Evidence map›Paper›PMID 35074498›Full record

ArticleCancer letters2022

PKC agonism restricts innate immune suppression, promotes antigen cross-presentation and synergizes with agonistic CD40 antibody therapy to activate CD8

Mehdi Chaib, Laura M Sipe, Johnathan R Yarbro, Margaret S Bohm, Brittany R Counts, Ubaid Tanveer, Ajeeth K Pingili, Deidre Daria, Tony N Marion, James A Carson and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer letters, 2022. 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
1.7field-weighted citation impact, top 16% 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, 20 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Mehdi ChaibDepartment of Pharmaceutical Sciences, College of Pharmacy, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Laura M SipeDepartment of Medicine, Division of Hematology and Oncology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Johnathan R YarbroDepartment of Medicine, Division of Hematology and Oncology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Margaret S BohmDepartment of Microbiology, Immunology, and Biochemistry, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Brittany R CountsDivision of Regenerative and Rehabilitation Sciences, College of Health Professions, UTHSC Memphis, USA.
Ubaid TanveerDepartment of Medicine, Division of Hematology and Oncology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Ajeeth K PingiliDepartment of Medicine, Division of Hematology and Oncology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Deidre DariaOffice of Vice Chancellor for Research, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Tony N MarionDepartment of Microbiology, Immunology, and Biochemistry, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA; Office of Vice Chancellor for Research, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
James A CarsonDivision of Regenerative and Rehabilitation Sciences, College of Health Professions, UTHSC Memphis, USA; UTHSC Center for Cancer Research, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Paul G ThomasDepartment of Microbiology, Immunology, and Biochemistry, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA; UTHSC Center for Cancer Research, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Liza MakowskiDepartment of Pharmaceutical Sciences, College of Pharmacy, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA; Department of Medicine, Division of Hematology and Oncology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA; Department of Microbiology, Immunology, and Biochemistry, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA; UTHSC Center for Cancer Research, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA. Electronic address: liza.makowski@uthsc.edu.
University of Tennessee Health Science Center · USSt. Jude Children's Research Hospital · US

Funding

Role of microbial-modulated bile acid receptor signaling in breast cancerR01CA253329 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI Katherine Loree Cook, Liza Makowski-Hayes · 2020 to 2026
$3.0M
Transdisciplinary Research in Energetics and Cancer (TREC) Training GrantR25CA203650 · NCI · YALE UNIVERSITY · PI IRWIN, MELINDA L · 2016 to 2025
$2.9M
Obesity-driven Metabolic and Molecular Biomarkers of Metformin Response in Endometrial CancerR37CA226969 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BAE-JUMP, VICTORIA LIN · 2018 to 2024
$2.5M
Determining susceptibility loci in triple negative breast cancer using a novel pre-clinical modelR01CA262112 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI Liza Makowski-Hayes · 2022 to 2026
$2.0M
The role of bile acids to ameliorate obesity driven triple negative breast cancerF32CA250192 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SIPE, LAURA MARIE · 2021 to 2022
$80k
PKC agonism restricts innate immune suppression and promotes antigen cross-presentation in Triple Negative Breast CancerF31CA268871 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CHAIB, MEHDI · 2022 to 2022
$33k
NCI NIH HHS F31 CA268871NCI NIH HHS F32 CA250192NCI NIH HHS R01 CA253329NCI NIH HHS R01 CA262112NCI NIH HHS R25 CA203650NCI NIH HHS R37 CA226969
6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) are an immature innate cell population that expands in pathological conditions such as cancer and suppresses T cells via production of immunosuppressive factors. Conversely, efficient cytotoxic T cell priming is dependent on the ability of antigen-presenting cells (APCs) to cross-present tumor antigens to CD8

Indexed as

Breast NeoplasmsCross-PrimingAnimalsCD40 AntigensCD8-Positive T-LymphocytesDendritic CellsFemaleHumansImmunity, InnateMiceTumor MicroenvironmentCD40 AntigensCD40Cross-presentationDCMDSCPKC

Identifiers

PMID35074498
PMCPMC9867936
OpenAlexW4205639547

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.