Autophagy in tumor and tumor microenvironment

This book deals with the paradoxical role of autophagy in tumor suppression and tumor promotion in cancer cells. Autophagy plays opposing, context-dependent roles in tumors; accordingly, strategies based on inhibiting or stimulating autophagy could offer as potential cancer therapies.

The book elucidates the physiological role of autophagy in modulating cancer metastasis, which is the primary cause of cancer-associated mortality. Further, it reviews its role in the differentiation, development, and activation of multiple immune cells, and its potential applications in tumor immunotherapy. In addition, it examines the effect of epigenetic modifications of autophagy-associated genes in regulating tumor growth and therapeutic response and summarizes autophagy’s role in the development of resistance to a variety of anti-cancer drugs in cancer cells. In closing, it assesses autophagy as a potential therapeutic target for cancer treatment. Given its scope, the book offers a valuable asset for all oncologists and researchers who wish to understand the potential role of autophagy in tumor biology.

Sujit Kumar Bhutia is currently working as an Associate Professor at the Department of Life Science, National Institute of Technology in Rourkela, India. He received his doctorate in cell biology and cancer from the Indian Institute of Technology, Kharagpur, India in 2008, and subsequently pursued post-doctoral research on autophagy and cancer at Virginia Commonwealth University, USA. His research interests are focused on understanding the role of autophagy and autophagy-dependent cell death in cancer for the development of novel therapeutics.

He has published more than 80 research articles in international peer-reviewed journals and authored or co-authored numerous books and book chapters. He is also serving as a referee for several international journals.  Prof. Bhutia has more than 10 years of teaching experience in the areas of cell biology, cell signaling, cancer biology, and cell death.