위점막에서의 장형 화생 아형과 위암종과의 관계

조중현(Joong Hyeon Cho),이정희(Jung Hee Lee),고경혁(Gyung Hyuck Ko),이호용(Ho Yong Lee),김현주(Hyun Ju Kim) 대한소화기학회 1997 대한소화기학회지 Vol.30 No.1

N/A Background/Aims: Gastric carcinoma is the mnost common tumor in Korea and is known to be associated with intestinal metaplasia. By the way, the intestinal metaplasia is classified into subtypes in recent years. This study is to see the relationship between the subtypes of intestinal metaplasia and gastric carcinoma. Methods: This study involved 850 patients with various gastric disorders. After diagnosis with hematoxlin-eosin stain, alcian blue pH 2.5/Periodic acid-Schiff and high iron diamine/alcian blue pH2.5 stains were performed to classify the intestinal metaplasia. Results: The, intestinal metaplasia was found in 465 patients(54.7 %): the prevalence of type I, II, and III intestinal metaplasia were 88.2%, 66.2%, and 22.4%, respectively. There are no difference in the prevalence of type I and II intestinal metaplasia among the various gastric disorders(p 0.05). But, type III was strongly associated with intestinal-type gastric carcinoma as compared to either benign gastric disorders(p(0.01) or diffuse-type gastric carcinoma(p(0.01). Conclusions: This results suggest that the type III intestinal metaplasia may play a special role in the histogenesis of intestinal-type carcinoma. (Korean J Gastroenterol 1997; 30:1 - 8)

위선암에서 장형화생의 변이형에 관한 연구

제갈승주,최영자,곽효일,노정섭,최찬 대한임상병리사협회 2001 대한임상병리사회지 Vol.21 No.1

위점막에서의 장형 화생 아형과 위암종과의 관계

이정희,김현주,이호용,조중현,고경혁 大韓消化器病學會 1997 大韓消化器病學會誌 Vol.30 No.1

조기위암과 그 주변점막병변에 있어서 Secretory Component의 출현에 관한 연구

김선영 최신의학사 1992 最新醫學 Vol.35 No.3

위의 장형화생-이형성증-암종의 구조적 Spectrum에 관한 형태계측학적 연구*

정상우,박동하,이지신,조규혁 대한병리학회 1993 Journal of Pathology and Translational Medicine Vol.27 No.1

위절제술을 시행한 조기위암환자에서 위치확인을 위한 위장조영검사와 위내시경검사의 비교분석에 따른 진단률 향상에 관한 연구 : 4cm미만의 조기위암 중심으로

고주영(Ju Young Ko),이보영(Bo Young Lee),김상균(Sang Gyun Kim),정재연(Jae Yeon Jeong),김금남(Geum Nam Kim),조영기(Young Gi Cho) 대한영상의학기술학회 2009 대한영상의학기술학회 논문지 Vol.2009 No.-

Purpose : It was prepared to help patients with early gastric cancer who underwent a gastrectomy to detect early gastric cancer by comparing observations from pre-operation UGI series and Endoscopy as well as post-operation pathological observations of type, size, and location. Materials and Methods : It targeted 27 cases who underwent a gastrectomy for early gastric cancer by visiting the department of surgery from February 2007 to September 2008 while the pathological observations of type, size, and location were compared and analyzed through observations from pre-operation gastroscopy and UGI series and medical record after the gastrectomy. Results : Considering the generation frequency after gastrectomy, pyloric antrum was the most with 15 cases (55.6%); specifically, lesser curvature of stomach was the most with 14 cases (51.9%). When 2 accompanied observations were combined, atrophic gastritis and intestinal metaplasia showed high frequencies with 23 cases (85.2%) and 22 cases(81.5%) respectively. Through radiologic severity, 14cases (51.8%) were judged as “concordance” while 13 cases (48.2%) were judged as “discordance”. In the origin site of the 13 cases judged as “discordance” in radiologic severity, pyloric antrum was the most with 9 cases (69.2%); specifically, lesser curvature of stomach was the most with 6 cases (41.6%). Lesser curvature and the anterior wall part of stomach are difficult to be technically depicted minutely during the UGI series, and they are parts where false positive rates are frequently generated. Conclusion : Observation of accompanied intestinal metaplasia(81.5%) is evaluated as the important standard in the discovery of early gastric cancer. Intensive tests are executed for intestinal metaplasia because it is considered as a high risk group and require follow up when suspected. In the result of radiologic severity, there were many observations which looked normal yet it was early gastric cancer in lesser curvature and the anterior wall of stomach including the gastric angle. Only habitual scans of that part with compression and flow technique, while at the same time, confirming the change of mucosa are thought to contribute to discovering early gastric cancer exactly and swiftly in gastric cancer screening tests.

