Evidence map›Paper›PMID 30061899›Full record

ReviewFrontiers in immunology2018

Notch Signaling as a Regulator of the Tumor Immune Response: To Target or Not To Target?

Mahnaz Janghorban, Li Xin, Jeffrey M Rosen, Xiang H-F Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
4.9field-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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Review
  9. Cancer stem cells and their role in metastasis.Central European journal of urology · 2025
    Review
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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

4 authors at 2 institutions in 1 country.

Mahnaz JanghorbanDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, United States.
Li XinDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, United States.
Jeffrey M RosenDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, United States.
Xiang H-F ZhangDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, United States.
Baylor College of Medicine · USChildren's Cancer Center · US

Funding

MALAT1 lncRNA as a Therapeutic Target in Triple Negative Breast CancerR01CA016303 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ROSEN, JEFFREY MARK · 1985 to 2022
$8.1M
Osteoclast-Independent Mechanisms of Early-Stage Bone Colonization of Breast CancerR01CA183878 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ZHANG, XIANG · 2014 to 2024
$3.5M
NCI NIH HHS R01 CA016303NCI NIH HHS R01 CA183878
6 · The paper itself

Abstract

The Notch signaling pathway regulates important cellular processes involved in stem cell maintenance, proliferation, development, survival, and inflammation. These responses to Notch signaling involving both canonical and non-canonical pathways can be spatially and temporally variable and are highly cell-type dependent. Notch signaling can elicit opposite effects in regulating tumorigenicity (tumor-promoting versus tumor-suppressing function) as well as controlling immune cell responses. In various cancer types, Notch signaling elicits a "cancer stem cell (CSC)" phenotype that results in decreased proliferation, but resistance to various therapies, hence potentially contributing to cell dormancy and relapse. CSCs can reshape their niche by releasing paracrine factors and inflammatory cytokines, and the niche in return can support their quiescence and resistance to therapies as well as the immune response. Moreover, Notch signaling is one of the key regulators of hematopoiesis, immune cell differentiation, and inflammation and is implicated in various autoimmune diseases, carcinogenesis (leukemia), and tumor-induced immunosuppression. Notch can control the fate of various T cell types, including Th1, Th2, and the regulatory T cells (Tregs), and myeloid cells including macrophages, dendritic cells, and myeloid-derived suppressor cells (MDSCs). Both MDSCs and Tregs play an important role in supporting tumor cells (and CSCs) and in evading the immune response. In this review, we will discuss how Notch signaling regulates multiple aspects of the tumor-promoting environment by elucidating its role in CSCs, hematopoiesis, normal immune cell differentiation, and subsequently in tumor-supporting immunogenicity.

Indexed as

cancer stem cellimmune responseimmune-suppressive microenvironmentNotchNotch therapy

Identifiers

PMID30061899
PMCPMC6055003
OpenAlexW2883609728

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.