Evidence map›Paper›PMID 25757734›Full record

ArticleBreast cancer research : BCR2015

Lobular breast cancer: molecular basis, mouse and cellular models.

Matthias Christgen, Patrick W B Derksen

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03620643 (Phase II Study of ROS1 Targeting With Crizotinib in Advanced E-cadherin Negative, ER Positive Lobular Breast Cancer, Diffuse Gastric Cancer, Triple Negative Lobular Breast Cancer or CDH1-mutated Solid Tumours), which is not on this map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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.

NCT03620643 phase2completednot on this mapstarted 2019, after this paper: background citation

Phase II Study of ROS1 Targeting With Crizotinib in Advanced E-cadherin Negative, ER Positive Lobular Breast Cancer, Diffuse Gastric Cancer, Triple Negative Lobular Breast Cancer or CDH1-mutated Solid Tumours

TypeinterventionalSponsorRoyal Marsden NHS Foundation TrustRan2019 to 2024Enrolled33ConditionsLobular Breast Carcinoma, Gastric Cancer, Triple Negative Breast Cancer, CDH1 Gene MutationArmsCrizotinib Oral Capsule [Xalkori], Fulvestrant 50 MG/ML Prefilled Syringe [Faslodex or generic]
3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Toward targeted therapeutics for lobular breast cancer.The Journal of clinical investigation · 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

2 authors at 2 institutions in 2 countries.

Matthias ChristgenInstitute of Pathology, Hannover Medical School, Carl-Neuberg-Straße 1, 30625, Hannover, Germany. Christgen.Matthias@MH-Hannover.de.
Patrick W B DerksenDepartment of Pathology, Utrecht University Medical Center, Heidelberglaan 100, 3584, Utrecht, The Netherlands. pderksen@umcutrecht.nl.
Heidelberg University · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infiltrating lobular breast cancer (ILC) is the most common special breast cancer subtype. With mutational or epigenetic inactivation of the cell adhesion molecule E-cadherin (CDH1) being confined almost exclusively to ILC, this tumor entity stands out from all other types of breast cancers. The molecular basis of ILC is linked to loss of E-cadherin, as evidenced by human CDH1 germline mutations and conditional knockout mouse models. A better understanding of ILC beyond the level of descriptive studies depends on physiologically relevant and functional tools. This review provides a detailed overview on ILC models, including well-characterized cell lines, xenograft tumors and genetically engineered mouse models. We consider advantages and limitations of these models and evaluate their representativeness for human ILC. The still incompletely defined mechanisms by which loss of E-cadherin drives malignant transformation are discussed based on recent findings in these models. Moreover, candidate genes and signaling pathways potentially involved in ILC development and progression as well as anticancer drug and endocrine resistance are highlighted.

Indexed as

AnimalsBreast NeoplasmsCadherinsCarcinoma, LobularCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalDNA-Binding ProteinsDNA HelicasesFemaleGene Expression ProfilingGene Knockout TechniquesGerm-Line MutationHeterograftsHumansMiceCadherinsCHD1 protein, humanDNA-Binding ProteinsDNA Helicases

Identifiers

PMID25757734
PMCPMC4320436
OpenAlexW2152305619

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.