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Gastric cancers develop from single cells, based on data from clonality analysis in C3H/HeN ⇔ BALB/c chimeric mice. We can conclude that IM is important not as a precancerous lesion but as a paracancerous cord from such studies of clonality of gastric cancers and of phenotypic expression of each intestinal metaplastic or stomach cancer cell. Intestinalization progresses from G, through GI, to I types in noncancerous and cancerous tissue independently, accompanied by homeotic transformation of underlying control factors. H. pylori is not an initiator, but rather a strong promoter in gastric carcinogenesis, and its eradication, together with reduction in salt intake, might effectively prevent gastric cancer development.

The history of basic and clinical research in gastric cancer originated from the 19th century in Europe, but surprisingly rapid response to this flow abroad occurred in Japan in every aspect of research and treatment of this disease. Researchers in early days devoted their best efforts to conquer the most frequent cancer in Japan. Diagnosis of gastric cancer has been highly elaborated with the aid of the double-contrast method of X-ray fluoroscopy and meticulous endoscopic apparatus, which facilitated both minimum and extended surgery according to the extent of disease. Effective anticancer drugs are available now, some of which were developed originally in our country. Daily use of gene diagnosis and treatment could be expected in the near future. Now we can enjoy a high level of treatment results in the fields of surgery and chemotherapy and should try to establish a global standard of diagnosis and treatment of gastric cancer. International corroboration is mandatory to achieve these goals, and we could expect the International and Japanese Gastric Cancer Associations and the WHO Collaborating Center for Primary Prevention, Diagnosis and Treatment of Gastric Cancer (chaired by Suemasu, Maruyama, Sasako) will take a leading role in this field. Gastric cancer still remains one of the prevailing cancers in our country, and our next goal should be based in prophylaxis to reduce the incidence of gastric cancer.

In the course of multistep carcinogenesis of the stomach, various alterations of oncogenes, tumor suppressor genes, DNA repair genes, growth factors/receptors, cell-cycle regulators, and cell adhesion molecules are accumulated. Some of these changes occur commonly in both well-differentiated and poorly differentiated types and some differ depending on the histological types. Among various epigenetic alterations, modified gene expression through DNA methylation and chromatin remodeling by histone modification are the most important events. Genetic polymorphism is a crucial endogenous cause and fundamental factor of cancer risk. Using genomic science including novel techniques for global analysis of gene expression and bioinformatics, the individual character of each person and cancer can be dissected precisely, which is directly connected to personalized medicine and cancer prevention. Understanding of the diversity of gastric cancer must be critical in the era of genomic medicine at the clinical setting.

Clinical diversity of Hp infection may be caused by variation of Hp itself and host reaction, other factors such as food intake, and interaction of these factors. The present carcinogenesis model employing MGs and epidemiological study have demonstrated a causal link of Hp infection and gastric cancer development. In vitro experiments have showed the mechanisms by which Hp infection inflict injury on gastric mucosal cells. From the point of view of “tailor-made medicine,” these in vivo and in vitro experiments may contribute to the development of more effective treatment for Hp infection.

1. Histological diversity of mixed figures is found in tumors more than 5mm in size. 2. As size of GC becomes larger, histological diversity increases. 3. As GC invades the submucosa, histological diversity increases. 4. Both components of tub2 and por show various histological figures. 5. Despite diversity, early GC is classified into DCA and UCA.

Hepatoid adenocarcinoma is an extrahepatic carcinoma with functionally and structurally distinctive foci of hepatocellular differentiation. The usual presence of adenocarcinoma indicates the emergence of hepatocellular transdifferentiation from adenocarcinoma cells. Hepatoid adenocarcinoma most commonly occurs in the stomach, but other gastrointestinal and genitourinary organs are also common sites of origin. Master transcriptional regulators, particularly liver-enriched nuclear factors, might be involved in the transdifferentiation process, as well as in the biology of hepatoid adenocarcinoma tissues.