Evidence map›Paper›PMID 27226587›Full record

ArticleThe Journal of biological chemistry2016

Reprogramming Nurse-like Cells with Interferon γ to Interrupt Chronic Lymphocytic Leukemia Cell Survival.

Shalini Gautam, Kavin Fatehchand, Saranya Elavazhagan, Brenda F Reader, Li Ren, Xiaokui Mo, John C Byrd, Susheela Tridandapani, Jonathan P Butchar

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

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  15. [Tumor-associated macrophages and hematologic malignancies].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2018
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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

9 authors at 1 institution in 2 countries.

Shalini GautamDepartment of Internal Medicine, Ohio State University, Columbus, Ohio 43210.
Kavin FatehchandDepartment of Internal Medicine, Ohio State University, Columbus, Ohio 43210.
Saranya ElavazhaganDepartment of Internal Medicine, Ohio State University, Columbus, Ohio 43210.
Brenda F ReaderDepartment of Internal Medicine, Ohio State University, Columbus, Ohio 43210.
Li RenDepartment of Internal Medicine, Ohio State University, Columbus, Ohio 43210; Key Laboratory for Molecular Enzymology and Engineering, Ministry of Education, Jilin University, Jilin 130000, China.
Xiaokui MoCenter for Biostatistics, Ohio State University, Columbus, Ohio 43210.
John C ByrdDepartment of Internal Medicine, Ohio State University, Columbus, Ohio 43210.
Susheela TridandapaniDepartment of Internal Medicine, Ohio State University, Columbus, Ohio 43210. Electronic address: tridandapani.2@osu.edu.
Jonathan P ButcharDepartment of Internal Medicine, Ohio State University, Columbus, Ohio 43210. Electronic address: butchar.2@osu.edu.
The Ohio State University · US

Funding

TWO SIGNAL REQUIREMENT FOR NATURAL KILLER IMMUNITYP01CA095426 · NCI · OHIO STATE UNIVERSITY · PI MUTHUSAMY, NATARAJAN · 2002 to 2016
$29.6M
Targeted Therapy for LeukemiaR35CA197734 · NCI · UNIVERSITY OF CINCINNATI · PI BYRD, JOHN C. · 2015 to 2021
$6.6M
MOLECULAR MECHANISMS OF LUNG INFLAMMATIONT32HL007946 · NHLBI · OHIO STATE UNIVERSITY · PI WEWERS, MARK DAMIAN · 2000 to 2017
$3.1M
Novel monocyte effector function in CLL immune therapyR01CA162411 · NCI · OHIO STATE UNIVERSITY · PI BYRD, JOHN C., TRIDANDAPANI, SUSHEELA · 2013 to 2017
$1.6M
NCI NIH HHS P01 CA095426NCI NIH HHS R01 CA162411NCI NIH HHS R35 CA197734NHLBI NIH HHS T32 HL007946
6 · The paper itself

Abstract

Nurse-like cells (NLCs) play a central role in chronic lymphocytic leukemia (CLL) because they promote the survival and proliferation of CLL cells. NLCs are derived from the monocyte lineage and are driven toward their phenotype via contact-dependent and -independent signals from CLL cells. Because of the central role of NLCs in promoting disease, new strategies to eliminate or reprogram them are needed. Successful reprogramming may be of extra benefit because NLCs express Fcγ receptors (FcγRs) and thus could act as effector cells within the context of antibody therapy. IFNγ is known to promote the polarization of macrophages toward an M1-like state that is no longer tumor-supportive. In an effort to reprogram the phenotype of NLCs, we found that IFNγ up-regulated the M1-related markers CD86 and HLA-DR as well as FcγRIa. This corresponded to enhanced FcγR-mediated cytokine production as well as rituximab-mediated phagocytosis of CLL cells. In addition, IFNγ down-regulated the expression of CD31, resulting in withdrawal of the survival advantage on CLL cells. These results suggest that IFNγ can re-educate NLCs and shift them toward an effector-like state and that therapies promoting local IFNγ production may be effective adjuvants for antibody therapy in CLL.

Indexed as

Cell SurvivalB7-2 AntigenCells, CulturedHLA-DR AntigensHumansInterferon-gammaLeukemia, Lymphocytic, Chronic, B-CellPhagocytosisReceptors, IgGB7-2 AntigenFCGR1A protein, humanHLA-DR AntigensInterferon-gammaReceptors, IgGcell-cell interactionFc receptorinterferonsignal transductiontumor immunology

Identifiers

PMID27226587
PMCPMC4933188
OpenAlexW2387035878

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.