Inverse association between programmed death ligand 1 and genes in the VEGF pathway in primary clear cell renal cell carcinoma.

Abstract:

:Increased angiogenesis and tumor-induced immune evasion are two mechanisms by which clear cell renal cell carcinoma (ccRCC) proliferate and metastasize; however, the relationship between these pathways in human ccRCC is poorly understood. We conducted a nested case-control study using 98 archived tumor samples from patients diagnosed with primary ccRCC between 1990 and 2006, half of which were identified by immunohistochemistry (IHC) as either programmed death ligand 1 (PDL-1)-positive or PDL-1-negative. RNAs were extracted from the formalin-fixed paraffin-embedded tumor slides and the expression of the VEGFA, VEGFR1, VEGFR2, and PDL-1 genes was quantified. We assessed the presence of tumor-infiltrating lymphocytes (TIL) by IHC for CD3, and then analyzed the relationship among VEGFA, VEGFR1, VEGFR2, CD3, and PDL-1. When analyzed as a continuous variable, PDL-1 protein expression by IHC inversely correlates with the expression of the three VEGF-related genes: VEGFA (r = -0.23; P = 0.01), VEGFR1 (r = -0.34; P < 0.001), and VEGFR2 (r = -0.23; P = 0.01). When dichotomized, the PDL-1-positive cohort trended toward a lower expression of VEGFA (fold change = 0.72; P = 0.056) and VEGFR1 (fold change = 0.69; P = 0.057). In addition, there was a significant and positive relationship between the presence of TIL as assessed by IHC for CD3 and PDL-1 by IHC (r = 0.25; P = 0.015), and there was a trend toward an inverse relationship between TIL and VEGFA gene expression (r = -0.18; P = 0.089). In conclusion, this is the first demonstration of an inverse association between the angiogenesis and PDL-1 pathways in tumor samples from primary ccRCC, and this relationship may be related to the immunosuppressive effects of VEGF signaling.

journal_name

Cancer Immunol Res

authors

Joseph RW,Parasramka M,Eckel-Passow JE,Serie D,Wu K,Jiang L,Kalari K,Thompson RH,Huu Ho T,Castle EP,Cheville J,Kwon ED,Thompson EA,Parker A

doi

10.1158/2326-6066.CIR-13-0042

subject

Has Abstract

pub_date

2013-12-01 00:00:00

pages

378-85

issue

6

eissn

2326-6066

issn

2326-6074

pii

2326-6066.CIR-13-0042

journal_volume

1

pub_type

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