Abstract
c-Met overexpression has been observed in renal cell carcinoma (RCC). However, its clinicopathological impacts remain uncertain. We performed this meta-analysis to evaluate the pathologic and prognostic impacts of high c-Met expression in patients with RCC. A systematic computerized search of the electronic databases PubMed and Embase was performed. From 12 studies, 1,724 patients with RCC were included in the meta-analysis. Compared with RCCs showing low c-Met expression, tumors with high c-Met expression showed significantly higher nuclear grade (odds ratio = 2.45 [95% CI: 1.43–4.19], P = 0.001) and pT stage (odds ratio = 2.18 [95% CI: 1.27–3.72], P = 0.005). In addition, patients with c-Met-high RCC showed significantly worse overall survival than those with c-Met-low tumor (hazard ratio = 1.32 [95% CI: 1.12–1.56], P = 0.0009). In conclusion, this meta-analysis demonstrates that high c-Met expression correlate with significantly worse pathological features and overall survival, indicating c-Met overexpression is a potential adverse prognostic marker for patients with RCC.
Highlights
Renal cell carcinoma (RCC) is the most common malignant renal neoplasm, accounting for approximately 85% of kidney cancers [1, 2]
Visual inspection of the funnel plots for nuclear grade, pT stage, and OS showed symmetry, indicating there were no substantial publication biases (Figure 5). In this meta-analysis, we evaluated the pathologic and prognostic impact of c-Met overexpression in patients with renal cell carcinoma (RCC)
The results show that high c-Met expression is associated with significantly worse pathological features and prognosis
Summary
Renal cell carcinoma (RCC) is the most common malignant renal neoplasm, accounting for approximately 85% of kidney cancers [1, 2]. Most patients without metastases can be cured by nephrectomy alone. Immunotherapeutic agents (interferon-α and interleukin-2) had been the main treatment option for patients with metastatic RCC, despite marginal benefits and significant toxicities [4, 5]. With understanding of molecular mechanisms of carcinogenesis, treatment of RCC has dramatically changed. The molecular targeted agents such as sorafenib, sunitinib, axitinib, pazopanib, or temsirolimus are currently recommended with improved outcomes for patients with metastatic RCC [6,7,8,9,10]. Most tumors eventually develop resistance and their survival benefits are still disappointing. C-Met has recently emerged as a possible therapeutic target in various tumors including RCC [11,12,13] Efforts to identify novel therapeutic targets and develop more effective targeted drugs are still required. c-Met has recently emerged as a possible therapeutic target in various tumors including RCC [11,12,13]
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