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Introduction: Surgery is the only potentially curative treatment for patients with colorectal liver metastases, resulting in 5-year survival rates of 36–58%. Although many studies have been performed to determine prognostic factors for tumor recurrence and survival after resection of colorectal liver metastases, there are few prognostic scoring systems stratifying patients undergoing surgery for colorectal liver metastases into risk group models. Objectives: To identify, evaluate and compare the existing prognostic scores for survival after surgery for resection of colorectal liver metastases. Material and Methods: Electronic search in PubMed, Cochrane and Embase from 1990 to 2013 using the terms ‘hepatic resection’, ‘colorectal cancer’, ‘liver metastasis’, ‘hepatectomy’, ‘prognostic’, and ‘score‘. Only studies proposing a prognostic model or risk stratification based on clinical and/or pathological variables were included. Results: From 1996 to June 2013, 19 scoring systems were identified, including one nomogram. Thirty prognostic factors were identified although none of the factors was common to all prognostic models. The 4 factors most often included were: number of liver metastases, regional lymph node metastization of primary tumor, preoperative CEA level and maximum size of metastases. The median study sample size was 305 patients (81-1 568 patients) and median follow-up was 33 months (16-54 months). All studies were retrospective and used the Cox proportional hazards model for multi-variable analysis. Conclusion: Several factors have been constantly reported as having prognostic value after liver resection of colorectal liver metastases, although there is no consensus on the ideal scoring system.

The osteolytic nature of bone metastasis results from a tumor-driven increased bone resorption. Bone remodeling is orchestrated by the molecular triad RANK-RANKL-OPG. This process is dysregulated in bone metastases, mostly via induction of RANKL by tumor-derived factors. These factors increase expression of RANKL, which induce osteoclast formation, function, and survival, thereby increasing bone resorption. RANK is unexpectedly expressed by cancer cells, and the activation of RANKL-RANK pathway correlates with an increased invasive phenotype. To investigate the interaction between RANK expression in human breast and prostate cancer cells and their pro-metastatic phenotype we analyzed the activation of RANKL-RANK pathway and its effects on cell migration, invasion, gene expression in vitro, and osteolysis-inducing ability in vivo. RANKL activates kinase signaling pathways, stimulates cell migration, increases cell invasion, and up-regulates MMP-1 expression. In vivo, MMP-1 knockdown resulted in smaller x-ray osteolytic lesions and osteoclastogenesis, and decreased tumor burden. Therefore, RANKL inhibition in bone metastatic disease may decrease the levels of the osteoclastogenesis inducer MMP-1, contributing to a better clinical outcome.