Evidence map›Paper›PMID 42409767›Full record

ArticleCell death & disease2026

mTORC1 suppression by Trp53 mutation drives resistance to immune checkpoint blockade.

Alireza Labani-Motlagh, Yang Li, David Shihong Gao, Eunseuk Lee, Vincent Chen, Lixian Yi, Fei Gao, Runzi Sun, Junchi Xu, Jason Shoush and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2026. 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
–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

1 citing paper in PubMed.

  1. Article
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

14 authors.

Alireza Labani-Motlagh *Center for Discovery and Innovation, Hackensack Meridian Health, Nutley, NJ, USA.
Yang Li *Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
David Shihong Gao *Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Eunseuk LeeCenter for Discovery and Innovation, Hackensack Meridian Health, Nutley, NJ, USA.ORCID http://orcid.org/0009-0004-3761-576X
Vincent ChenDepartment of Medical Sciences, Hackensack Meridian School of Medicine, Nutley, NJ, USA.
Lixian YiDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Fei GaoDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Runzi SunDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Junchi XuDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Jason ShoushDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Zoi KykrouDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Minxin LiangDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Xinghua LuBiomedical Informatics Training Program, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Binfeng LuCenter for Discovery and Innovation, Hackensack Meridian Health, Nutley, NJ, USA. binfeng.lu@hmh-cdi.org.ORCID http://orcid.org/0000-0002-7822-5950

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53 is a critical tumor suppressor gene that inhibits cancer development by regulating cell cycle arrest, apoptosis, DNA repair, and metabolism. However, recent studies examining TP53 mutations in cancer immunotherapy have yielded inconsistent results, likely due to differences in tumor mutational burden (TMB) and the context-dependent roles of specific p53 mutants. In this study, we assessed the function of G242V and S258I Trp53 mutations in MC38 cells in the context of immunotherapy by generating Trp53 deletion and observed significantly enhanced responses to anti-PD-1 therapy. Trp53-null tumors showed increased CD8

Indexed as

Drug Resistance, NeoplasmImmune Checkpoint InhibitorsMechanistic Target of Rapamycin Complex 1MutationTumor Suppressor Protein p53AnimalsApoptosisAutophagyCell Line, TumorHumansMiceSignal TransductionImmune Checkpoint InhibitorsMechanistic Target of Rapamycin Complex 1Tumor Suppressor Protein p53

Identifiers

PMID42409767
PMCPMC13620114

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.