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Treatment planning plays an important role in the process of radiotherapy (RT). The quality of the treatment plan directly and significantly affects patient treatment outcomes. In the past decades, technological advances in computer and software have promoted the development of RT treatment planning systems with sophisticated dose calculation and optimization algorithms. Treatment planners now have greater flexibility in designing highly complex RT treatment plans in order to mitigate the damage to healthy tissues better while maximizing radiation dose to tumor targets. Nevertheless, treatment planning is still largely a time-inefficient and labor-intensive process in current clinical practice. Artificial intelligence, including machine learning (ML) and deep learning (DL), has been recently used to automate RT treatment planning and has gained enormous attention in the RT community due to its great promises in improving treatment planning quality and efficiency. In this article, we reviewed the historical advancement, strengths, and weaknesses of various DL-based automated RT treatment planning techniques. We have also discussed the challenges, issues, and potential research directions of DL-based automated RT treatment planning techniques.

BackgroundKDM5B is a jmjc domain-containing histone demethylase which remove tri-, di-, and monomethyl groups from histone H3 lysine 4 (H3K4). KDM5B has been determined as an oncogene in many malignancies. However, its expression and role in hepatocellular carcinoma (HCC) remain unknown.MethodsWe detected the expression of KDM5B in HCC tissues and cell lines. Cell proliferation was performed to reveal the role of KDM5B depletion on HCC cells both in vivo and in vitro. Flow cytometry was used to analyze the cell cycle and chip analysis was conducted to determine the direct target of KDM5B.ResultsKDM5B is frequently up-regulated in HCC specimens compared with adjacent normal tissues and its expression level was significantly correlated with tumor size, TNM stage, and Edmondson grade. Moreover, Kaplan-Meier survival analysis showed that patients with high levels of KDM5B expression had a relatively poor prognosis. Knockdown of KDM5B notably inhibits HCC cell proliferation both in vivo and in vitro via arresting the cell cycle at G1/S phase partly through up-regulation of p15 and p27. Further molecular mechanism study indicates that silencing of KDM5B promotes p15 and p27 expression by increasing histone H3K4 trimethylation in their promoters.ConclusionsKDM5B could be a potentially therapeutic target, which provides a rationale for the development of histone demethylase inhibitors as a strategy against HCC.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-016-0311-5) contains supplementary material, which is available to authorized users.

Aim. To investigate the expression of miR-940 in the hepatocellular carcinoma (HCC) and its impact on function and biological mechanism in the HCC cells. Methods. Quantitative RT-PCR analysis was used to quantify miR-940 expression in 46 cases of tissues and cells. Transfection of HCC cell lines was performed by miR-940 mimics; the abilities of invasion and migration were assessed through Transwell array. Western blot represents the alteration in expression of CXCR2 by miR-940 mimics. Results. miR-940 expression was decreased significantly in the HCC tissues and the relevant cell lines. miR-940 upregulation suppressed the invasion and migration of HCC cells in vitro. Furthermore, the CXCR2 was downregulated to suppress invasion and migration after miR-940 mimics. Moreover, decreased miR-940 expression was negatively correlated with Edmondson grade (P = 0.008), tumor microsatellite or multiple tumors (P = 0.04), vascular invasion (P = 0.035), and recurrence and metastasis (P = 0.038). Kaplan-Meier analysis demonstrated that decreased miR-940 expression contributed to poor overall survival (P < 0.05). Conclusions. Our findings present that miR-940 acts as a pivotal adaptor of CXCR2 and its transcription downregulated CXCR2 expression to decrease HCC invasion and migration in vitro. Our study suggests that miR-940 may be a novel poor prognostic biomarker for HCC.