Helicobacter pylori is the strongest known risk factor for gastric cancer, which is the third leading cause of cancer-related deaths globally. H. pylori is one of the four main cancer-causing pathogens listed in the Texas Cancer Plan. It is not listed in Goal 5, which seeks to increase vaccination rates for the prevention of cancer because there is no available vaccine. Also it is resident in over 4.4 billion human beings and there is some evidence of beneficial health effects from this infection. And yet close to 700,000 deaths globally are attributable to gastric cancer every year. Even in the United States, 1 out of every 95 men will develop gastric cancer and the greatest H. pylori burd...

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Helicobacter pylori is the strongest known risk factor for gastric cancer, which is the third leading cause of cancer-related deaths globally. H. pylori is one of the four main cancer-causing pathogens listed in the Texas Cancer Plan. It is not listed in Goal 5, which seeks to increase vaccination rates for the prevention of cancer because there is no available vaccine. Also it is resident in over 4.4 billion human beings and there is some evidence of beneficial health effects from this infection. And yet close to 700,000 deaths globally are attributable to gastric cancer every year. Even in the United States, 1 out of every 95 men will develop gastric cancer and the greatest H. pylori burden is borne by those of lower socio-economic class. The current treatment is antibiotics for those with ulcers or gastritis, the precursors to gastric cancer, but antibiotic resistance is developing to a degree where sustainability of this approach is questioned. I propose to solve this complex problem using an inexpensive engineered probiotic treatment. Engineered probiotics are now the central technology of several new companies and represent an emerging technology. I have developed a probiotic that eliminates H. pylori from mouse stomach by targeting the protein, VacA, that makes H. pylori cause ulcers and cancer. I use the host receptor protein that VacA binds to as my targeting agent so that the hunted becomes the hunter. My proposal is now to clearly demonstrate the obvious: if H. pylori develops resistance to this treatment, then it will no longer bind this host receptor and it will not longer cause disease. My technology will then be shown to not only knock down H. pylori, but keep any recurring H. pylori "toothless" so that they will not cause cancer. These results would provide the basis for clinical studies for an inexpensive probiotic product that would provide long term protection from gastric cancer.

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