Evidence map›Paper›PMID 31076951›Full record

ReviewCancer metastasis reviews2019

The role of carbonic anhydrase IX in cancer development: links to hypoxia, acidosis, and beyond.

Silvia Pastorekova, Robert J Gillies

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 238 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
238citing papers in PubMed, 1 pooled it
15.3field-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

238 citing papers in PubMed, 1 synthesis or guideline pooled it, 425 citations in OpenAlex.

  1. High IntratumoralInternational journal of molecular sciences · 2026
    Pooled it
  2. Evaluation of the safety, biodistribution, dosimetry of [European journal of nuclear medicine and molecular imaging · 2025
    Trial
  3. Article
  4. Dual-target carbonic anhydrase inhibitors in cancer therapy: progress, challenges, and opportunities.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
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  6. Progress in the application ofAnnals of nuclear medicine · 2026
    Review
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178 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

2 authors at 2 institutions in 2 countries.

Silvia PastorekovaDepartment of Tumor Biology, Institute of Virology, Biomedical Research Center, University Science Park for Biomedicine, Slovak Academy of Sciences, Dúbravská cesta 9, 845 05, Bratislava, Slovakia. silvia.pastorekova@savba.sk.
Robert J GilliesDepartment of Cancer Physiology, H. Lee Moffitt Cancer Center, 12902 Magnolia Avenue, Tampa, FL, 33612, USA.
Biomedical Research Center of the Slovak Academy of Sciences · SKMoffitt Cancer Center · US

Funding

"Research Supplement to Promote Diversity in Health-Related Research", as part of Moffitt PS-OC, "Cancer as a Complex adaptive System"U54CA193489 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI ANDERSON, ALEXANDER ROBERTSON ALLAN, GATENBY, ROBERT A · 2015 to 2020
$12.5M
Causes & Consequences of Acid pH in TumorsR01CA077575 · NCI · UNIVERSITY OF ARIZONA · PI GILLIES, ROBERT J. · 1999 to 2018
$8.5M
NCI NIH HHS R01 CA077575NCI NIH HHS U54 CA193489
6 · The paper itself

Abstract

Cancer development is a complex process that follows an intricate scenario with a dynamic interplay of selective and adaptive steps and an extensive cast of molecules and signaling pathways. Solid tumor initially grows as an avascular bulk of cells carrying oncogenic mutations until diffusion distances from the nearest functional blood vessels limit delivery of nutrients and oxygen on the one hand and removal of metabolic waste on the other one. These restrictions result in regional hypoxia and acidosis that select for adaptable tumor cells able to promote aberrant angiogenesis, remodel metabolism, acquire invasiveness and metastatic propensity, and gain therapeutic resistance. Tumor cells are thereby endowed with capability to survive and proliferate in hostile microenvironment, communicate with stroma, enter circulation, colonize secondary sites, and generate metastases. While the role of oncogenic mutations initializing and driving these processes is well established, a key contribution of non-genomic, landscaping molecular players is still less appreciated despite they can equally serve as viable targets of anticancer therapies. Carbonic anhydrase IX (CA IX) is one of these players: it is induced by hypoxia, functionally linked to acidosis, implicated in invasiveness, and correlated with therapeutic resistance. Here, we summarize the available experimental evidence supported by accumulating preclinical and clinical data that CA IX can contribute virtually to each step of cancer progression path via its enzyme activity and/or non-catalytic mechanisms. We also propose that targeting tumor cells that express CA IX may provide therapeutic benefits in various settings and combinations with both conventional and newly developed treatments.

Indexed as

AcidosisAnimalsCarbonic Anhydrase IXCell HypoxiaHumansNeoplasmsCarbonic Anhydrase IXAcidosisCancer progressionCarbonic anhydrase IXHypoxiapH regulationTumor microenvironment

Identifiers

PMID31076951
PMCPMC6647366
OpenAlexW2944503022

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.