위축 위염과 장형화생에서의 마이크로어레이를 이용한 유전자 발현

김경래 ( Kyong Rae Kim ),오수연 ( Soo Youn Oh ),박웅채 ( Ung Chae Park ),왕준호 ( Joon Ho Wang ),이재동 ( Jae Dong Lee ),권혁중 ( Hyuk Jung Kweon ),김상윤 ( Sang Yoon Kim ),박승화 ( Seung Hwa Park ),최동국 ( Dong Kug Choi ),김찬길 대한소화기학회 2007 대한소화기학회지 Vol.49 No.4

목적: 장형화생을 동반한 위축 위염은 최근까지 위암발생의 중요한 요인으로 여겨져 왔다. 그러나 아직 장형화생과 위축 위염에 발현하는 주요 유전자에 관해서 거의 알려진 것이 없다. 이번 연구는 기존의 유전자 탐색에 사용되었던 어떤 방법보다도 많은 장점을 가지고 있는 올리고뉴클레오티드 마이크로어레이를 이용하여 전반적인 유전자 변화와 함께 위암과의 관련성을 알아보고자 하였다. 대상 및 방법: 장형화생을 동반한 위축 위염환자의 위점막과 정상 점막에서 올리고뉴클레오티드 마이크로어레이 기술을 이용하여 대량의 유전자 정보를 얻었으며, 유전자들의 확인을 위해 SAM (Significance Analysis of Microarrays) package 방법을 사용하였다. Global normalization, intensity dependent normalization 그리고 box plot normalization를 사용하여 결과를 분석하였다. 결과: FABP, REG, OR6C1, MEP1, SLC6A1, SI, Mucin 1, RAB23 등 8개 유전자는 정상점막에 비해 10배이상 과발현되었고, LOC44119유전자 하나만이 10배 이상 저발현되었다. 알려진 위암의 발암과정에 관여된 유전자로는 FN1, SRMS, TP53, TP53IMP2, TP53I3, FGFR4, TGFB1, TGFA 등 모두 8개에서 공통적으로 2배 이상의 발현 증감을 보였다. 결론: 저자들은 위암의 전단계병변인 장형화생을 동반한 위축 위염에서 암화와 관련한 유전자를 확인할 수 있었으며, 이번 연구 결과는 위암 진단 및 치료와 같은 임상적용을 위한 분자생물학적인 특성을 이해하는 데에 도움이 될 것이다. Background/Aims: The atrophic gastritis with intestinal metaplasia of gastric mucosa has been considered to be the major factor of carcinogenesis in the stomach. However, the key molecules are still poorly understood. To elucidate the molecular genetic basis, we report the results of our initial microarray data to analyze the genome pattern in patients with atrophic gastritis and intestinal metaplasia of the stomach. Methods: We used oligonucleotide microarray technique to evaluate the gene expression profiles in atrophic gastritis with intestinal metaplasia, in comparison with those of normal mucosa. For the identification of differentially expressed genes, Significance Analysis of Microarrays (SAM) package method was used. The results were analyzed using global normalization, intensity dependent normalization, and box plot normalization. Results: Eight genes including FABP, REG, OR6C1, MEP1, SLC6A1, SI, Mucin 1, and RAB23 in mucosa of atrophic gastritis and intestinal metaplasia were up-regulated by more than 10 times as compared with normal gastric mucosa. Only one gene, LOC44119 was down-regulated by more than 10 times of the expression as compared with normal gastric mucosa. In respect to the expression of known genes related to gastric carcinogenesis, 8 genes including FN1, SRMS, TP53, TP53IMP2, TP53I3, FGFR4, TGFB1, and TGFA showed up- and down-regulations more than 2 folds in expression pattern. Conclusions: We could identify a total genome pattern in patient with atrophic gastritis and intestinal metaplasia using oligonucleotide microarray. We believe that the current results will serve as a fundamental bioinformative basis for clinical applications in diagnosis and treatment of gastric cancer and precancerous lesion in the future. (Korean J Gastroenterol 2007;49:209-224)

CpG Island Hypermethylation in Gastric Carcinoma and Its Premalignant Lesions

강경훈 대한병리학회 2012 Journal of Pathology and Translational Medicine Vol.46 No.1

Gastric cancers arise through a multistep process characterized by the progressive accumulation of molecular alterations in which genetic and epigenetic mechanisms have been implicated. Gastric cancer is one of the human malignancies in which aberrant promoter CpG island hypermethylation is frequently found. Helicobacter pylori and Epstein-Barr virus, which are known carcinogens for gastric cancer, are closely associated with enhanced hypermethylation of CpG island loci in gastric non-neoplastic epithelial cells and cancer cells, respectively. Aberrant CpG island hypermethylation occurs early in the multistep cascade of gastric carcinogenesis and tends to increase with the step-wise progression of the lesion. Approximately 400 genes that are actively expressed in normal gastric epithelial cells are estimated to be inactivated in gastric cancers as a result of promoter CpG island hypermethylation. In this review, a variety of information is summarized regarding CpG island hypermethylation in gastric cancer.

