Abstract
Purpose: Evasion of the immune system by cancer cells allows for the progression of tumors. Antitumor immunotherapy has shown remarkable effects in a diverse range of cancers. The aim of this study was to determine the clinicopathological significance of human epidermal growth factor receptor 2 (HER2), indoleamine 2,3-dioxygenase (IDO), and programmed death ligand-1 (PD-L1) expression in urothelial carcinoma of the bladder (UCB). Materials and Methods: We retrospectively studied 97 patients with UCB. We performed an immunohistochemical study to measure the expression levels of HER2, IDO, and PD-L1 in UCB tissue from these 97 patients. Results: In all 97 cases, the PD-L1 expression of tumor-infiltrating immune cells (ICs) was significantly correlated with higher pathologic tumor stage (pT). In pT2–pT4 cases (n = 69), higher levels of HER2 and IDO expression in invasive tumor cells (TCs) were associated with shorter periods of disease-free survival (DFS). Conclusion: These results imply that the expression of PD-L1 in ICs of the UCB microenvironment is associated with cancer invasion and the expression of HER2 or IDO in the invasive cancer cell and suggestive of the potential for cancer recurrence. We suggest that the expression levels of IDO, HER2, and PD-L1 could be useful as targets in the development of combined cancer immunotherapeutic strategies.
Highlights
Urothelial carcinoma of the bladder (UCB) remains one of the most common malignant cancers of the genitourinary tract [1]
We tried to identify the correlation between immune cell infiltration of this cancer and survival by using the TIMER (Tumor IMmune Estimation Resource) database
These results are in line with the tumorcidial function of CD8+ T in immune cells, which can be mitigated by the immune escape mechanism [27]
Summary
Urothelial carcinoma of the bladder (UCB) remains one of the most common malignant cancers of the genitourinary tract [1]. Among UCB patients, approximately 30% will have muscle invasion at diagnosis, show rapid progression to metastatic disease, and succumb to their disease [2]. There are several different treatment regimens, very poor treatment outcomes have been reported in locally advanced and metastatic UCB patients, and this trend has remained unchanged in the last few decades [3,4]. One barrier limiting the efficacy of classic cancer therapies is the interactions of cancer cells with their microenvironment, which determine whether the primary tumor is eradicated, metastasizes, or establishes dormant micrometastases [5]. The tumor microenvironment can determine treatment outcome and resistance [6]. Future anticancer treatment strategies should act directly on the proliferative processes of transformed cells and interrupt the crosstalk circuits established by tumor cells with the host microenvironment [7]
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