Evidence map›Paper›PMID 28546110›Full record

ReviewSeminars in cancer biology2018

Hypoxia driven glycation: Mechanisms and therapeutic opportunities.

Mohammad Imran Khan, Suvasmita Rath, Vaqar Mustafa Adhami, Hasan Mukhtar

Abstract readReview
In one paragraph

Review in Seminars in cancer biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.9field-weighted citation impact, top 17% 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

39 citing papers in PubMed, 61 citations in OpenAlex.

  1. Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

4 authors at 1 institution in 1 country.

Mohammad Imran KhanDepartment of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison, WI-53706, USA.
Suvasmita RathDepartment of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison, WI-53706, USA.
Vaqar Mustafa AdhamiDepartment of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison, WI-53706, USA.
Hasan MukhtarDepartment of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison, WI-53706, USA. Electronic address: hmukhtar@dermatology.wisc.edu.
University of Wisconsin–Madison · US

Funding

Targeting PI3K/Akt/mTOR for the management of psoriasisR01AR059742 · NIAMS · UNIVERSITY OF WISCONSIN-MADISON · PI MUKHTAR, HASAN · 2010 to 2019
$3.3M
Skin Diseases Research Center at the University of WisconsinP30AR066524 · NIAMS · UNIVERSITY OF WISCONSIN-MADISON · PI WOOD, GARY S · 2014 to 2018
$2.6M
Developing Fisetin for the Managment of Prostate CancerR01CA160867 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI MUKHTAR, HASAN · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA160867NIAMS NIH HHS P30 AR066524NIAMS NIH HHS R01 AR059742
6 · The paper itself

Abstract

Tumor masses are deprived of oxygen and characterized by enhanced glucose uptake followed by glycolysis. Elevated glucose levels induce non-enzymatic glycosylation or glycation of proteins which leads to accumulation of advanced glycation end products (AGE). These AGE molecules bind to their respective receptors called the receptor for advanced glycation end products (RAGE) and initiate several aberrant signaling pathways leading to onset of diseases such as diabetes, Alzheimer's, atherosclerosis, heart failure and cancer. The role of AGE in cancer progression is being extensively studied in recent years. As cancer cells are hypoxic in nature and adapted to glycolysis, which induces glycation, its effects need to be understood in greater detail. Since AGE-RAGE signaling is involved in cancer progression, inhibition of AGE-RAGE interaction could be a potential therapeutic target. The purpose of this review is to highlight the role of AGE-RAGE interaction in hypoxic cancer cells.

Indexed as

GlycosylationAnimalsAntineoplastic AgentsCell Transformation, NeoplasticGlycation End Products, AdvancedHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMolecular Targeted TherapyProtein BindingReceptor for Advanced Glycation End ProductsSignal TransductionAntineoplastic AgentsGlycation End Products, AdvancedHypoxia-Inducible Factor 1, alpha SubunitReceptor for Advanced Glycation End ProductsAdvanced glycation end productsCancerGlycationHif1αHypoxiaRAGE

Identifiers

PMID28546110
PMCPMC5699980
OpenAlexW2617569755

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.