Evidence map›Paper›PMID 29110374›Full record

ReviewCancer science2018

Towards understanding the mechanisms of actions of carcinoembryonic antigen-related cell adhesion molecule 6 in cancer progression.

Balsam Rizeq, Zain Zakaria, Allal Ouhtit

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 121 citations in OpenAlex.

  1. Article
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  5. Exploring the interactions of integrins and CEACAM6 (Review).Experimental and therapeutic medicine · 2025
    Review
  6. A unified framework for identification of cell-type-specific spatially variable genes in spatial transcriptomic studies.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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11 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Balsam RizeqDepartment of Biological and Environmental Sciences, College of Arts and Science, Qatar University, Doha, Qatar.ORCID http://orcid.org/0000-0001-5859-3804
Zain ZakariaDepartment of Biological and Environmental Sciences, College of Arts and Science, Qatar University, Doha, Qatar.
Allal OuhtitDepartment of Biological and Environmental Sciences, College of Arts and Science, Qatar University, Doha, Qatar.ORCID http://orcid.org/0000-0002-2455-5014
Qatar University · QA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human carcinoembryonic antigen (CEA) is the prototypic member of a family of highly related cell surface glycoproteins that includes carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) and others. CEACAM6 (formerly NCA), which belongs to the immunoglobulin superfamily, is a cell adhesion protein of the CEA family. It is normally expressed on the epithelial surfaces and on the surface of myeloid cells (CD66c). CEACAM6 is a multi-functional glycoprotein that mediates homotypic binding with other CEA family members and heterotypic binding with integrin receptors. It functions by organizing tissue architecture and regulating different signal transduction, while aberrant expression leads to the development of human malignancies. It was first discovered in proliferating cells of adenomas and hyperplastic polyps in comparison to benign colonic tissue when overexpressed on the surface of various cell types in model systems. CEACAM6 functions as a pan-inhibitor of cell differentiation and cell polarization, and it also causes distortion of tissue architecture. Moreover, overexpression of CEACAM6 modulates cancer progression through aberrant cell differentiation, anti-apoptosis, cell growth and resistance to therapeutic agents. In addition, CEACAM6 overexpression in multiple malignancies promotes cell invasion and metastasis, thereby representing an acquired advantage of tumor cells directly responsible for an invasive phenotype. This review focuses on the findings supporting the mechanisms of actions linking the oncogenic potential of CEACAM6 to the onset of cancer progression and pathogenesis, especially in breast cancer, and to validating CEACAM6 as a target to pave the way towards the design of efficient therapeutic strategies against breast cancer.

Indexed as

Up-RegulationAntigens, CDCell Adhesion MoleculesCell DifferentiationCell PolarityDisease ProgressionGene Expression Regulation, NeoplasticGPI-Linked ProteinsHumansNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsSignal TransductionAntigens, CDCEACAM6 protein, humanCell Adhesion MoleculesGPI-Linked ProteinsadhesioncancerCEACAM6invasion and metastasisreview

Identifiers

PMID29110374
PMCPMC5765285
OpenAlexW2767830882

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.