Evidence map›Paper›PMID 25815848›Full record

ReviewCancer journal (Sudbury, Mass.)

Metabolism and its sequelae in cancer evolution and therapy.

Robert J Gillies, Robert A Gatenby

Open access · greenAbstract readReview
In one paragraph

Review in Cancer journal (Sudbury, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 76 citations in OpenAlex.

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  9. Preclinical Evaluation of AZD6422, an Armored Chimeric Antigen Receptor T Cell Targeting CLDN18.2 in Gastric, Pancreatic, and Esophageal Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
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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

2 authors at 1 institution in 1 country.

Robert J GilliesFrom the Departments of Cancer Imaging and Metabolism and Radiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.
Robert A Gatenby
Moffitt Cancer Center · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
Causes & Consequences of Acid pH in TumorsR01CA077575 · NCI · UNIVERSITY OF ARIZONA · PI GILLIES, ROBERT J. · 1999 to 2018
$8.5M
Integrative Molecular Epidemiology WorkshopR25CA174664 · NCI · AMERICAN ASSOCIATION FOR CANCER RESEARCH · PI Shelley S Tworoger · 2013 to 2026
$2.8M
NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA077575NCI NIH HHS R25 CA174664
6 · The paper itself

Abstract

Cancers progress through a series of events that can be characterized as "somatic evolution." A central premise of Darwinian evolutionary theory is that the environment imparts pressure to select for species that are most fit within that particular microenvironmental context. Furthermore, the rate of evolution is proportional to both (1) the strength of the environmental selection and (2) the phenotypic variance of the selected population. It is notable that, during the progression of cancers from carcinogenesis to local invasion to metastasis, the selective landscape continuously changes, and throughout this process, there is increased selection for cells that have altered metabolic phenotypes: implying that these phenotypes impart a selective advantage during the process of environmental selection. One of the most prevalent selected phenotypes is that of aerobic glycolysis, that is, the continued fermentation of glucose even in the presence of adequate oxygen. The mechanisms of this so-called "Warburg effect" have been well studied, and there are multiple models to explain how this occurs at the molecular level. Herein, we propose that unifying insights can be gained by evaluating the environmental context within which this phenotype arises. In other words, we focus not on the "how" but the "why" do cancer cells exhibit high aerobic glycolysis. This is best approached by examining the sequelae of aerobic glycolysis that may impart a selective advantage. Many of these have been considered, including generation of anabolic substrates, response rates of glycolysis vis-à-vis respiration, and generation of antioxidants. A further sequeala considered here is that aerobic glycolysis results in a high rate of lactic acid production; resulting in acidification of the extracellular space. Indeed, it has been shown that a low extracellular pH promotes local invasion, promotes metastasis, and inhibits antitumor immunity. In naturally occurring cancers, low extracellular pH is a strong negative prognostic indicator of metastasis-free survival. Furthermore, it has been shown that inhibition of extracellular acidosis can inhibit metastasis and promote antitumor immunity. Hence, we propose that excess acid production confers a selective advantage for cells during the somatic evolution of cancers.

Indexed as

Energy MetabolismAnimalsCell Transformation, NeoplasticDisease ProgressionHumansHypoxiaNeoplasm InvasivenessNeoplasmsPhenotypeTumor Microenvironment

Identifiers

PMID25815848
PMCPMC4446699
OpenAlexW2069809499

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.