Programmed cell death 1 and programmed cell death ligand 1 expression in invasive breast carcinoma using CAL10 and NAT105 immunostaining.
Breast
CAL10
NAT105
cancer
human
immunohistochemistry
immunotherapy
programmed cell death 1
programmed cell death ligand 1
programmed cell death ligand 2
tissue microarray
Journal
Biotechnic & histochemistry : official publication of the Biological Stain Commission
ISSN: 1473-7760
Titre abrégé: Biotech Histochem
Pays: England
ID NLM: 9107378
Informations de publication
Date de publication:
Feb 2023
Feb 2023
Historique:
pubmed:
26
10
2022
medline:
8
2
2023
entrez:
25
10
2022
Statut:
ppublish
Résumé
Increased incidence of breast cancer has stimulated development of new diagnostic and therapeutic methods. The programmed cell death 1 (PD1) pathway and its inhibitors are promising avenues for investigation. PD1 includes PD ligands 1 (PDL1) and 2 (PDL2). We investigated the expression of PD1 and PDL1 in invasive breast carcinomas using immunohistochemical staining. We used 171 invasive breast carcinoma specimens from which tissue microarray blocks were created. Immunohistochemical staining of PD1 using NAT105, and PDL1 using CAL10 was performed on tissue microarray sections. NAT105 and CAL10 are useful clones for detecting expression of PD1 and PDL1. PD1 and PDL1 immunostaining was significantly stronger in carcinomas with basal-like phenotype compared to other molecular breast cancer types. PD1 and PDL1 expression also was associated with a high histologic grade and a high Ki-67 index. PD1 expression also was associated with lymphovascular invasion and axillary metastasis. PD1 and PDL1 expression is associated with aggressive tumor behavior and a basal-like phenotype in breast cancer. We suggest that inhibition of the PD1/PDL1 pathway, particularly in triple negative breast carcinomas with basal-like phenotype, might be useful for targeted immunotherapy.
Identifiants
pubmed: 36281760
doi: 10.1080/10520295.2022.2137586
doi:
Substances chimiques
Ligands
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM