Evidence map›Paper›PMID 29355844›Full record

ArticleThe Journal of clinical investigation2018

Endothelial Tie1-mediated angiogenesis and vascular abnormalization promote tumor progression and metastasis.

Silvia La Porta, Lise Roth, Mahak Singhal, Carolin Mogler, Carleen Spegg, Benjamin Schieb, Xianghu Qu, Ralf H Adams, H Scott Baldwin, Soniya Savant and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 102 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Multi-omic Profiling of Recurrence Risk Across Breast Cancer Subtypes.medRxiv : the preprint server for health sciences · 2026
    Article
  5. Article
  6. Article
  7. Vascular changes and their implications in lipedema.Frontiers in cell and developmental biology · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

11 authors at 3 institutions in 2 countries.

Silvia La PortaDivision of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), Heidelberg, Germany.
Lise RothDivision of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), Heidelberg, Germany.
Mahak SinghalDivision of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), Heidelberg, Germany.
Carolin MoglerDivision of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), Heidelberg, Germany.
Carleen SpeggDivision of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), Heidelberg, Germany.
Benjamin SchiebDivision of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), Heidelberg, Germany.
Xianghu QuDepartment of Pediatrics, Division of Cardiology, and.
Ralf H AdamsDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
H Scott BaldwinDepartment of Pediatrics, Division of Cardiology, and.
Soniya SavantDivision of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), Heidelberg, Germany.
Hellmut G AugustinDivision of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), Heidelberg, Germany.
German Cancer Research Center · DEVanderbilt University · USUniversity of Münster · DE

Funding

Developmental Determinants of Cardiovascular DiseaseT32HL105334 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BALDWIN, H SCOTT · 2011 to 2021
$4.3M
Tie Tek Modulation of Cardiac DevelopmentR01HL118386 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BALDWIN, H SCOTT · 2013 to 2017
$2.1M
NHLBI NIH HHS R01 HL118386NHLBI NIH HHS T32 HL105334
6 · The paper itself

Abstract

The endothelial tyrosine kinase receptor Tie1 remains poorly characterized, largely owing to its orphan receptor status. Global Tie1 inactivation causes late embryonic lethality, thereby reflecting its importance during development. Tie1 also plays pivotal roles during pathologies such as atherosclerosis and tumorigenesis. In order to study the contribution of Tie1 to tumor progression and metastasis, we conditionally deleted Tie1 in endothelial cells at different stages of tumor growth and metastatic dissemination. Tie1 deletion during primary tumor growth in mice led to a decrease in microvessel density and an increase in mural cell coverage with improved vessel perfusion. Reduced angiogenesis and enhanced vascular normalization resulted in a progressive increase of intratumoral necrosis that caused a growth delay only at later stages of tumor progression. Concomitantly, surgical removal of the primary tumor decreased the number of circulating tumor cells, reduced metastasis, and prolonged overall survival. Additionally, Tie1 deletion in experimental murine metastasis models prevented extravasation of tumor cells into the lungs and reduced metastatic foci. Taken together, the data support Tie1 as a therapeutic target by defining its regulatory functions during angiogenesis and vascular abnormalization and identifying its role during metastasis.

Indexed as

Neoplasm MetastasisNeovascularization, PathologicAnimalsCell Line, TumorDisease ProgressionEndothelial CellsFemaleGene DeletionHumansHuman Umbilical Vein Endothelial CellsLung NeoplasmsMaleMelanoma, ExperimentalMiceMice, KnockoutNecrosisReceptor, TIE-1AngiogenesisCancerendothelial cellsOncology

Identifiers

PMID29355844
PMCPMC5785248
OpenAlexW2784469476

What OpenQuestion holds

Textmetadata
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.