PD-L1 Expression is Associated With Poor Prognosis in Renal Cell CarcinomaShow others and affiliations
2020 (English)In: Applied immunohistochemistry & molecular morphology (Print), ISSN 1541-2016, E-ISSN 1533-4058, Vol. 28, no 3, p. 213-220Article in journal (Refereed) Published
Abstract [en]
Programmed death ligand 1 (PD-L1) is a protein which, when interacting with its receptor programmed death 1, acts as a negative regulator of the antitumor T-cell-mediated immune response. The prognostic value of PD-L1 expression in renal cell carcinoma (RCC) has been controversial. In this study, the prognostic value of PD-L1 expression in RCC was evaluated by analyzing PD-L1 immunoreactivity in tumor cells and tumor-infiltrating immune cells (TIICs) in 346 RCC patients with long-term follow-up. PD-L1 positivity in tumor cells was associated with higher World Health Organization nucleolar grade (P<0.001), recurrence (P=0.011), and death due to RCC (P=0.031). PD-L1 positivity in TIICs was associated with higher nucleolar grade (P<0.001), higher T-stage (P=0.031), higher N-stage (P=0.01), recurrence (P=0.007), and death due to RCC (P=0.001). A significant positive association of time to cancer-specific death with both PD-L1-positive tumor cells and TIICs were also found. The data indicate that RCC patients with PD-L1-positive tumor cells and TIICs are at significant risk for cancer progression and the expression may be used as a complementary prognostic factor in the management of RCC patients.
Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2020. Vol. 28, no 3, p. 213-220
Keywords [en]
programmed death ligand 1, antitumor immunity, RCC, TIICs, prognostic marker
National Category
Urology and Nephrology Cancer and Oncology
Identifiers
URN: urn:nbn:se:oru:diva-74192DOI: 10.1097/PAI.0000000000000766ISI: 000525011200009PubMedID: 31058656OAI: oai:DiVA.org:oru-74192DiVA, id: diva2:1315265
Note
Funding Agencies:
Örebro County Council Research Committee
Lions Cancer Foundation, Sweden
2019-05-132019-05-132020-12-01Bibliographically approved