Helicobacter pylori are bacteria that are most commonly found in the stomach and/or small intestine of humans. It is Gram-negative spiral shaped bacteria and it is estimated that it colonizes in nearly fifty percent of all humans (7). H. pylorus was discovered in the 1980's by researcher Robin Warren and Barry Marshall. For their discovery they both received the prestigious Nobel Prize (7). H. Pylori were not discovered until the 1980's because for many years scientists believed that the stomach was a sterile organ due to its extremely high acid concentration. However Helicobacter pylori have been able to evolve other thousands of years to be able to survive in the harsh environment (4). According to the National Cancer Institute Helicobacter pylori bacteria is able to secrete urease, which is a special enzyme that converts urea to ammonia; ammonia reduces the acidity in the stomach making it an environment where H. pylori can survive. Helicobacter pylori are unique in that their ability to survive in the stomach. Because of their ability to survive in the stomach lining, the white blood cells that recognize them are not able to attack. White blood cells respond to the site of infection but are unable to cross from the blood vessels to the stomach lining. White blood cells die at the infection site and release nutrients the ironically feed the H. pylori bacteria (4).
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When H. pylori were discovered in the 1980's, it was found in the tissue samples from people who were suffering with ulcers in the stomach and the upper small intestine. Barry Marshall and Robin Warren suspected that H. pylori were the actual cause of the ulcers and tried to prove this. Frustrated with the lack of good quality animal models, Barry Marshall infected himself with the Helicobacter pylori bacteria (4). Marshall developed ulcers in his stomach and provided cultures from his own ulcers. Warren and Marshall were able to prove that the H. pylori microbe was in fact the cause of stomach ulcers (4).
According to the Centers for Disease Control and Prevention, approximately more than two-thirds of the humans carry H. pylori bacteria, most prevalently in developing nations. Usually infection happens during the human's childhood by contaminated food or water. It lives in the human's stomach and about twenty percent of the people infected will develop ulcers later on in life (4). It has been found that there is a correlation between people who suffer from stomach ulcers and people who later on develop stomach cancer (3). Much research has been and is still been conducted in the link between H. pylori and gastric cancer. Many scientists believe that H. pylori are a risk factor to developing gastric cancer.
In a study that was published in 2006 in the Alimentary Pharmacology & Therapeutics Journal several scientists conducted a study to find out if there was a link between H. pylori and gastric cancer. The scientists gathered information on areas where there was a high prevalence of people infected with H. pylori bacteria. In conducting the gathering of data, the scientists had two separate groups; a group of people who had gastric cancer and the other group of people who did not have gastric cancer. They gather blood samples and studied the results. They concluded that eighty-four percent of gastric cancer patients showed that there we positive for H. pylori antibody in comparison with non gastric cancer patients, who showed that only sixty-six percent of the people had the H. pylori antibody (2). They concluded that there was a very strong link between H. pylori and a risk for stomach cancer.
There have been many other studies that proved the relationship between H. pylori and stomach cancer. Another study that was published in 2006, doctors gathered a controlled group of 213 people who had already been diagnosed with stomach cancer. Titers were collected from the group to determine the prevalence of H. pylori antibody (1). Out of the 213 people with gastric cancer, 163 people tested positive to carrying the H. pylori antibody. This study concluded once again that H. pylori could in fact be a contributing factor to early gastric cancer. There were many more studies conducted to continue proving the link between H. pylori and gastric cancer. Scientist discovered that more than likely H. pylori were to blame for noncardia stomach cancer.
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Once the link was established, scientists wanted to learn how H. pylori was possibly contributing to gastric cancer and why even though a large amount of the world's population carried the bacteria only a small amount developed into stomach cancer. They decided to look at H. pylori and determine if there are different types of strands and which ones are the strands that could possibly cause gastric cancer. In a study conducted in 2008, a strain was isolated from a person with gastric cancer and also a person suffering from gastric ulcer disease (6). Their genome was analyzed and the researchers came to the conclusion that their genome sequences were not identical. Each strain had original genes that were not present in each other, or other genomes previously studied.
While more extensive research still has to be conducted in order to learn how various strands of H. pylori behave some scientists wanted to know if treating H. pylori infections could prevent a person from developing stomach cancer. In 2008, yet another research was conducted to find out whether treatment would prevent stomach cancer. The research was conducted in gerbils; gerbils were infected with H. pylori for four to eight weeks and then treated with antimicrobial therapy (8). The study concluded that if H. pylorus was treated within four weeks there were no cases of carcinoma present. But of treatment was delayed till after eight weeks of infection there were cases of inflammation, dysplasia, and carcinoma that developed shortly (8).
In another study conducted in 2003, scientists decided they wanted to look at the relationship between H. pylori and gastric cancer tumor size. The researchers gathered fifty-one patients who were all diagnosed with stomach cancer. Thirty-three of them were positive for H. pylori bacteria, six of the patients were H. pylori negative, and twelve of the patients had been diagnosed with gastric cancer after the eradication of H. pylori (9). The scientists gathered data and discovered significant differences in the sizes of the tumor in the three categories. They concluded that H. pylori infection was in fact associated with cell production, and that suppression influenced tumor vascularity of gastric cancer. Consequently, they concluded that H. pylori eradication therapy could contribute to the suppression of tumor growth (9).
Although extensive research has been conducted to better understand the link between Helicobacter pylori and stomach cancer; there is still plenty more research to be done to be able to understand how H. pylorus triggers cancer in the stomach. H. pylori accounts for about seventy to ninety percent of all cases of stomach cancer (5), as a result it is very important to better understand how H. pylorus affects gastric cancer. Hopefully future research will be able to give us the answers we need to be able to prevent and treat gastric cancer.