Evidence map›Paper›PMID 26798421›Full record

ReviewOxidative medicine and cellular longevity2016

The Interplay of Reactive Oxygen Species, Hypoxia, Inflammation, and Sirtuins in Cancer Initiation and Progression.

Marco Tafani, Luigi Sansone, Federica Limana, Tania Arcangeli, Elena De Santis, Milena Polese, Massimo Fini, Matteo A Russo

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
207citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

207 citing papers in PubMed, 1 synthesis or guideline pooled it, 361 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. How telomere attrition protects against cancer.Nature reviews. Genetics · 2026
    Review
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  15. Hypoxic adaptation theory of cancer.Frontiers in cell and developmental biology · 2026
    Article
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  20. Review

147 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

8 authors at 3 institutions in 1 country.

Marco TafaniDepartment of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy; Department of Cellular and Molecular Pathology, IRCCS San Raffaele, 00166 Rome, Italy.ORCID 0000-0001-7128-810X
Luigi SansoneDepartment of Cellular and Molecular Pathology, IRCCS San Raffaele, 00166 Rome, Italy.
Federica LimanaConsortium MEBIC, San Raffaele University, 00166 Rome, Italy.
Tania ArcangeliDepartment of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy.
Elena De SantisDepartment of Gynecological-Obstetrical Sciences and Urological Sciences, Sapienza University of Rome, 00161 Rome, Italy.
Milena PoleseDepartment of Human Anatomy, Sapienza University of Rome, 00161 Rome, Italy.
Massimo FiniDepartment of Cellular and Molecular Pathology, IRCCS San Raffaele, 00166 Rome, Italy.
Matteo A RussoConsortium MEBIC, San Raffaele University, 00166 Rome, Italy.
Istituti di Ricovero e Cura a Carattere Scientifico · ITSapienza University of Rome · ITSan Raffaele University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The presence of ROS is a constant feature in living cells metabolizing O2. ROS concentration and compartmentation determine their physiological or pathological effects. ROS overproduction is a feature of cancer cells and plays several roles during the natural history of malignant tumor. ROS continuously contribute to each step of cancerogenesis, from the initiation to the malignant progression, acting directly or indirectly. In this review, we will (a) underline the role of ROS in the pathway leading a normal cell to tumor transformation and progression, (b) define the multiple roles of ROS during the natural history of a tumor, (c) conciliate many conflicting data about harmful or beneficial effects of ROS, (d) rethink the importance of oncogene and tumor suppressor gene mutations in relation to the malignant progression, and (e) collocate all the cancer hallmarks in a mechanistic sequence which could represent a "physiological" response to the initial growth of a transformed stem/pluripotent cell, defining also the role of ROS in each hallmark. We will provide a simplified sketch about the relationships between ROS and cancer. The attention will be focused on the contribution of ROS to the signaling of HIF, NFκB, and Sirtuins as a leitmotif of cancer initiation and progression.

Indexed as

Disease ProgressionAnimalsCarcinogenesisHumansHypoxiaInflammationReactive Oxygen SpeciesSirtuinsReactive Oxygen SpeciesSirtuins

Identifiers

PMID26798421
PMCPMC4699039
OpenAlexW2177051273

What Socratic 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 Socratic graph.