Evidence map›Paper›PMID 30034942›Full record

ArticleAmerican journal of cancer research2018

Blocking LLT1 (CLEC2D, OCIL)-NKRP1A (CD161) interaction enhances natural killer cell-mediated lysis of triple-negative breast cancer cells.

Armando M Marrufo, Stephen O Mathew, Pankaj Chaudhary, Joseph D Malaer, Jamboor K Vishwanatha, Porunelloor A Mathew

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

40 citing papers in PubMed, 50 citations in OpenAlex.

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  19. SARS-CoV-2 infection impairs NK cell functionsFrontiers in immunology · 2023
    Article
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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

6 authors at 1 institution in 1 country.

Armando M MarrufoDepartment of Microbiology, Immunology and Genetics, University of North Texas Health Science Center Fort Worth 76107, TX, USA.
Stephen O MathewDepartment of Microbiology, Immunology and Genetics, University of North Texas Health Science Center Fort Worth 76107, TX, USA.
Pankaj ChaudharyDepartment of Microbiology, Immunology and Genetics, University of North Texas Health Science Center Fort Worth 76107, TX, USA.
Joseph D MalaerDepartment of Microbiology, Immunology and Genetics, University of North Texas Health Science Center Fort Worth 76107, TX, USA.
Jamboor K VishwanathaDepartment of Microbiology, Immunology and Genetics, University of North Texas Health Science Center Fort Worth 76107, TX, USA.
Porunelloor A MathewDepartment of Microbiology, Immunology and Genetics, University of North Texas Health Science Center Fort Worth 76107, TX, USA.
University of North Texas · US

Funding

Molecular Characterization of NKp44 Ligand on AstrocytesR03NS101481 · NINDS · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI MATHEW, PORUNELLOOR ABRAHAM · 2017 to 2018
$146k
NINDS NIH HHS R03 NS101481
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is the most invasive form of breast cancer due to an absence of estrogen (ER), progesterone (PR), and human epidermal growth factor-2 (HER2) receptors on the cell surface. TNBC accounts for approximately 12 to 20 percent of all breast cancer cases. The absence of ER, PR, and HER2 receptors on TNBCs and its ability to develop drug resistance renders it difficult to eradicate or retrogress tumor growth with hormonal therapy and chemotherapy. Triple-negative breast cancer is associated with poorer prognosis, increased chance of relapse, and lower chance of survival. Patients with TNBC have poorer outcome to conventional treatments than patients with other types of breast cancer. Natural killer cell-mediated immunotherapy is a promising therapeutic option for patients with TNBC. Natural killer cells contribute to the immune system by recognizing tumor cells through interactions between ligands on tumor cells and natural killer cell receptors. NK cell function is regulated by a net balance of signals from activating and inhibitory receptors interacting with ligands on target cells. Lectin-like Transcript-1 (LLT1, CLEC2D, OCIL) is a ligand that interacts with NK cell receptor NKRP1A (CD161) and inhibits NK cell activation. In this study, we have identified expression of LLT1 on TNBC cell lines MDA-MB-231 and MDA-MB-436 through flow cytometry, western blot, and confocal microscopy. We have demonstrated that blocking LLT1 on TNBCs with antibodies disrupts interaction with NKRP1A and enhances lysis of TNBCs by primary natural killer cells. We have also shown that a gene knockdown of

Indexed as

breast cancerlectin-like transcript-1LLT1LLT1-NKRP1A interactionnatural killer cellsNKRP1A (CD161)TNBCtriple-negative breast cancer

Identifiers

PMID30034942
PMCPMC6048397
OpenAlexW2981198889

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.