2020

Vol 2, No.2 CANCER+ (Call for Papers)

Table of Contents

Review Articles

by Mengran Shi, Luyao Wang, Zhao Yang, Chong Li
56 Views, 33 PDF Downloads

Bladder cancer (BC) is one of the most common types of cancers in the world. Despite various treatments are currently in place, the prognosis of BC does not seem to improve. Therefore, this prompts us to search for alternative treatments. The understanding of the molecular changes in cancer offers the prospect of targeting the key elements responsible for cancer development and progression, and thus, helps to develop a more effective and robust targeted therapy that does not endanger normal cells. At present, protein-based therapeutic targets such as programmed death ligand 1, epidermal growth factor receptor and aberrantly glycosylated integrin-α3β1, and genetic targets such as p53, human EGF receptor-2, and miR-23b are promising targets for BC treatment. In addition, predictive markers of treatment efficacy for BC, such as meiotic recombination 11, excision repair cross-complementing group 1, and multidrug resistance 1 gene are essential in facilitating clinicians to design and implement suitable and effective therapies for BC patients. This review discusses the pivotal role of these markers in the development of targeted therapy and the estimation of the clinical outcome of BC.

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Review Articles

by Chen Ge, Haiyang Wang, Haixu Chen, Wen Yue, Xinlong Yan
38 Views, 8 PDF Downloads
DNA methylation abnormalities in tumors often manifest as an increase or decrease of 5-methylcytosine at the genomic level or individual promoter sites. The mechanism of DNA demethylation by ten-eleven translocation proteins (TET) in maintaining the stability of global genome methylation level has attracted extensive attention. The biological functions of TET1-mediated hydroxymethylation differ among cancers due to tumor heterogeneity. Herein, recent updates on the effects of TET1 on tumor proliferation, migration, and invasion by altering DNA methylation levels are reviewed, and the direct and indirect roles of TET1 in activating or suppressing tumor progression are also discussed. Besides, the potential uses of DNA methylation analysis in clinical diagnosis and research of tumor microenvironment in relation to epigenetics are prospected. In conclusion, further studies about the dual characteristics of TET1 in cancer diseases are warranted to expand our understanding of the effects of DNA methylation in tumor which could be instrumental in the development of tumor treatment.
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