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2 cm Å©±âÀÇ À§ SMT°¡ ¹ß°ßµÇ¾î ½Ã¼ú Àü Á¶Á÷°Ë»ç¿¡¼ ¾ÏÀ¸·Î ³ª¿ÀÁö ¾ÊÀº »óÅ·ΠÀÇ·ÚµÈ È¯ÀÚÀÔ´Ï´Ù. Wedge resectionÀ» ½ÃÇàÇÏ¿´°í ³î¶ø°Ôµµ ¾Æ·¡¿Í °°Àº °á°ú°¡ ³ª¿Ô½À´Ï´Ù. Á¶Á÷°Ë»ç À§Ä¡¸¦ ¹Ù²Ù¾î º¸¾Ò´Ù¸é ¼ö¼ú Àü À§¾ÏÀ» Áø´ÜÇÒ ¼ö ÀÖÁö ¾Ê¾ÒÀ»±î »ý°¢ÇØ º¸¾Ò½À´Ï´Ù. ¿©ÇÏÆ° herniated gastric mucosa·Î ÀÎÇÏ¿© SMTó·³ À¶±âµÈ ºÎÀ§ÀÇ Á¡¸· top¿¡¼ ¹ß»ýÇÑ À§¾ÏÀ̶ó°í °á·ÐÁö¾ú½À´Ï´Ù. Ȥ½Ã À§¾ÏÀÌ ¸ÕÀúÀÌ°í ÀÌ·Î ÀÎÇÏ¿© gastric mucosaÀÇ herniationÀÌ ¹ß»ýÇÑ °ÍÀº ¾Æ´Ò±îµµ »ý°¢ÇØ º¸¾Ò½À´Ï´Ù. ¸¶Ä¡ gastritis cystica profunda¿Í ºñ½ÁÇÏ°Ô ¸»ÀÔ´Ï´Ù. Á¤´äÀÌ ¾ø´Â Áú¹®À» È¥ÀÚ ÇØ º¸¸é¼ ¿ô¾ú½À´Ï´Ù.
- Histologic type : tubular adenocarcinoma, well differentiated
- Size : 1.5x1.5x1.0 cm
- Depth of invasion : extension to mucosa (muscularis mucosa) (pT1a)
- Resection margin: free from carcinoma
- Associated findings : herniated gastric mucosa in the submucosa
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1) ÀÏ¿äÀÏ Æ¯°¿¬ÀÚÀ̽Š¿¬¼¼´ëÇб³ ÀÇ°ú´ëÇÐ ÀÇ»ý¸í°úÇкΠ³²±âÅà ±³¼ö´Ô²²¼ SPEM(Spasmoltic Polypeptide Expressing Metaplasia)À» ¼Ò°³ÇØ Áּ̽À´Ï´Ù. ¿À·¡ÀüºÎÅÍ SPEMÀÌ chief cell¿¡¼ originÇÏÁö ¾ÊÀ»±î ÃßÃøÇÏ¿© ¿Ô´Âµ¥ lineage tracing(»óÇǼ¼Æ÷ÀÇ stem cell marker¸¦ Áõ¸íÇÏ´Â ¹æ¹ýÀÓ. Stem cell¿¡ beta-GalÀ» taggingÇÏ¿© ´Ù¸¥ ¼¼Æ÷·Î ºÐÈÇØ °¡´Â °ÍÀ» Áõ¸íÇÏ´Â ¹æ¹ý)À» ÅëÇÏ¿© Áõ¸íÇÒ ¼ö ÀÖ¾ú´Ù°í ÇÕ´Ï´Ù.
Spasmoltic Polypeptide Expressing Metaplasia (SPEM)
- Marker: TFF2 (trefoil factor2), MUC 6 (Âü°í·Î intestinal metaplasiaÀÇ marker´Â TFF3, MUC2)
- Present in fundic/oxyntic mucosa
- Associated with oxyntic atrophy (parietal cell loss)
- Arises from the base of the glands (antralization / pseudopyloric metaplasia)
- > 90% of cancer resection specimens contain SPEM in adjacent mucosa
- 52% of early gastric cancers stain for TFF2
Âü°í¹®Çå 1: Goldenring & Nam. Prog Mol Biol Transl Sci (2010) Review; Oxyntic atrophy, metaplasia, and gastric cancer - Gastric carcinogenesis involves the loss of parietal cells (oxyntic atrophy) and subsequent replacement of the normal gastric lineages with metaplastic cells. In humans, two metaplastic lineages develop as sequelae of chronic Helicobacter pylori infection: intestinal metaplasia and spasmolytic polypeptide-expressing metaplasia (SPEM). Mouse models of both chronic Helicobacter infection and acute pharmacological oxyntic atrophy have led to the discovery that SPEM arises from transdifferentiation of mature chief cells. The presence of inflammation promotes the expansion of SPEM in mice. Furthermore, studies in Mongolian gerbils as well as increasing evidence from human studies indicate that SPEM likely represents a precursor for the development of intestinal metaplasia. These findings suggest that loss of parietal cells, augmented by chronic inflammation, leads to a cascade of metaplastic events. Identification of specific biomarkers for SPEM and intestinal metaplasia hold promise for providing both early detection of preneoplasia and information on prognostic outcome following curative resection.
Âü°í¹®Çå 2: Nam. Gut (2012) Spasmolytic polypeptide-expressing metaplasia (SPEM) in the gastric oxyntic mucosa does not arise from Lgr5-expressing cells
Âü°í¹®Çå 3: Nam. Gastroenterology (2010) Mature chief cells are cryptic progenitors for metaplasia in the stomach (PDF)
Âü°í¹®Çå 4: Weis & Goldenring. Gastric Cancer (2009) Current understanding of SPEM and its standing in the preneoplastic process
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