Current best practices and rationalistic perspectives in causation-based prevention, early detection and multidisciplinary treatment of breast and gastric cancer

Gastric & Breast Cancer
DOI: 10.2122/gbc.2003.0023


Carcinogenesis in the stomach: Hypotheses, Facts and Future
Gastric cancer is the end result of multistep, multifactorial, long-term, complex interaction between environmental and genetic factors. In contrast to other common sporadic cancer types, as breast or prostate cancer, in which inherited effects have a greater contribution to cancer risk, epigenetic events that lie outside the cancer cells are essential in gastric carcinogenesis.
H pylori infection has been identified as an essential exogenous causative factor in the initiations of gastric carcinogenesis, but additional other factors, which promote the process of precursor lesions to invasive cancer, are largely unknown.

Three rational major theories, including host polymorphisms, H. pylori genotypes and most recently specific combinations of both, have been suggested to explain why a minority only of infected subjects develops invasive gastric cancer.

Recently, a tumor suppressor gene, the RUNX3 involved in gastric cancer has been identified and several mutations (MLH1/microsatelite instability, loss of TP53) have been described, but the underlying molecular mechanisms responsible to progression of epithelial gastric mucosal cells to cancer cells are poorly understood. Identification of key events in carcinogenic pathway will open the way for the development of highly-targeted preventative drugs.

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Online ISSN : 1109 - 7647
   Print ISSN : 1109 - 7655

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last update: 3 February 2004