Evidence map›Paper›PMID 31548239›Full record

ArticleMolecular cancer research : MCR2019

Phosphoinositide 3-Kinase Signaling Can Modulate MHC Class I and II Expression.

Sanjay Chandrasekaran, Maiko Sasaki, Christopher D Scharer, Haydn T Kissick, Dillon G Patterson, Kelly R Magliocca, John T Seykora, Bishu Sapkota, David A Gutman, Lee A Cooper and 8 more

Abstract read
In one paragraph

Article in Molecular cancer research : MCR, 2019. 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
–field-weighted citation impact
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.

  1. Article
  2. Review
  3. OncogenicJournal for immunotherapy of cancer · 2026
    Article
  4. Article
  5. CD20Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. EGFR: New Insights on Its Activation and Mutation in Tumor and Tumor Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

18 authors.

Sanjay ChandrasekaranDepartment of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia.ORCID 0000-0002-6289-5327
Maiko SasakiAtlanta Veterans Affairs Medical Center, Atlanta, Georgia.
Christopher D ScharerDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia.
Haydn T KissickDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia.
Dillon G PattersonDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia.ORCID 0000-0001-6053-5216
Kelly R MaglioccaWinship Cancer Institute of Emory University School of Medicine, Atlanta, Georgia.
John T SeykoraDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Bishu SapkotaAtlanta Veterans Affairs Medical Center, Atlanta, Georgia.
David A GutmanDepartment of Neurology, Emory University School of Medicine, Atlanta, Georgia.
Lee A CooperDepartment of Biomedical Informatics, Emory University School of Medicine, Atlanta, Georgia.ORCID 0000-0002-3504-4965
Gregory B LesinskiDepartment of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia.
Edmund K WallerDepartment of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia.
Susan N ThomasWinship Cancer Institute of Emory University School of Medicine, Atlanta, Georgia.
Sergei V KotenkoDepartment of Biochemistry and Molecular Biology, Rutgers New Jersey Medical School, Newark, New Jersey.
Jeremy M BossDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia.
Carlos S MorenoWinship Cancer Institute of Emory University School of Medicine, Atlanta, Georgia.ORCID 0000-0002-5582-0028
Robert A SwerlickAtlanta Veterans Affairs Medical Center, Atlanta, Georgia.ORCID 0000-0002-9802-4144
Brian P PollackAtlanta Veterans Affairs Medical Center, Atlanta, Georgia. bppolla@emory.edu.

Funding

Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Suresh S Ramalingam · 2009 to 2026
$47.5M
Atlanta Clinical and Translational Science Institute (ACTSI) RenewalUL1TR000454 · NCATS · EMORY UNIVERSITY · PI STEPHENS, DAVID S · 2012 to 2016
$25.8M
Tissue and Animal UseU54CA119338 · NCI · EMORY UNIVERSITY · PI BAO, GANG · 2005 to 2009
$18.4M
TARGETING DEATH RECEPTOR-MEDIATED APOPTOSIS FOR HEAD AND NECK CANCERP50CA128613 · NCI · EMORY UNIVERSITY · PI SHIN, DONG M · 2007 to 2011
$12.0M
Melanoma immunotherapy targeting sentinel lymph nodesR01CA207619 · NCI · GEORGIA INSTITUTE OF TECHNOLOGY · PI THOMAS, SUSAN NAPIER · 2016 to 2020
$2.0M
Translational Physician-Scientist Training Program in OncologyT32CA160040 · NCI · EMORY UNIVERSITY · PI SHIN, DONG M · 2013 to 2017
$1.2M
BLRD VA I01 BX001922NCATS NIH HHS UL1 TR000454NCI NIH HHS P30 CA138292NCI NIH HHS P50 CA128613NCI NIH HHS R01 CA207619NCI NIH HHS T32 CA160040NCI NIH HHS U54 CA119338
6 · The paper itself

Abstract

Molecular events activating the PI3K pathway are frequently detected in human tumors and the activation of PI3K signaling alters numerous cellular processes including tumor cell proliferation, survival, and motility. More recent studies have highlighted the impact of PI3K signaling on the cellular response to interferons and other immunologic processes relevant to antitumor immunity. Given the ability of IFNγ to regulate antigen processing and presentation and the pivotal role of MHC class I (MHCI) and II (MHCII) expression in T-cell-mediated antitumor immunity, we sought to determine the impact of PI3K signaling on MHCI and MHCII induction by IFNγ. We found that the induction of cell surface MHCI and MHCII molecules by IFNγ is enhanced by the clinical grade PI3K inhibitors dactolisib and pictilisib. We also found that PI3K inhibition increases STAT1 protein levels following IFNγ treatment and increases accessibility at genomic STAT1-binding motifs. Conversely, we found that pharmacologic activation of PI3K signaling can repress the induction of MHCI and MHCII molecules by IFNγ, and likewise, the loss of PTEN attenuates the induction of MHCI, MHCII, and STAT1 by IFNγ. Consistent with these

Indexed as

Antigen PresentationBinding SitesCell ProliferationDNA-Binding ProteinsGene Expression Regulation, NeoplasticGenes, MHC Class IGenes, MHC Class IIGenomicsHumansInterferon-gammaPhosphatidylinositol 3-KinaseProtein BindingProtein Kinase InhibitorsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionDNA-Binding ProteinsIFNG protein, humanInterferon-gammaPhosphatidylinositol 3-KinaseProtein Kinase InhibitorsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID31548239
PMCPMC7339488

What OpenQuestion holds

Textmetadata
LicenceTDM
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.