Current
best practices and rationalistic perspectives in causation-based
prevention, early detection and multidisciplinary treatment
of breast and gastric cancer
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Gastric & Breast Cancer
DOI: 10.2122/gbc.2003.0023
Perspective
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Carcinogenesis
in the stomach: Hypotheses, Facts and Future |
Abstract |
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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