J W Shay

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  5. Sorafenib, rapamycin, and venetoclax attenuate doxorubicin-induced senescence and promote apoptosis in HCT116 cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
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  18. Article
  19. Gene Expression Studies for the Development of Particle Therapy.International journal of particle therapy · 2018
    Article
  20. 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

8 authors at 1 institution in 2 countries.

S B KimDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
R G BozemanDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
A KaisaniDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
W KimDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
L ZhangDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
J A RichardsonDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
W E WrightDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
J W ShayDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
The University of Texas Southwestern Medical Center · US

Funding

UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI BYERS, LAUREN AVERETT · 1996 to 2024
$57.4M
Cell Biology Research Improvements and RenovationsC06RR030414 · NCRR · UT SOUTHWESTERN MEDICAL CENTER · PI FITZ, JOHN GREGORY · 2010 to 2010
$15.0M
Cancer Biology Training GrantT32CA124334 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI SHAY, JERRY WILLIAM · 2007 to 2021
$5.3M
NCI NIH HHS P50 CA070907NCI NIH HHS T32 CA124334NCRR NIH HHS C06 RR030414
6 · The paper itself

Abstract

Proton radiotherapy is becoming more common as protons induce more precise DNA damage at the tumor site with reduced side effects to adjacent normal tissues. However, the long-term biological effects of proton irradiation in cancer initiation compared with conventional photon irradiation are poorly characterized. In this study, using a human familial adenomatous polyposis syndrome susceptible mouse model, we show that whole-body irradiation with protons are more effective in inducing senescence-associated inflammatory responses (SIRs), which are involved in colon cancer initiation and progression. After proton irradiation, a subset of SIR genes (Troy, Sox17, Opg, Faim2, Lpo, Tlr2 and Ptges) and a gene known to be involved in invasiveness (Plat), along with the senescence-associated gene (P19Arf), are markedly increased. Following these changes, loss of Casein kinase Iα and induction of chronic DNA damage and TP53 mutations are increased compared with X-ray irradiation. Proton irradiation also increases the number of colonic polyps, carcinomas and invasive adenocarcinomas. Pretreatment with the non-steroidal anti-inflammatory drug, 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid-ethyl amide (CDDO-EA), reduces proton irradiation-associated SIR and tumorigenesis. Thus exposure to proton irradiation elicits significant changes in colorectal cancer initiation and progression that can be mitigated using CDDO-EA.

Indexed as

Adenomatous Polyposis ColiAgingAnimalsColorectal NeoplasmsDisease Models, AnimalDisease ProgressionDNA DamageGene Expression Regulation, NeoplasticHumansInflammationMice, Inbred C57BLMice, KnockoutMutationOleanolic AcidOxidative StressProton Therapy2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid ethyl amideOleanolic AcidTumor Suppressor Protein p53

Identifiers

PMID26477319
PMCPMC4837107
OpenAlexW2174570955

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.