Prognostic role of lymphocyte to monocyte ratio for patients with cancer: evidence from a systematic review and meta-analysis

MicroRNAs as prognostic molecular signatures in renal cell carcinoma: a systematic review and meta-analysis MicroRNAs as prognostic molecular signatures in renal cell carcinoma: a systematic review and meta-analysis

CD44 is a marker of cancer stem-like cells in renal cell carcinoma (RCC). However, the prognostic value of CD44 in RCC remains controversial. This study evaluated the correlation of CD44 expression with the clinicopathological features of RCC through a meta-analysis. We systematically searched PubMed, ISI Web of Science and Embase for relevant studies until February 2015. We collected and analysed data on clinical stage, Fuhrman grade, microvascular invasion, recurrence, five-year overall survival (OS), disease-specific survival (DSS) and disease-free survival (DFS). Twenty studies involving 1672 patients satisfied the inclusion criteria. Results showed that high CD44 expression in RCC was a poor prognostic marker for five-year OS (RR = 0.69, 95% CI 0.60–0.78) in a fixed-effects model and for five-year DSS (RR = 0.46, 95% CI 0.27–0.80) and five-year DFS (RR = 0.63, 95% CI 0.43–0.93) in a random-effects model. CD44 expression also correlated with Furhman grade (RR = 0.61, 95% CI 0.48–0.77), tumour recurrence (RR = 7.42, 95% CI 3.74–14.70) and MVI (Microvascular invasion) (RR = 3.63, 95% CI 1.97–6.71). This meta-analysis suggests that CD44 is a prognostic marker in RCC. High CD44 expression correlates with high Fuhrman grade, recurrence, MVI and poor prognosis.

Clear cell renal cell carcinoma (ccRCC) is a gender-biased tumor. Here we report that there is also a gender difference between pulmonary metastasis and lymph node metastasis showing that the androgen receptor (AR)-positive ccRCC may prefer to metastasize to lung rather than to lymph nodes. A higher AR expression increases ccRCC hematogenous metastasis yet decreases ccRCC lymphatic metastases. Mechanism dissection indicates that AR enhances miR-185-5p expression via binding to the androgen response elements located on the promoter of miR-185-5p, which suppresses VEGF-C expression via binding to its 3′ UTR. In contrast, AR-enhanced miR-185-5p also promotes HIF2α/VEGF-A expression via binding to the promoter region of HIF2α. Together, these results provide a unique mechanism by which AR can either increase or decrease ccRCC metastasis at different sites and may help us to develop combined therapies using anti-AR and anti-VEGF-C compounds to better suppress ccRCC progression.