The roles of gene transcription in cancer have long been appreciated. However, posttranscriptional processes also contribute significantly to alterations in gene expression that lead to tumor initiation, formation, and progression.We have known for decades that alterations in the expression of key genes, such as those involved in cell proliferation, signaling, apoptosis, and immune responses, are major molecular events in cancer. This book presents our current understanding of selected posttranscriptional control mechanisms and the RNAs that they regulate. Each chapter provides an overview of a specific RNA-directed regulatory system and the RNA/protein factors involved, then discusses major findings in the field and their relationships to the development and/or treatment of cancer and associated diseases. Future questions serve to address "where do we go from here" and stimulate the reader’s thinking about these important problems.This compendium of chapters from experts in the field is essential reading for anyone interested in the myriad ways that RNAs contribute to tumorigenesis: from graduate students, researchers, and clinical scientists interested in mRNA processing and translation, RNA-binding proteins that promote turnover/stability of specific mRNAs, how small noncoding RNAs control inflammation and signaling, roles of the epitranscriptome, and future and emerging RNA-based, anti-tumor therapeutics.Key Features: oWith the Covid-19 pandemic, caused by the RNA virus SARS-CoV-2, together with the recently available, RNA-based vaccines against CoV-2, RNA has drawn significant media and societal attention worldwideoNumerous types of RNAs play unique roles in cancer, and this book serves to draw attention to their importanceoMost chapters describe unique types of RNA-based gene regulation and their roles in cancer specifically; other chapters cover mTOR signaling, a major pathway in many cancersoAll chapters are written by established, eminent scientists or newly emerging scientists, all experts in their fields

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