Stomach Cancer: just watch your habits

· TGI - Cancer
Authors

Carcinoma of the stomach is the second most common cause of cancer death worldwide. Despite advances in diagnosis and treatment, the 5-year survival rate of stomach cancer is only 20 per cent. Stomach cancer can be classified into intestinal and diffuse types. The development of gastric cancer is a complex, multistep process involving multiple genetic and epigenetic alterations of oncogenes, tumor suppressor genes, DNA repair genes, cell cycle regulators, and signaling molecules. According to the OMIM database, 90 per cent of gastric cancers are sporadic, whereas 10 per cent are hereditary.

Endoscopic image of linitis plastica, where th...

Endoscopic image of linitis plastica, where the entire stomach is invaded with gastric cancer, leading to a leather bottle like appearance. Released into public domain on permission of patient — Samir धर्म 08:44, 7 June 2006 (UTC) Category:Endoscopic images (Photo credit: Wikipedia)

EPIDEMIOLOGY:

Age: known to increase with age with the peak incidence occurring at 60-80 years. Cases in patients younger than 30 years are very rare. In India, the age range for stomach cancer is 35-55 years in the South and 45-55 years in the North.

Sex: The disease shows a male preponderance in almost all countries, with rates two to four times higher among males than females.

Cancer location: it can develop both in the proximal and the distal region.

  1. Distal gastric cancers predominate in developing countries and in the lower socio-economic groups. Dietary factors and Helicobacter pylori (H. pylori) infection are major risk factors for the development of distal tumors. Exception: Distal tumors continue to predominate in Japan in contrast to the increasing prevalence of proximal tumors in the rest of the world.
  2. Proximal tumors are more common in developed countries and in higher socio-economic classes. The major risk factors for proximal cancers are GastroEsophageal Reflux Disease (GERD) & Obesity.

The etiology of gastric cancer is multifactorial and includes both dietary and non-dietary factors.

  1. High content of nitrates and High salt intake. Dietary salt intake was directly associated with risk of gastric cancer in prospective population studies, with progressively increasing risk across consumption levels. Populations at high risk for stomach cancer have been shown to consume diets rich in starch and poor in protein quality, and are not inclined to eat fresh fruits and vegetables. Both high starch and low protein diet may favor acid-catalyzed nitrosation in the stomach and cause mechanical damage to the gastric mucosa. One study found a positive association between salt/sodium intake and gastric cancer mortality. Another study reported a direct correlation between dietary salt intake and risk of gastric cancer with progressively increasing risk across consumption levels based on a meta-analysis of prospective studies.
  2. Helicobacter pylori (H. pylori) infection. (more than 80% of cases have been attributed to H. pylori infection). In 1994, the International Agency for Research on Cancer categorized H. pylori as a “Group 1 human carcinogen”. Approximately 50 per cent of the world’s population is infected by H. pylori. A combination of a virulent organism, a permissive environment, and a genetically susceptible host is considered essential for H. pylori-induced gastric cancer. H. pylori has been suggested to trigger a cascade of events that promote the sequential progression of normal gastric epithelium through atrophic gastritis, intestinal metaplasia, and dysplasia to carcinoma. The bacterium secretes several products that cause gastric mucosal damage such as urease, protease, phospholipase, ammonia, and acetaldehyde. H. pylori disrupts gastric barrier function via urease-mediated myosin II activation. Generation of oxidative stress is recognized as a virulence factor in H. pylori-infected hosts –      H.Pylori induces the production of reactive oxygen and nitrogen species and suppresses the host antioxidant defense mechanisms, leading to oxidative DNA damage. It has been demonstrated that H. pylori infection promotes gastric carcinogenesis by increasing endogenous DNA damage whilst decreasing repair activities and by inducing mutations in the mitochondrial and nuclear DNA. Aberrant DNA methylation induced by H. pylori infection has been found to be a significant risk factor for gastric cancer.
  3. Alcohol &  Tobacco: A direct correlation was observed between consumption of alcohol and tobacco and the risk of gastric cancer in a population-based prospective cohort study. Smokers tend to have a higher incidence of H. pylori infection and gastro-duodenal inflammation than non-smokers.

How to Prevent it?

A plausible program for gastric cancer prevention involves:

  1. intake of a balanced diet containing vegetables and fruits
  2. low intake of Salt and salted diet including roasted, grilled, baked, and deep fried in open furnaces etc., as all of which increase the formation of carcinogenic N-nitroso compounds (NNC).
  3. low intake of nitrates – natural (dietary nitrates are found naturally in foods such as cabbage, cauliflower, carrot, celery, radish, beets, and spinach) or added during preservation. Gastric acid converts these Nitrates in to carcinogenic N-nitroso compounds (NNC), thereby increasing the risk. {Imagine: high intake of nitrates + high salt intake combined with cooking practices like broiling of meats, roasting, grilling, baking, and deep frying in open furnaces, sun drying, salting, curing, and pickling.}
  4. Avoid completely where possible (or minimize) Tobacco and Alcohol consumption
  5. improved sanitation and hygiene
  6. screening and treatment of H. pylori infection, and
  7. follow-up of precancerous lesions recognizable precursors are inflammation – metaplasia – dysplasia. Following is the “Summary of proposed management for patients with atrophic gastritis, gastric intestinal metaplasia and gastric epithelial dysplasia”.
Summary of proposed management for patients with atrophic gastritis, gastric intestinal metaplasia and gastric epithelial dysplasia.

Summary of proposed management for patients with atrophic gastritis, gastric intestinal metaplasia and gastric epithelial dysplasia.

The fact that diet plays an important role in the etiology of gastric cancer offers scope for nutritional chemoprevention.

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