Targeting an alternate Wilms' tumor antigen 1 peptide bypasses immunoproteasome dependency.
Journal
Science translational medicine
ISSN: 1946-6242
Titre abrégé: Sci Transl Med
Pays: United States
ID NLM: 101505086
Informations de publication
Date de publication:
09 02 2022
09 02 2022
Historique:
entrez:
9
2
2022
pubmed:
10
2
2022
medline:
12
4
2022
Statut:
ppublish
Résumé
Designing effective antileukemic immunotherapy will require understanding mechanisms underlying tumor control or resistance. Here, we report a mechanism of escape from immunologic targeting in an acute myeloid leukemia (AML) patient, who relapsed 1 year after immunotherapy with engineered T cells expressing a human leukocyte antigen A*02 (HLA-A2)-restricted T cell receptor (TCR) specific for a Wilms' tumor antigen 1 epitope, WT1
Identifiants
pubmed: 35138909
doi: 10.1126/scitranslmed.abg8070
pmc: PMC8985599
mid: NIHMS1784706
doi:
Substances chimiques
Antigens, Neoplasm
0
Epitopes
0
HLA-A2 Antigen
0
Peptides
0
Receptors, Antigen, T-Cell
0
WT1 Proteins
0
Proteasome Endopeptidase Complex
EC 3.4.25.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
eabg8070Subventions
Organisme : NCI NIH HHS
ID : K08 CA169485
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA018029
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA080416
Pays : United States
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