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BackgroundWe explored risk factors for bone metastasis (BMs) in colorectal cancer (CRC) to improve in early diagnosis and follow-up and to reduce bone metastasis.MethodsWith a retrospective analysis of 2066 patients with CRC treated in our institution from January 2006 to January 2015, we assessed high-risk variables associated with bone metastasis using univariate and multivariate analyses.ResultsOf those subjects studied, 102 patients developed BMs, including 62 of 1014 the rectal cancer patients and 40 of the 1052 colon cancer patients. Lung metastases were accounting for 59.8% of the BMs (χ2 = 17.7, p<0.01) and hepatic metastases were accounting for 34.3% of BMs (χ2 = 3.06,p >0.05). BMs were diagnosed more rapidly in the presence of lung metastases(6.9 months versus 11.6 months for liver metastases). Univariate analysis revealed that BMs were associated with primary tumor location (p < 0.001), lung metastases (p < 0.001), initial stage (p = 0.001), radiotherapy (p < 0.001) and serum carcinoembryonic antigen (CEA) (p=0.001). Multivariate analysis revealed that primary tumor location (rectum), lung metastases, and serum CEA (>5 μg/L) were statistically significant (p <0.05).ConclusionsBMs in rectal cancer occur more frequently than in colon cancer. Lung metastases predicted potential progression to bone in CRCs more than liver metastases. Primary rectal locations, lung metastases and serum CEA were independent risk factors for BMs in CRC. Thus, patients should receive early bones scanning when presenting with CRC.

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Neuroblastoma (NB) is one of the most common solid tumors in childhood. To date, targeting MYCN, a well-established driver gene in high-risk neuroblastoma, is still challenging. In recent years, inhibition of bromodomain and extra terminal (BET) proteins shows great potential in multiple of Myc-driven tumors. ARV-825 is a novel BET inhibitor using proteolysis-targeting chimera (PROTAC) technology which degrades target proteins by the proteasome. In this study, we investigated the effect of ARV-825 in neuroblastoma in vitro and in vivo. Our results showed that ARV-825 treatment robustly induced proliferative suppression, cell cycle arrest, and apoptosis in NB cells. Moreover, ARV-825 efficiently depleted BET protein expression, subsequently repressing the expression of MYCN or c-Myc. In the NB xenograft model, ARV-825 profoundly reduced tumor growth and led to the downregulation of BRD4 and MYCN expression in mice. Taken together, these findings provide evidence that PROTAC BET inhibitor is an efficient way to achieve MYCN/c-Myc manipulation, and ARV-825 can be used as a potential therapeutic strategy for the treatment of neuroblastoma.

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Our results demonstrate successful functional and clinical outcomes for treatment of severe anophthalmic orbital syndrome using microvascular radial forearm free flaps. However, further prospective, long-term studies are recommended.