Evidence map›Paper›PMID 30760857›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2019

The molecular mechanisms underlying reduced E-cadherin expression in invasive ductal carcinoma of the breast: high throughput analysis of large cohorts.

Mansour Alsaleem, Michael S Toss, Chitra Joseph, Mohammed Aleskandarany, Sasagu Kurozumi, Ibrahim Alshankyty, Angela Ogden, Padmashree C G Rida, Ian O Ellis, Ritu Aneja and 3 more

Open access · bronzeAbstract read
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In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Pitfalls in the Histological Diagnosis of Morphologic Variants of Invasive Lobular Carcinoma of the Breast.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Engineering the Interactions of Classical Cadherin Cell-Cell Adhesion Proteins.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Review
  11. HighMedicina (Kaunas, Lithuania) · 2023
    Article
  12. Article
  13. Article
  14. Molecular mechanism for strengthening E-cadherin adhesion using a monoclonal antibody.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Article
  16. Article
  17. Article
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  19. Article
  20. Review
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

13 authors at 3 institutions in 4 countries.

Mansour AlsaleemNottingham Breast Cancer Research Centre, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, UK.
Michael S TossNottingham Breast Cancer Research Centre, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, UK.ORCID http://orcid.org/0000-0002-9077-3984
Chitra JosephNottingham Breast Cancer Research Centre, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, UK.ORCID http://orcid.org/0000-0003-2631-9266
Mohammed AleskandaranyNottingham Breast Cancer Research Centre, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, UK.
Sasagu KurozumiNottingham Breast Cancer Research Centre, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, UK.
Ibrahim AlshankytyFaculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia.
Angela OgdenDepartment of Biology, Georgia State University, Atlanta, GA, USA.
Padmashree C G RidaDepartment of Biology, Georgia State University, Atlanta, GA, USA.
Ian O EllisNottingham Breast Cancer Research Centre, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, UK.
Ritu AnejaDepartment of Biology, Georgia State University, Atlanta, GA, USA.
Andrew R GreenNottingham Breast Cancer Research Centre, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, UK.ORCID http://orcid.org/0000-0002-0488-5913
Nigel P MonganCancer Biology and Translational Research, Faculty of Medicine and Health Sciences, University of Nottingham, Nottingham, UK.ORCID http://orcid.org/0000-0001-5438-1126
Emad A RakhaNottingham Breast Cancer Research Centre, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, UK. Emad.Rakha@nottingham.ac.uk.
University of Nottingham · GBGeorgia State University · USKing Abdulaziz University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

E-cadherin is a tumor suppressor gene in invasive lobular breast cancer. However, a proportion of high-grade ductal carcinoma shows reduced/loss of E-cadherin. In this study, we assessed the underlying mechanisms and molecular implications of E-cadherin loss in invasive ductal carcinoma. This study used large, well-characterized cohorts of early-stage breast cancer-evaluated E-cadherin expression via various platforms including immunohistochemistry, microarray analysis using Illumina HT-12 v3, copy number analysis using Affymetrix SNP 6.0 arrays, and next-generation sequencing for differential gene expression. Our results showed 27% of high-grade invasive ductal carcinoma showed reduced/loss of E-cadherin membranous expression. CDH1 copy number loss was in 21% of invasive ductal carcinoma, which also showed low CDH1 mRNA expression (p = 0.003). CDH1 copy number was associated with copy number loss of TP53, ATM, BRCA1, and BRCA2 (p < 0.001). Seventy-nine percent of invasive ductal carcinoma with reduced CDH1 mRNA expression showed elevated expression of E-cadherin transcription suppressors TWIST2, ZEB2, NFKB1, LLGL2, CTNNB1 (p < 0.01). Reduced/loss E-cadherin expression was associated with differential expression of 2143 genes including those regulating Wnt (FZD2, GNG5, HLTF, WNT2, and CER1) and PIK3-AKT (FGFR2, GNF5, GNGT1, IFNA17, and IGF1) signaling pathways. Interestingly, key genes differentially expressed between invasive lobular carcinoma and invasive ductal tumors did not show association with E-cadherin loss in invasive ductal carcinoma. We conclude that E-cadherin loss in invasive ductal carcinoma is likely a consequence of genomic instability occurring during carcinogenesis. Potential novel regulators controlling E-cadherin expression in invasive ductal carcinoma warrant further investigation.

Indexed as

AdolescentAdultAgedAged, 80 and overBreast NeoplasmsCadherinsCarcinoma, Ductal, BreastFemaleGenomic InstabilityHigh-Throughput Nucleotide SequencingHumansImmunohistochemistryMiddle AgedTissue Array AnalysisYoung AdultCadherins

Identifiers

PMID30760857
OpenAlexW2913977697

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.