Evidence map›Paper›PMID 26475630›Full record

ArticleGut2017

Clinical significance of SNORA42 as an oncogene and a prognostic biomarker in colorectal cancer.

Yoshinaga Okugawa, Yuji Toiyama, Shusuke Toden, Hiroki Mitoma, Takeshi Nagasaka, Koji Tanaka, Yasuhiro Inoue, Masato Kusunoki, C Richard Boland, Ajay Goel

Open access · greenAbstract readValidation Study
In one paragraph

Article in Gut, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 2 pooled it
4.7field-weighted citation impact, top 4% 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

100 citing papers in PubMed, 2 syntheses or guidelines pooled it, 147 citations in OpenAlex.

  1. What is the Role of SNORA42 in Carcinogenesis? A Systematic Review.Asian Pacific journal of cancer prevention : APJCP · 2023
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  15. SnoRNAs: The promising targets for anti-tumor therapy.Journal of pharmaceutical analysis · 2024
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40 more citing papers are in PubMed but not listed here.

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 3 countries.

Yoshinaga OkugawaCenter for Gastrointestinal Cancer Research; Center for Epigenetics, Cancer Prevention and Cancer Genomics, Baylor Research Institute and Charles A. Sammons Cancer Center, Baylor University Medical Center, Dallas, Texas, USA.
Yuji ToiyamaCenter for Gastrointestinal Cancer Research; Center for Epigenetics, Cancer Prevention and Cancer Genomics, Baylor Research Institute and Charles A. Sammons Cancer Center, Baylor University Medical Center, Dallas, Texas, USA.
Shusuke TodenCenter for Gastrointestinal Cancer Research; Center for Epigenetics, Cancer Prevention and Cancer Genomics, Baylor Research Institute and Charles A. Sammons Cancer Center, Baylor University Medical Center, Dallas, Texas, USA.
Hiroki MitomaBaylor Institute for Immunology Research, Baylor Research Institute, Baylor Health Care System, Dallas, Texas, USA.
Takeshi NagasakaDepartment of Gastroenterological Surgery and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Koji TanakaDepartment of Gastrointestinal and Pediatric Surgery, Division of Reparative Medicine, Institute of Life Sciences, Mie University Graduate School of Medicine, Mie, Japan.
Yasuhiro InoueDepartment of Gastrointestinal and Pediatric Surgery, Division of Reparative Medicine, Institute of Life Sciences, Mie University Graduate School of Medicine, Mie, Japan.
Masato KusunokiDepartment of Gastrointestinal and Pediatric Surgery, Division of Reparative Medicine, Institute of Life Sciences, Mie University Graduate School of Medicine, Mie, Japan.
C Richard BolandCenter for Gastrointestinal Cancer Research; Center for Epigenetics, Cancer Prevention and Cancer Genomics, Baylor Research Institute and Charles A. Sammons Cancer Center, Baylor University Medical Center, Dallas, Texas, USA.
Ajay GoelCenter for Gastrointestinal Cancer Research; Center for Epigenetics, Cancer Prevention and Cancer Genomics, Baylor Research Institute and Charles A. Sammons Cancer Center, Baylor University Medical Center, Dallas, Texas, USA.
Center for Cancer Research · USMie University · JPBaylor Scott & White Health · USBaylor University Medical Center · USInstitute of Life Sciences · INOkayama University · JP

Funding

The Biology and Diagnosis of HNPCCR01CA072851 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI GOEL, AJAY · 1996 to 2019
$6.6M
Aspirin and Cancer Prevention in Lynch Syndrome: From Cell to Population DataU01CA187956 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI GOEL, AJAY, WODARZ, DOMINIK F · 2014 to 2018
$2.7M
METHYLATION BIOMARKER DEVELOPMENT FOR NONINVASIVE DETECTION OF COLORECTAL CANCERR01CA181572 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI GOEL, AJAY · 2014 to 2018
$1.6M
NCI NIH HHS R01 CA072851NCI NIH HHS R01 CA181572NCI NIH HHS U01 CA187956
6 · The paper itself

Abstract

purposeDespite recent advances in colorectal cancer (CRC) treatment, the prognosis of patients suffering from this malignancy still remains substandard, and metastatic recurrence following curative surgery is the leading cause of mortality. Therefore, it is imperative to identify prognostic markers to predict the clinical outcome of CRC patients. Recent evidence revealed the new role of small nucleolar RNAs (snoRNAs) in oncogenesis. Herein, we systematically evaluated dysregulation of snoRNAs in CRC and clarified their biomarker potential and biological significance in CRC. EXPERIMENTAL

designWe analysed expression levels of 4 snoRNAs in 274 colorectal tissues from 3 independent cohorts and 6 colon cancer cell lines. The functional characterisation for the role of SNORA42 in CRC was investigated through a series of in vitro and in vivo experiments.

resultsIn the screening phase, expression levels of all four snoRNAs were significantly elevated in CRC tissues than in corresponding normal mucosa. In the clinical validation cohort, increased SNORA42 expression was an independent prognostic factor for overall survival and disease-free survival, and was a risk factor for distant metastasis. SNORA42 expression negatively correlated with overall survival in an additional independent cohort and identified the patients with high risk for recurrence and poor prognosis in stage II CRC. Furthermore, in vitro and in vivo analyses showed that SNORA42 overexpression resulted in enhanced cell proliferation, migration, invasion, anoikis resistance and tumorigenicity.

conclusionsSNORA42 appears to be a novel oncogene and could serve as a promising predictive biomarker for recurrence and prognosis in patients with CRC.

Indexed as

AgedAnimalsAnoikisBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticColorectal NeoplasmsDisease-Free SurvivalFemaleGene Knockdown TechniquesHEK293 CellsHumansMaleMiceBiomarkers, TumorRNA, Small NucleolarCOLORECTAL CANCER

Identifiers

PMID26475630
PMCPMC4860159
OpenAlexW2173066718

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.