Evidence map›Paper›PMID 36765663›Full record

ArticleCancers2023

Deletion of Glycogen Synthase Kinase 3 Beta Reprograms NK Cell Metabolism.

Marcelo S F Pereira, Kinnari Sorathia, Yasemin Sezgin, Aarohi Thakkar, Colin Maguire, Patrick L Collins, Bethany L Mundy-Bosse, Dean A Lee, Meisam Naeimi Kararoudi

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

9 authors at 2 institutions in 1 country.

Marcelo S F PereiraCenter for Childhood Cancer and Blood Disease, Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH 43205, USA.ORCID 0000-0001-7069-5328
Kinnari SorathiaCenter for Childhood Cancer and Blood Disease, Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH 43205, USA.
Yasemin SezginCenter for Childhood Cancer and Blood Disease, Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH 43205, USA.
Aarohi ThakkarCenter for Childhood Cancer and Blood Disease, Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH 43205, USA.ORCID 0000-0001-6515-8747
Colin MaguireCenter for Childhood Cancer and Blood Disease, Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH 43205, USA.
Patrick L CollinsDepartment of Microbial Infection and Immunity, The Ohio State University, Columbus, OH 43210, USA.ORCID 0000-0003-4550-4272
Bethany L Mundy-BosseDepartment of Internal Medicine, Division of Hematology, The Ohio State University, Columbus, OH 43210, USA.
Dean A LeeCenter for Childhood Cancer and Blood Disease, Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH 43205, USA.ORCID 0000-0001-6693-5392
Meisam Naeimi KararoudiCenter for Childhood Cancer and Blood Disease, Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH 43205, USA.
Nationwide Children's Hospital · USThe Ohio State University · US

Funding

Project 4:Targeting M2-like Macrophages and MDSC with Myelolytic-VirotherapyU54CA232561 · NCI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI CAIRO, MITCHELL S., CRIPE, TIMOTHY P · 2019 to 2023
$12.1M
Dysregulation of Innate Lymphoid Immunity in Acute Myeloid LeukemiaR01CA255860 · NCI · OHIO STATE UNIVERSITY · PI MUNDY-BOSSE, BETHANY, OAKES, CHRISTOPHER C. · 2021 to 2025
$2.5M
Gene regulatory architecture of CD56 bright natural killer cellsR21AI156411 · NIAID · OHIO STATE UNIVERSITY · PI COLLINS, PATRICK LEONARD · 2021 to 2022
$433k
NCI NIH HHS R01 CA255860NCI NIH HHS U54 CA232561NIAID NIH HHS R21 AI156411NIH HHS U54-CA232561
6 · The paper itself

Abstract

Loss of cytotoxicity and defective metabolism are linked to glycogen synthase kinase 3 beta (GSK3β) overexpression in natural killer (NK) cells from patients with acute myeloid leukemia or from healthy donors after expansion ex vivo with IL-15. Drug inhibition of GSK3β in these NK cells improves their maturation and cytotoxic activity, but the mechanisms of GSK3β-mediated dysfunction have not been well studied. Here, we show that expansion of NK cells with feeder cells expressing membrane-bound IL-21 maintained normal GSK3β levels, allowing us to study GSK3β function using CRISPR gene editing. We deleted

Indexed as

AMLCas9/RNPCRISPRGSK3βmetabolismnatural killer cellsNK cellsOXPHOS

Identifiers

PMID36765663
PMCPMC9913837
OpenAlexW4318042578

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.