Evidence map›Paper›PMID 37349410›Full record

ReviewNature reviews. Cancer2023

Understanding tumour endothelial cell heterogeneity and function from single-cell omics.

Qun Zeng, Mira Mousa, Aisha Shigna Nadukkandy, Lies Franssens, Halima Alnaqbi, Fatima Yousif Alshamsi, Habiba Al Safar, Peter Carmeliet

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing 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

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

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73 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

8 authors.

Qun ZengLaboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven and Center for Cancer Biology, VIB, Leuven, Belgium.ORCID 0000-0003-0859-3894
Mira Mousa *Center for Biotechnology, Khalifa University of Science and Technology, Abu Dhabi, UAE.ORCID 0000-0002-5676-3221
Aisha Shigna Nadukkandy *Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven and Center for Cancer Biology, VIB, Leuven, Belgium.
Lies Franssens *Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven and Center for Cancer Biology, VIB, Leuven, Belgium.
Halima Alnaqbi *Center for Biotechnology, Khalifa University of Science and Technology, Abu Dhabi, UAE.ORCID 0000-0002-7799-8038
Fatima Yousif Alshamsi *Department of Biomedical Engineering, Khalifa University of Science and Technology, Abu Dhabi, UAE.ORCID 0000-0002-4378-6598
Habiba Al SafarCenter for Biotechnology, Khalifa University of Science and Technology, Abu Dhabi, UAE. habiba.alsafar@ku.ac.ae.
Peter CarmelietLaboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven and Center for Cancer Biology, VIB, Leuven, Belgium. peter.carmeliet@kuleuven.be.ORCID 0000-0001-7961-1821

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-angiogenic therapies (AATs) are used to treat different types of cancers. However, their success is limited owing to insufficient efficacy and resistance. Recently, single-cell omics studies of tumour endothelial cells (TECs) have provided new mechanistic insight. Here, we overview the heterogeneity of human TECs of all tumour types studied to date, at the single-cell level. Notably, most human tumour types contain varying numbers but only a small population of angiogenic TECs, the presumed targets of AATs, possibly contributing to the limited efficacy of and resistance to AATs. In general, TECs are heterogeneous within and across all tumour types, but comparing TEC phenotypes across tumours is currently challenging, owing to the lack of a uniform nomenclature for endothelial cells and consistent single-cell analysis protocols, urgently raising the need for a more consistent approach. Nonetheless, across most tumour types, universal TEC markers (ACKR1, PLVAP and IGFBP3) can be identified. Besides angiogenesis, biological processes such as immunomodulation and extracellular matrix organization are among the most commonly predicted enriched signatures of TECs across different tumour types. Although angiogenesis and extracellular matrix targets have been considered for AAT (without the hoped success), the immunomodulatory properties of TECs have not been fully considered as a novel anticancer therapeutic approach. Therefore, we also discuss progress, limitations, solutions and novel targets for AAT development.

Indexed as

Endothelial CellsNeoplasmsHumansNeovascularization, PathologicPhenotype

Identifiers

What OpenQuestion holds

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Registered trials

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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.