Evidence map›Paper›PMID 25621294›Full record

ArticleOncoscience2014

Glycolysis, tumor metabolism, cancer growth and dissemination. A new pH-based etiopathogenic perspective and therapeutic approach to an old cancer question.

Khalid O Alfarouk, Daniel Verduzco, Cyril Rauch, Abdel Khalig Muddathir, H H Bashir Adil, Gamal O Elhassan, Muntaser E Ibrahim, Julian David Polo Orozco, Rosa Angela Cardone, Stephan J Reshkin and 1 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Oncoscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

125 citing papers in PubMed, 245 citations in OpenAlex.

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65 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 5 countries.

Khalid O AlfaroukUniversity of Khartoum, Khartoum, Sudan.
Daniel VerduzcoH. Lee Moffitt Cancer Center, Tampa, FL, USA.
Cyril RauchUniversity of Nottingham, Sutton Bonington, Leicestershire, Nottingham, UK.
Abdel Khalig MuddathirUniversity of Khartoum, Khartoum, Sudan.
H H Bashir AdilUniversity of Khartoum, Khartoum, Sudan.
Gamal O ElhassanUnizah Pharmacy Collage, Qassim University, Unizah, AL-Qassim, King of Saudi Arabia ; Omdurman Islamic University, Omdurman, Sudan.
Muntaser E IbrahimUniversity of Khartoum, Khartoum, Sudan.
Julian David Polo OrozcoInstitute of Clinical Biology and Metabolism, Vitoria, Spain.
Rosa Angela CardoneUniversity of Bari, Bari, Italy.
Stephan J ReshkinUniversity of Bari, Bari, Italy.
Salvador HarguindeyInstitute of Clinical Biology and Metabolism, Vitoria, Spain.
University of Khartoum · SDUniversity of Bari Aldo Moro · ITMoffitt Cancer Center · USOmdurman Islamic University · SDUniversity of Nottingham · GB

Funding

Wellcome Trust 100715
6 · The paper itself

Abstract

Cancer cells acquire an unusual glycolytic behavior relative, to a large extent, to their intracellular alkaline pH (pHi). This effect is part of the metabolic alterations found in most, if not all, cancer cells to deal with unfavorable conditions, mainly hypoxia and low nutrient supply, in order to preserve its evolutionary trajectory with the production of lactate after ten steps of glycolysis. Thus, cancer cells reprogram their cellular metabolism in a way that gives them their evolutionary and thermodynamic advantage. Tumors exist within a highly heterogeneous microenvironment and cancer cells survive within any of the different habitats that lie within tumors thanks to the overexpression of different membrane-bound proton transporters. This creates a highly abnormal and selective proton reversal in cancer cells and tissues that is involved in local cancer growth and in the metastatic process. Because of this environmental heterogeneity, cancer cells within one part of the tumor may have a different genotype and phenotype than within another part. This phenomenon has frustrated the potential of single-target therapy of this type of reductionist therapeutic approach over the last decades. Here, we present a detailed biochemical framework on every step of tumor glycolysis and then proposea new paradigm and therapeutic strategy based upon the dynamics of the hydrogen ion in cancer cells and tissues in order to overcome the old paradigm of one enzyme-one target approach to cancer treatment. Finally, a new and integral explanation of the Warburg effect is advanced.

Indexed as

cancer growthcancer treatmentmetastatic processnew paradigm in oncologypH and cancerpH and glycolysisproton transport inhibitorsTumor glycolysis

Identifiers

PMID25621294
PMCPMC4303887
OpenAlexW2122012410

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.