Evidence map›Paper›PMID 31796022›Full record

ArticleBMC cancer2019

The notch target gene HEYL modulates metastasis forming capacity of colorectal cancer patient-derived spheroid cells in vivo.

Sarah Weber, Sebastian E Koschade, Christopher M Hoffmann, Taronish D Dubash, Klara M Giessler, Sebastian M Dieter, Friederike Herbst, Hanno Glimm, Claudia R Ball

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  3. HEYL-mediated activation of LAMA3 influences radiotherapy response in esophageal cancer.Esophagus : official journal of the Japan Esophageal Society · 2025
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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

9 authors at 2 institutions in 1 country.

Sarah WeberTranslational Functional Cancer Genomics, National Center for Tumor Diseases (NCT) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Sebastian E KoschadeGerman Cancer Consortium (DKTK) Frankfurt am Main, Frankfurt am Main, Germany.
Christopher M HoffmannTranslational Functional Cancer Genomics, National Center for Tumor Diseases (NCT) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Taronish D DubashTranslational Functional Cancer Genomics, National Center for Tumor Diseases (NCT) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Klara M GiesslerTranslational Functional Cancer Genomics, National Center for Tumor Diseases (NCT) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Sebastian M DieterTranslational Functional Cancer Genomics, National Center for Tumor Diseases (NCT) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Friederike HerbstTranslational Functional Cancer Genomics, National Center for Tumor Diseases (NCT) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Hanno GlimmTranslational Functional Cancer Genomics, National Center for Tumor Diseases (NCT) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Claudia R BallTranslational Functional Cancer Genomics, National Center for Tumor Diseases (NCT) and German Cancer Research Center (DKFZ), Heidelberg, Germany. claudia.ball@nct-dresden.de.ORCID http://orcid.org/0000-0002-1749-3791
German Cancer Research Center · DEGoethe University Frankfurt · DE

Funding

Deutsche Krebshilfe Colon-Resist-NetDeutsches Krebsforschungszentrum NCT3.0_2015.04 TransOncoDeutsches Krebsforschungszentrum NCT3.0_2015.54 DysregPTTRANSCAN-2 ERA-NET TACTIC
6 · The paper itself

Abstract

backgroundWhile colorectal cancer (CRC) patients with localized disease have a favorable prognosis, the five-year-survival rate in patients with distant spread is still below 15%. Hence, a detailed understanding of the mechanisms regulating metastasis formation is essential to develop therapeutic strategies targeting metastasized CRC. The notch pathway has been shown to be involved in the metastatic spread of various tumor entities; however, the impact of its target gene HEYL remains unclear so far.

methodsIn this study, we functionally assessed the association between high HEYL expression and metastasis formation in human CRC. Therefore, we lentivirally overexpressed HEYL in two human patient-derived CRC cultures differing in their spontaneous metastasizing capacity and analyzed metastasis formation as well as tumor cell dissemination into the bone marrow after xenotransplantation into NOD.Cg-Prkdc

resultsHEYL overexpression decreased tumor cell dissemination and the absolute numbers of formed metastases in a sub-renal capsular spontaneous metastasis formation model, addressing all steps of the metastatic cascade. In contrast, metastatic capacity was not decreased following intrasplenic xenotransplantation where the cells are placed directly into the blood circulation.

conclusionThese results suggest that HEYL negatively regulates metastasis formation in vivo presumably by inhibiting intravasation of metastasis-initiating cells.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsBiomarkers, TumorBone Marrow NeoplasmsCell Line, TumorCell ProliferationColorectal NeoplasmsFemaleHeterograftsHumansMaleMiceMice, Inbred NODMice, SCIDReceptor, Notch1Repressor ProteinsBasic Helix-Loop-Helix ProteinsBiomarkers, TumorHEYL protein, humanNOTCH1 protein, humanReceptor, Notch1Repressor ProteinsColorectal cancerHEYLMetastasisXenotransplantation

Identifiers

PMID31796022
PMCPMC6892194
OpenAlexW2994452501

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.