Cancer-Specific Loss of p53 Leads to a Modulation of Myeloid and T Cell Responses.
Kras
T cell response
myeloid cells
p53
tumor
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
14 01 2020
14 01 2020
Historique:
received:
21
02
2019
revised:
19
07
2019
accepted:
06
12
2019
entrez:
16
1
2020
pubmed:
16
1
2020
medline:
13
2
2021
Statut:
ppublish
Résumé
Loss of p53 function contributes to the development of many cancers. While cell-autonomous consequences of p53 mutation have been studied extensively, the role of p53 in regulating the anti-tumor immune response is still poorly understood. Here, we show that loss of p53 in cancer cells modulates the tumor-immune landscape to circumvent immune destruction. Deletion of p53 promotes the recruitment and instruction of suppressive myeloid CD11b
Identifiants
pubmed: 31940491
pii: S2211-1247(19)31678-X
doi: 10.1016/j.celrep.2019.12.028
pmc: PMC6963783
pii:
doi:
Substances chimiques
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
481-496.e6Subventions
Organisme : Wellcome Trust
ID : FC001202
Pays : United Kingdom
Organisme : Cancer Research UK
ID : FC001169
Pays : United Kingdom
Organisme : Cancer Research UK
ID : C596/A10419
Pays : United Kingdom
Organisme : Cancer Research UK
ID : FC001557
Pays : United Kingdom
Organisme : Cancer Research UK
ID : C596/A17196
Pays : United Kingdom
Organisme : Cancer Research UK
ID : C596/A26855
Pays : United Kingdom
Organisme : Wellcome Trust
ID : FC001557
Pays : United Kingdom
Organisme : Cancer Research UK
ID : FC001202
Pays : United Kingdom
Organisme : Medical Research Council
ID : FC001557
Pays : United Kingdom
Organisme : Cancer Research UK
ID : FC001202
Pays : United Kingdom
Organisme : Wellcome Trust
ID : FC001169
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.
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