Evidence map›Paper›PMID 24409151›Full record

ReviewFrontiers in physiology2014

Carbonic anhydrase IX, a hypoxia-induced catalytic component of the pH regulating machinery in tumors.

Olga Sedlakova, Eliska Svastova, Martina Takacova, Juraj Kopacek, Jaromir Pastorek, Silvia Pastorekova

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 2 pooled it
10.0field-weighted citation impact, top 1% 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

98 citing papers in PubMed, 2 syntheses or guidelines pooled it, 195 citations in OpenAlex.

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  12. Di-Journal of medicinal chemistry · 2025
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  15. Tumor Hypoxia: How Conventional Histology Is Reshaped in Breast Carcinoma.International journal of molecular sciences · 2025
    Review
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38 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

6 authors at 1 institution in 1 country.

Olga SedlakovaDepartment of Molecular Medicine, Institute of Virology, Slovak Academy of Sciences Bratislava, Slovakia.
Eliska SvastovaDepartment of Molecular Medicine, Institute of Virology, Slovak Academy of Sciences Bratislava, Slovakia.
Martina TakacovaDepartment of Molecular Medicine, Institute of Virology, Slovak Academy of Sciences Bratislava, Slovakia.
Juraj KopacekDepartment of Molecular Medicine, Institute of Virology, Slovak Academy of Sciences Bratislava, Slovakia.
Jaromir PastorekDepartment of Molecular Medicine, Institute of Virology, Slovak Academy of Sciences Bratislava, Slovakia.
Silvia PastorekovaDepartment of Molecular Medicine, Institute of Virology, Slovak Academy of Sciences Bratislava, Slovakia.
Institute of Virology of the Slovak Academy of Sciences · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acidic tissue microenvironment contributes to tumor progression via multiple effects including the activation of angiogenic factors and proteases, reduced cell-cell adhesion, increased migration and invasion, etc. In addition, intratumoral acidosis can influence the uptake of anticancer drugs and modulate the response of tumors to conventional therapy. Acidification of the tumor microenvironment often develops due to hypoxia-triggered oncogenic metabolism, which leads to the extensive production of lactate, protons, and carbon dioxide. In order to avoid intracellular accumulation of the acidic metabolic products, which is incompatible with the survival and proliferation, tumor cells activate molecular machinery that regulates pH by driving transmembrane inside-out and outside-in ion fluxes. Carbonic anhydrase IX (CA IX) is a hypoxia-induced catalytic component of the bicarbonate import arm of this machinery. Through its catalytic activity, CA IX directly participates in many acidosis-induced features of tumor phenotype as demonstrated by manipulating its expression and/or by in vitro mutagenesis. CA IX can function as a survival factor protecting tumor cells from hypoxia and acidosis, as a pro-migratory factor facilitating cell movement and invasion, as a signaling molecule transducing extracellular signals to intracellular pathways (including major signaling and metabolic cascades) and converting intracellular signals to extracellular effects on adhesion, proteolysis, and other processes. These functional implications of CA IX in cancer are supported by numerous clinical studies demonstrating the association of CA IX with various clinical correlates and markers of aggressive tumor behavior. Although our understanding of the many faces of CA IX is still incomplete, existing knowledge supports the view that CA IX is a biologically and clinically relevant molecule, exploitable in anticancer strategies aimed at targeting adaptive responses to hypoxia and/or acidosis.

Indexed as

carbonic anhydrase IXhypoxiapH regulationtumor microenvironment

Identifiers

PMID24409151
PMCPMC3884196
OpenAlexW1983080825

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.