Evidence map›Paper›PMID 31239543›Full record

ArticleBritish journal of cancer2019

Notch2 pathway mediates breast cancer cellular dormancy and mobilisation in bone and contributes to haematopoietic stem cell mimicry.

Mattia Capulli, Dayana Hristova, Zoé Valbret, Kashmala Carys, Ronak Arjan, Antonio Maurizi, Francesco Masedu, Alfredo Cappariello, Nadia Rucci, Anna Teti

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 74 citations in OpenAlex.

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  7. HES1 oscillations are required for cell cycle reentry in oestrogen receptor-positive breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

10 authors at 1 institution in 1 country.

Mattia CapulliDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila Via Vetoio - Coppito 2, 67100, L'Aquila, Italy.
Dayana HristovaDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila Via Vetoio - Coppito 2, 67100, L'Aquila, Italy.
Zoé ValbretDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila Via Vetoio - Coppito 2, 67100, L'Aquila, Italy.
Kashmala CarysDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila Via Vetoio - Coppito 2, 67100, L'Aquila, Italy.
Ronak ArjanDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila Via Vetoio - Coppito 2, 67100, L'Aquila, Italy.
Antonio MauriziDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila Via Vetoio - Coppito 2, 67100, L'Aquila, Italy.
Francesco MaseduDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila Via Vetoio - Coppito 2, 67100, L'Aquila, Italy.
Alfredo CapparielloDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila Via Vetoio - Coppito 2, 67100, L'Aquila, Italy.
Nadia RucciDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila Via Vetoio - Coppito 2, 67100, L'Aquila, Italy.
Anna TetiDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila Via Vetoio - Coppito 2, 67100, L'Aquila, Italy. annamaria.teti@univaq.it.
University of L'Aquila · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecurrence after >5-year disease-free survival affects one-fifth of breast cancer patients and is the clinical manifestation of cancer cell reactivation after persistent dormancy.

methodsWe investigated cellular dormancy in vitro and in vivo using breast cancer cell lines and cell and molecular biology techniques.

resultsWe demonstrated cellular dormancy in breast cancer bone metastasis, associated with haematopoietic stem cell (HSC) mimicry, in vivo competition for HSC engraftment and non-random distribution of dormant cells at the endosteal niche. Notch2 signal implication was demonstrated by immunophenotyping the endosteal niche-associated cancer cells and upon co-culture with sorted endosteal niche cells, which inhibited breast cancer cell proliferation in a Notch2-dependent manner. Blocking this signal by in vivo acute administration of the γ-secretase inhibitor, dibenzazepine, induced dormant cell mobilisation from the endosteal niche and colonisation of visceral organs. Sorted Notch2

conclusionsNotch2 represents a key determinant of breast cancer cellular dormancy and mobilisation in the bone microenvironment.

Indexed as

AnimalsBone NeoplasmsBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationDibenzazepinesDrug Resistance, NeoplasmFemaleHematopoietic Stem CellsHumansMiceMice, Inbred BALB COsteoblastsReceptor, Notch2Signal TransductiondibenzazepineDibenzazepinesNOTCH2 protein, humanReceptor, Notch2

Identifiers

PMID31239543
PMCPMC6738045
OpenAlexW2954433278

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.