Evidence map›Paper›PMID 28467356›Full record

ArticleGenes2017

AKR1C1 as a Biomarker for Differentiating the Biological Effects of Combustible from Non-Combustible Tobacco Products.

Sangsoon Woo, Hong Gao, David Henderson, Wolfgang Zacharias, Gang Liu, Quynh T Tran, G L Prasad

Open access · goldAbstract read
In one paragraph

Article in Genes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Secretome analysis of oral keratinocytes chronically exposed to shisha.Cancer biomarkers : section A of Disease markers · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Nicotine mediated epithelial modulations: AnJournal of oral biology and craniofacial research
    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

7 authors at 2 institutions in 1 country.

Sangsoon WooStatistical Genetics, Axio Research LLC, 4th Ave. Suite 200, Seattle, WA 98121, USA. sangsoonw@axioresearch.com.
Hong GaoDepartment of Medicine, James Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY 40202, USA. kygaohong@gmail.com.
David HendersonStatistical Genetics, Axio Research LLC, 4th Ave. Suite 200, Seattle, WA 98121, USA. davidh@axioresearch.com.
Wolfgang ZachariasDepartment of Medicine, James Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY 40202, USA. wolfgang.zacharias@louisville.edu.
Gang LiuRAI Services Company, 401 N. Main Street, Winston-Salem, NC 27101, USA. liug@rjrt.com.
Quynh T TranRAI Services Company, 401 N. Main Street, Winston-Salem, NC 27101, USA. trann1@rjrt.com.
G L PrasadRAI Services Company, 401 N. Main Street, Winston-Salem, NC 27101, USA. prasadg@rjrt.com.
Research Applications (United States) · USUniversity of Louisville · US

Funding

WV INBRE: The Inhibitor of Growth Family Member 4 (ING4) inhibits L-Type Amino Acid Transporter 1 (LAT1) expression to suppress Breast CancerP20GM103434 · NIGMS · MARSHALL UNIVERSITY · PI Travis Salisbury · 2012 to 2026
$61.1M
PILOT PROJECT PROGRAMP30GM106396 · NIGMS · UNIVERSITY OF LOUISVILLE · PI MILLER, DONALD M. · 2013 to 2017
$5.4M
NIGMS NIH HHS P20 GM103434NIGMS NIH HHS P30 GM106396
6 · The paper itself

Abstract

Smoking has been established as a major risk factor for developing oral squamous cell carcinoma (OSCC), but less attention has been paid to the effects of smokeless tobacco products. Our objective is to identify potential biomarkers to distinguish the biological effects of combustible tobacco products from those of non-combustible ones using oral cell lines. Normal human gingival epithelial cells (HGEC), non-metastatic (101A) and metastatic (101B) OSCC cell lines were exposed to different tobacco product preparations (TPPs) including cigarette smoke total particulate matter (TPM), whole-smoke conditioned media (WS-CM), smokeless tobacco extract in complete artificial saliva (STE), or nicotine (NIC) alone. We performed microarray-based gene expression profiling and found 3456 probe sets from 101A, 1432 probe sets from 101B, and 2717 probe sets from HGEC to be differentially expressed. Gene Set Enrichment Analysis (GSEA) revealed xenobiotic metabolism and steroid biosynthesis were the top two pathways that were upregulated by combustible but not by non-combustible TPPs. Notably, aldo-keto reductase genes,

Indexed as

aldo-keto reductasescigarette smokenicotineoral cavity cellssmokeless tobacco productsxenobiotic metabolism

Identifiers

PMID28467356
PMCPMC5448006
OpenAlexW2583063260

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.