Publisher's Synopsis
Each day, some 1,600 people die of cancer in the United States. That number goes up 10-fold, up to 21,000 if you include the global population. Cancer is a global scourge and is far from being controlled. However, decades of my research has exposed the fact that electronically modified oxygen derivatives (EMODs) are a major factor leading to cellular suicide (apoptosis) for cancerous cells, across a wide spectrum of human cell types. In fact, I have found that over 30 cell types of human cancer are killed by EMOD induced apoptosis. Most amazingly, prooxidant EMODs selectively kill cancer cells and do not harm normal cells. This prooxidant approach is gaining ground as a primary means of treating cancer. Altered metabolism, together with activated oncogenic signaling and deregulation of mitochondrial function, typically results in an increase in the generation of reactive oxygen species (ROS, EMODs) in cancer cells. Interestingly, this phenomenon leads to a differential redox homeostasis in normal and malignant cells that is gaining ground as a promising target for the design of more selective and effective anticancer agents. Oxidant-induced upregulation of cellular reactive oxygen species (ROS, EMODs) should selectively target cancer cells without compromising the viability of untransformed, normal cells. Consequently, a pro-oxidant deviation well-tolerated by nonmalignant cells might rapidly reach a cell-death threshold in malignant cells already at a high set point for constitutive EMOD stress or EMOD mediated apoptosis (cancer cell death). Prooxidative (EMOD) therapies are compatible with chemotherapy, radiation therapy and surgery. There is no reason to avoid it because it will only complement other forms of cancer treatment. Please remember that chemotherapy and radiation therapy can wipe out your immune system, speed up cancer's spread and destroy your oxidative ability to kill cancer. Thus, you must be willing to boost or restore your EMODs to a point of "oxidative bliss." The reason for the failed war against cancer stems from a flawed theoretical paradigm that categorized cancer as primarily a "free radical disease." My prooxidant approach lends the potential to treat all types of cancer because it exploits the one weakness that is common to every cancer cell: a higher electronically modified oxygen derivative (EMOD, ROS) level than normal cells and therefore, a lower threshold of death. This will take into account the unique metabolic signature of each individual and of each cancer cell type. I believe that a primary understanding of mutagenesis and prevention should be based on redox (oxidation/reduction) biochemistry and on the crucial role played by electronically modified oxygen derivatives (EMODs). No doubt, EMOD induced apoptosis (cellular suicide) is at the heart of a successful approach in conquering cancer. By controlling metabolic redox minutia, we can show that EMOD induced apoptosis (cellular suicide) is crucial for a successful clinical approach in dealing with cancer. I present the "Howes Cancer Unification Principles (HCUP)" that personalized prooxidant molecular therapy, based on electronically modified oxygen derivative (EMOD) biochemistry, hold the key to conquering cancer. First, the HCUP states that EMODs are proven killers of cancer cells and second, excessive levels of antioxidants can shield or protect cancer cells. By elegantly regulating both our local and systemic redox milieu and oxidative capacity, we can arrive at a point of "oxidative bliss" (the holy grail) and thereby kill cancer cells (and metastatic cells) and not harm normal cells. This will require "stacking" of prooxidant methodologies in a safe and effective manner. I present overwhelming scientific evidence to support this premise and offer new insights into cancer cell killing, suppression and protection.
