Evidence map›Paper›PMID 33530455›Full record

ReviewCancers2021

The CXCL12 Crossroads in Cancer Stem Cells and Their Niche.

Juan Carlos López-Gil, Laura Martin-Hijano, Patrick C Hermann, Bruno Sainz

Abstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  16. Tumor hypoxia shapes natural killer cell anticancer activities.Journal of molecular medicine (Berlin, Germany) · 2025
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  18. Cancer stem cells in meningiomas: novel insights and therapeutic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
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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

4 authors.

Juan Carlos López-GilDepartment of Cancer Biology, Instituto de Investigaciones Biomédicas "Alberto Sols" (IIBM), CSIC-UAM, 28029 Madrid, Spain.ORCID 0000-0003-4988-8648
Laura Martin-HijanoDepartment of Cancer Biology, Instituto de Investigaciones Biomédicas "Alberto Sols" (IIBM), CSIC-UAM, 28029 Madrid, Spain.ORCID 0000-0003-0666-533X
Patrick C HermannDepartment of Internal Medicine I, Ulm University, 89081 Ulm, Germany.ORCID 0000-0003-0418-0478
Bruno SainzDepartment of Cancer Biology, Instituto de Investigaciones Biomédicas "Alberto Sols" (IIBM), CSIC-UAM, 28029 Madrid, Spain.ORCID 0000-0003-4829-7651

Funding

Deutsche Krebshilfe Max Eder Fellowship 111746Deutsche Stiftung Friedensforschung 316249678 - SFB 1279Fundación Científica Asociación Española Contra el Cáncer GC16173694BARBFundación Fero n/aHector Foundation Cancer Research grant M65.1
6 · The paper itself

Abstract

Cancer stem cells (CSCs) are defined as a subpopulation of "stem"-like cells within the tumor with unique characteristics that allow them to maintain tumor growth, escape standard anti-tumor therapies and drive subsequent repopulation of the tumor. This is the result of their intrinsic "stem"-like features and the strong driving influence of the CSC niche, a subcompartment within the tumor microenvironment that includes a diverse group of cells focused on maintaining and supporting the CSC. CXCL12 is a chemokine that plays a crucial role in hematopoietic stem cell support and has been extensively reported to be involved in several cancer-related processes. In this review, we will provide the latest evidence about the interactions between CSC niche-derived CXCL12 and its receptors-CXCR4 and CXCR7-present on CSC populations across different tumor entities. The interactions facilitated by CXCL12/CXCR4/CXCR7 axes seem to be strongly linked to CSC "stem"-like features, tumor progression, and metastasis promotion. Altogether, this suggests a role for CXCL12 and its receptors in the maintenance of CSCs and the components of their niche. Moreover, we will also provide an update of the therapeutic options being currently tested to disrupt the CXCL12 axes in order to target, directly or indirectly, the CSC subpopulation.

Indexed as

cancer stem cellsCSC nicheCXCL12CXCR4CXCR4 inhibitors

Identifiers

PMID33530455
PMCPMC7866198

What OpenQuestion holds

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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.