Problem statement and importance for society: Gastric Cancer is the fifth most common malignancy in the world and third leading cause of death. It has affected a major part of the world population, more than 70% cases (677,000) has occurred in the developing countries or in low-and-middle-income countries (LMIC). According to the International Agency for Research on Cancer, 89% of all gastric cancer cases are attributed to infection from Helicobacter Pylori, morphologically a spiral-shaped bacteria which grows underneath the mucosal layer of the human stomach. It is a well recognized germ, which has coexisted within the human stomach for many thousands of years. Its global prevalence was estimated to 4.4 billion people in 2015, which is more than half of the world’s population.
H. pylori has a unique, acid gated membrane channel, which effectively controls the amount of alkali produced by the bacteria to combat gastric acid which allows it to survive in stomach. For maintaining prevalence, H. pylori produce an enzyme called urease, which converts urea (present in gastric secretion) into ammonia and CO2. The production of ammonia (alkaline buffer zone) around h. pylori neutralizes the acidity of the stomach, making it more hospitable to colonize and survive. In the presence of gastric acid, the membrane channel increases the amount of urea entering the bacterial cytoplasm by 300-fold, resulting into a significant production of ammonia for endemic acid neutralization. Due to this, sufficient ammonia is produced to neutralize the area between inner and outer layer of the bacterial cell membrane. In addition, the helical shape of h. pylori allows it to burrow into the sub-mucosa, which is less acidic than the inside space, or lumen, of the stomach. H. pylori attach to the cells that line the inner surface of the stomach. Such behavior subverts the innate immunity and then modulates the adaptive immune system. As a result, the immune system of stomach is silenced against digested microbes. This condition may lead to formation of gastric ulcer in stomach and duodenum, which in turn causes indigestion. Once the h. pylori population helps in establishing the ulcers, these ulcers penetrate deep into the endothelium and start damaging the surrounding tissue. This causes bleeding or perforation in the stomach surface. Early diagnosis of H. pylori is important for understanding the pathology of gastric cancer and starting early therapy. But the high cost, ambiguous diagnosis and poor patient engagement of existing diagnostic methods lead to late/advanced stage diagnosis of cancer. Patients spend $700-$1800 for a standard 2-week triple-drug therapy. Such high cost in the LMIC is a burden where 33 million individuals face catastrophic health expense and cancer take their toll at the cost of human life.
Objective: My vision is to demonstrate the “proof-of-concept” of a device, with three different techniques together for (A) Single stop, low cost, easily accessible, portable, unambiguous, instantaneous gastric cancer screening, which results in (B) Increased patient engagement with no waiting for medical reports and quick medication. This project aims to reduce the cost by performing early diagnosis with single stop, easily accessible, portable, unambiguous, instantaneous screening device, which results in increased patient engagement with no waiting for medical reports and quick medication. This is made possible through the combination of laser-based Raman/Fourier Transform Infrared, and Chitosan-Magnetic-Swob spectroscopy, which will offer an addendum tool for h-pylori diagnosis using standard endoscopy, suitable not only for in-theatre but also for portable/accessible use in the LMIC regions.
