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tuberculosis dissemination. Copyright © 2020 Moule and Cirillo.Senescence is the irreversible arrest of cell proliferation that has now been shown to play an important role in both health and disease. With increasing age senescent cells accumulate throughout the body, including the bone marrow and this has been associated with a number of age-related pathologies including malignancies. It has been shown that the senescence associated secretory phenotype (SASP) creates a pro-tumoural environment that supports proliferation and survival of malignant cells. Understanding the role of senescent cells in tumor development better may help us to identify new treatment targets to impair tumor survival and reduce treatment resistance. In this review, we will specifically discuss the role of senescence in the aging bone marrow (BM) microenvironment. Many BM disorders are age-related diseases and highly dependent on the BM microenvironment. Despite advances in drug development the prognosis particularly for older patients remains poor and new treatment approaches are needed to improve outcomes for patients. In this review, we will focus on the relationship of senescence and hematological malignancies, how senescence promotes cancer development and how malignant cells induce senescence. Copyright © 2020 Hellmich, Moore, Bowles and Rushworth.Being the second most common type of primary bone malignancy in children and adolescents, Ewing Sarcoma (ES) encounters the dilemma of low survival rate with a lack of effective treatments. As an emerging approach to combat cancer, RNA therapeutics may expand the range of druggable targets. Since the genome-derived oncolytic microRNA-34a (miR-34a) is down-regulated in ES, restoration of miR-34a-5p expression or function represents a new therapeutic strategy which is, however, limited to the use of chemically-engineered miRNA mimics. Very recently we have developed a novel bioengineering technology using a stable non-coding RNA carrier (nCAR) to achieve high-yield production of biocompatible miRNA prodrugs, which is a great addition to current tools for the assessment of RNA therapeutics. Herein, for the first time, we investigated the biochemical pharmacology of bioengineered miR-34a-5p prodrug (nCAR/miR-34a-5p) in the control of ES using human ES cells and xenograft mouse models. The bioengineered nCAR/miR-34a-5p was precisely processed to mature miR-34a-5p in ES cells and subsequently suppressed cell proliferation, attributable to the enhancement of apoptosis and induction of G2 cell cycle arrest through downregulation of SIRT-1, BCL-2 and CDK6 protein levels. Proteasome inhibitor Furthermore, systemic administration of nCAR/miR-34a-5p dramatically suppressed the ES xenograft tumor growth in vivo while showing biocompatibility. In addition, the antitumor effect of bioengineered nCAR/miR-34a-5p was associated with a lower degree of tumoral cell proliferation and greater extent of apoptosis. These findings demonstrate the efficacy of bioengineered miR-34a-5p prodrug for the treatment of ES and support the development of miRNA therapeutics using biocompatible bioengineered miRNA prodrugs. Copyright © 2020 Li, Yuan, Tu, Hu, Li, Yi, Li, Zhao, Cheng, Yu, Jian and Yu.[This corrects the article DOI 10.3389/fonc.2019.01563.]. Copyright © 2020 Wilson, Hammond, Higgins and Petersson.Metabolic reprogramming is prevalent in cancer, largely due to its altered chemical environments such as the distinct intracellular concentrations of O2, H2O2 and H+, compared to those in normal tissue cells. The reprogrammed metabolisms are believed to play essential roles in cancer formation and progression. However, it is highly challenging to elucidate how individual normal metabolisms are altered in a cancer-promoting environment; hence for many metabolisms, our knowledge about how they are changed is limited. We present a novel method, CaMeRe (CAncer MEtabolic REprogramming), for identifying metabolic pathways in cancer tissues. Based on the specified starting and ending compounds, along with gene expression data of given cancer tissue samples, CaMeRe identifies metabolic pathways connecting the two compounds via collection of compatible enzymes, which are most consistent with the provided gene-expression data. In addition, cancer-specific knowledge, such as the expression level of bottleneck enzymes in the pathways, is incorporated into the search process, to enable accurate inference of cancer-specific metabolic pathways. We have applied this tool to predict the altered sugar-energy metabolism in cancer, referred to as the Warburg effect, and found the prediction result is highly accurate by checking the appearance and ranking of those key pathways in the results of CaMeRe. Computational evaluation indicates that the tool is fast and capable of handling large metabolic network inference in cancer tissues. Hence, we believe that CaMeRe offers a powerful tool to cancer researchers for their discovery of reprogrammed metabolisms in cancer. The URL of CaMeRe is http//csbl.bmb.uga.edu/CaMeRe/. Copyright © 2020 Li, Zhou, Sun, Qiu, Gao and Xu.[This corrects the article DOI 10.3389/fonc.2019.00468.]. Copyright © 2020 Razak, Alam, Afsar, Abulmeaty, Almajwal and Jahan.Macrophages, which have functions of engulfing and digesting foreign substances, can clear away harmful matter, including cellular debris and tumor cells. Based on the condition of the internal environment, circulating monocytes give rise to mature macrophages, and when they are recruited into the tumor microenvironment and in suitable conditions, they are converted into tumor-associated macrophages (TAMs). Generally, macrophages grow into two main groups called classically activated macrophages (M1) and alternatively activated macrophages (M2). M2 and a small fraction of M1 cells, also known as TAMs, not only lack the function of phagocytizing tumor cells but also help these tumor cells escape from being killed and help them spread to other tissues and organs. In this review, we introduce several mechanisms by which macrophages play a role in the immune regulation of tumor cells, including both killing factors and promoting effects. Furthermore, the targeted therapy for treating tumors based on macrophages is also referred to in our review.