Role of intestinal metaplasia subtyping in the risk of gastric cancer in Korea

Kang, Kyung P,Lee, Hye S,Kim, Nayoung,Kang, Hyung M,Park, Young S,Lee, Dong H,Choe, Gheeyoung,Kim, Joo S,Jung, Hyun C,Song, In S Blackwell Publishing Asia 2009 Journal of gastroenterology and hepatology Vol.24 No.1

<P>Abstract</P><P>Background and Aim: </P><P>Gastric cancer is believed to develop by a multistage process. Intestinal metaplasia (IM) is regarded as a premalignant condition; it is classified into subtypes I, II and III. The aim of this study was to evaluate whether the subtypes of IM were associated with progression to gastric cancer.</P><P>Methods: </P><P>The study cohort consisted of 861 subjects, categorized as controls, gastric ulcers, dysplasia and cancer. The IM was scored histologically using the Sydney classification for the antrum and the body of the stomach. The biopsies were stained with high iron diamine and alcian blue (pH 2.5) (HID-AB2.5), and the IM was subtyped as I, II or III.</P><P>Results: </P><P>The proportion of IM subtypes I, II and III were 14.5%, 47.2% and 38.3% in the antrum, and 28.1%, 57.8% and 14.1% in the body of the stomach, respectively. These distributions did not show significant differences depending on disease or <I>Helicobacter pylori</I> positivity. In cases that were <I>H. pylori</I>-positive, the prevalence of IM subtype II in the cancer and dysplasia groups was higher than in the control group in the body of the stomach (<I>P</I> < 0.05). The proportion of IM subtype III in the antrum increased in proportion with age (<I>P</I> = 0.036).</P><P>Conclusions: </P><P>IM subtyping was not found to play a major role in the prediction of gastric cancer development in Korea. IM subtype III was associated with aging, and IM subtype II appeared to be related to gastric carcinogenesis in the presence of <I>H. pylori</I> infection.</P>

Comparative Analysis of Gastrointestinal Microbiota Between Normal and Caudal-Related Homeobox 2 (Cdx2) Transgenic Mice

( Hirotsugu Sakamoto ),( Takashi Asahara ),( Osamu Chonan ),( Norikatsu Yuki ),( Hiroyuki Mutoh ),( Shunji Hayashi ),( Hironori Yamamoto ),( Kentaro Sugano ) 대한장연구학회 2015 Intestinal Research Vol.13 No.1

Background/Aims: Caudal-related homeobox 2 (Cdx2) is expressed in the human intestinal metaplastic mucosa and induces intestinal metaplastic mucosa in the Cdx2 transgenic mouse stomach. Atrophic gastritis and intestinal metaplasia commonly lead to gastric achlorhydria, which predisposes the stomach to bacterial overgrowth. In the present study, we determined the differences in gut microbiota between normal and Cdx2 transgenic mice, using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Methods: Twelve normal (control) and 12 Cdx2 transgenic mice were sacrificed, and the gastric, jejunal, ileac, cecal and colonic mucosa, and feces were collected. To quantitate bacterial microbiota, we used real-time qRT-PCR with 16S rRNA gene-targeted, species-specific primers. Results: The total numbers of bacteria in the gastric, jejunal, ileac, cecal, and colonic mucosa of the Cdx2 transgenic mice were significantly higher than those of the normal mice. The Bacteroi-des fragilis group and also Prevotella were not detected in the stomach of the normal mice, although they were detected in the Cdx2 transgenic mice. Moreover, the Clostridium coccoides group, Clostridium leptum subgroup, Bacteroides fragilis group, and Prevotella were not detected in the jejunum or ileum of the normal mice, although they were detected in the Cdx2 transgenic mice. The fecal microbiota of the normal mice was similar to that of the Cdx2 transgenic mice. Conclusions: Our results showed the differences in composition of gut microbiota between normal and Cdx2 transgenic mice, which may be caused by the development of gastric achlorhydria and intestinal metaplasia in Cdx2 transgenic mice. (Intest Res 2015;13:39-49)