Evidence map›Paper›PMID 26171112›Full record

ReviewOxidative medicine and cellular longevity2015

Type 2 Diabetes and Breast Cancer: The Interplay between Impaired Glucose Metabolism and Oxidant Stress.

Patrizia Ferroni, Silvia Riondino, Oreste Buonomo, Raffaele Palmirotta, Fiorella Guadagni, Mario Roselli

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

46 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  12. Smad3 Phospho-Isoform Signaling in Nonalcoholic Steatohepatitis.International journal of molecular sciences · 2022
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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

6 authors.

Patrizia FerroniSan Raffaele Rome University, IRCCS San Raffaele Pisana, Research Center, Via di Val Cannuta 247, 00166 Rome, Italy.
Silvia RiondinoSan Raffaele Rome University, IRCCS San Raffaele Pisana, Research Center, Via di Val Cannuta 247, 00166 Rome, Italy ; Department of Systems Medicine, Medical Oncology, Tor Vergata Clinical Center, University of Rome Tor Vergata, Viale Oxford 81, 00133 Rome, Italy.
Oreste BuonomoDepartment of Surgery, Division of Surgical Oncology, Tor Vergata Clinical Center, University of Rome Tor Vergata, Viale Oxford 81, 00133 Rome, Italy.
Raffaele PalmirottaSan Raffaele Rome University, IRCCS San Raffaele Pisana, Research Center, Via di Val Cannuta 247, 00166 Rome, Italy.
Fiorella GuadagniSan Raffaele Rome University, IRCCS San Raffaele Pisana, Research Center, Via di Val Cannuta 247, 00166 Rome, Italy.
Mario RoselliDepartment of Systems Medicine, Medical Oncology, Tor Vergata Clinical Center, University of Rome Tor Vergata, Viale Oxford 81, 00133 Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic disorders, especially type 2 diabetes and its associated complications, represent a growing public health problem. Epidemiological findings indicate a close relationship between diabetes and many types of cancer (including breast cancer risk), which regards not only the dysmetabolic condition, but also its underlying risk factors and therapeutic interventions. This review discusses the advances in understanding of the mechanisms linking metabolic disorders and breast cancer. Among the proposed mechanisms to explain such an association, a major role is played by the dysregulated glucose metabolism, which concurs with a chronic proinflammatory condition and an associated oxidative stress to promote tumour initiation and progression. As regards the altered glucose metabolism, hyperinsulinaemia, both endogenous due to insulin-resistance and drug-induced, appears to promote tumour cell growth through the involvement of innate immune activation, platelet activation, increased reactive oxygen species, exposure to protumorigenic and proangiogenic cytokines, and increased substrate availability to neoplastic cells. In this context, understanding the relationship between metabolic disorders and cancer is becoming imperative, and an accurate analysis of these associations could be used to identify biomarkers able to predict disease risk and/or prognosis and to help in the choice of proper evidence-based diagnostic and therapeutic protocols.

Indexed as

Oxidative StressBreast NeoplasmsDiabetes Mellitus, Type 2FemaleGlucoseHumansHypoglycemic AgentsInflammationMitogen-Activated Protein KinasesReactive Oxygen SpeciesGlucoseHypoglycemic AgentsMitogen-Activated Protein KinasesReactive Oxygen Species

Identifiers

PMID26171112
PMCPMC4480937

What OpenQuestion holds

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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.