Special Issue "Oxidative Stress and Cancer"

Guest Editor
Prof. Dr. Alba Minelli
Cellular Biochemistry Unit, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Via del Giochetto, 06124, Perugia, Italy
E-Mail:
Phone: +39 075 7440
Fax: +39 075 7442
Interests: prostate cancer; oxidative stress; prostasomes; adenosine

Dear Colleagues,

Over 7,500 articles on oxidative stress related cancers are substantial evidence of the paramount importance of the control of cellular redox homeostasis which is challenged, throughout life, by sustained oxidative stress, chronic inflammation, and excessive antigen-loading. Oxidative stress-induced activation of NADPH oxidase and peroxisome proliferators-activated receptors, oxidants and inflammatory mediators, i.e. IL-6, IL-10, TNF-α, PGs, alterations of redox state of binding proteins, DNA mutations and induction of early response genes and hematopoietic activation seem to be common elements in the induction of hyperplasia, neoplasia, cancer metastasis, and angiogenesis. Therefore, potential health benefits of a number of antioxidants or anti-inflammatory agents, and maintenance of cellular oxido-redox status are crucial for optimal tissue function. This is a complicated topic which can be investigated from a number of perspectives. Our final goal is the compilation of a special issue providing an integrated understanding / identification of developmental phases of oxidative stress-induced cancers that will assist professionals towards effective progress on cancer war.

Thank you for your collaboration.

Prof. Dr. Alba Minelli
Guest Editor

Submission

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Type of Paper: Review
Title: Oxidative Stress-induced Tumor Stemness Switch: A New Perspective on Tumor Progression and Metastasis
Author: Bikul Das
Affiliation: Medical Oncology, Stanford University Medical School, CA, USA; E-Mail: bikuldas@stanford.edu
Abstract: One of the hallmarks of tumor microenvironment is the prevailing stress of hypoxia and oxidative stress injury. This “injured microenvironment” may act as a niche for tumor stem cells (TSC), and activate key signaling pathways that switch the quiescent population of TSC to an active mode of self-renewal and expansion (stemness switch)”. The stemness switch may be an important early event of tumor progression and metastasis. Signaling pathways such as HIF/VEGF mediated upregulation of stemenss related transcription factors such as Oct4 may be invoved in the oxidative-stress induced tumor stemness switch. The review will discuss the idea and preliminary findings on tumor stemness switch model.