• Title/Summary/Keyword: Gastric adenoma

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Early Gastric Mucosal Cancer Associated with Synchronous Liver Metastasis (위 점막암에 동반된 간전이 1예)

  • Bong Sung-Joon;Jun Kyong-Hwa;Chin Hyung-Min;Cho Hyeon-Min;Won Yong-Sung;Park Woo-Bae
    • Journal of Gastric Cancer
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    • v.4 no.4
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    • pp.277-281
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    • 2004
  • Early gastric cancer (EGC) is defined as a carcinoma confined to the mucosa or submucosa of the stomach, with or without lymph-node metastasis. Synchronous liver metastasis is 5. $12.8\%$ in advanced gastric cancer, but is very low in EGC. A 64-year-old woman was admitted to St. Vincent's Hospital with a complaint of epigastric pain. Gastrofiberscopic examination showed a polypoid mass on the gastric antrum. Abdominal computed tomography demonstrated an intraluminal polypoid mass in the gastric antrum, but no tumor mass in the liver. A laparotomy revealed a solitary liver metastasis, we performed a distal partial gastrectomy with a group-2 lymph-node dissection and resection of metastatic liver tumor. Histologic examination showed a tubular adenoma with a focal carcinomatous change, Which was confined to the gastric mucosa and to the metastatic adenocarcinoma in the liver. We present a case of early gastric mucosal cancer associated with synchronous liver metastasis, along with a review of the literature.

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Clonality Assay of Dysplastic Epithelial Lesions of the Stomach (위 이형성 상피 병변의 클론성에 대한 분자병리학적 연구)

  • Choi Ho Soo;Kim Mi Sook;Park Jae Woo;Park Chang Soo;Kim Young-Jin;Juhng Sang-Woo
    • Journal of Gastric Cancer
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    • v.1 no.3
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    • pp.129-135
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    • 2001
  • Purpose: Dysplasia or flat adenoma of the stomach is regarded as a precancerous lesion. However, the frequency and the evolutionary process of malignant transformation of gastric dysplasia are still debated. In order to see whether the lesion was a monoclonal or a polyclonal proliferation, clonality was assayed by X-linked HUMARA polymorphism. Materials and Methods: DNA was extracted from the paraffin-embedded tissue of 16 consecutive cases of endoscopic biopsy, eight of which supplied both dysplastic and nondysplastic tissue for comparison. HUMARA was amplified by PCR with or without pretreatment with methylationsensitive restriction enzyme, HpaII. The amplification products were electrophoresed on polyacrylamide gel and silver-stained. Results: Among the 16 cases, 13 cases were informative and 3 cases noninformative. Of the 13 cases, one case showed skewed lyonization, rendering 12 cases to be analyzed further. A monoclonal band pattern was noted in 2 cases, and a polyclonal band pattern in 10 cases. A review of the histopathologies of the monoclonal and the polyclonal cases did not reveal features discriminating the two groups. Conclusion: These results suggest that gastric dysplasia is a disease entity heterogeneous in the genetic level, and many cases may be non-neoplastic.

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Endoscopic Findings and Treatment of Gastric Neoplasms in Familial Adenomatous Polyposis

  • Sato, Chihiro;Takahashi, Kazuya;Sato, Hiroki;Naruse, Takumi;Nakajima, Nao;Takatsuna, Masafumi;Mizuno, Ken-ichi;Hashimoto, Satoru;Takeuchi, Manabu;Yokoyama, Junji;Kobayashi, Masaaki;Terai, Shuji
    • Journal of Gastric Cancer
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    • v.22 no.4
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    • pp.381-394
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    • 2022
  • Purpose: Gastric neoplasia is a common manifestation of familial adenomatous polyposis (FAP). This study aimed to elucidate the clinical characteristics, endoscopic features including fundic gland polyposis (FGPsis), and treatment outcomes of gastric neoplasms (GNs) in patients with FAP. Materials and Methods: A total of 35 patients diagnosed with FAP, including nine patients from four pedigrees who underwent esophagogastroduodenoscopy (EGD), were investigated regarding patient characteristics, GN morphology, and treatment outcomes. Results: Twenty-one patients (60.0%) had 38 GNs; 33 (86.8%) and 5 (13.2%) were histologically diagnosed with adenocarcinoma and adenoma, respectively. There were no specific patient characteristics related to GNs.Nodule-type GNs were more prevalent in patients with FGP than without (52.2% vs. 0.0%, P=0.002) in the upper body of the stomach. Conversely, depressed-type GNs were fewer in patients with FGPsis than in those without (13.0% vs. 73.3%, P<0.001). Slightly elevated-type GNs were observed in both groups (34.8% vs. 20.0%, P=0.538). Even within pedigrees, the background gastric mucosa and types of GNs varied. In total, 24 GNs were treated with endoscopic submucosal dissection (ESD) and eight with endoscopic mucosal resection (EMR). EMR was selected for GNs with FGPsis because of the technical difficulty of ESD, resulting in a lower en bloc resection rate (62.5% vs. 100%, P=0.014). Conclusions: Our study indicates the necessity of routine EGD surveillance in patients diagnosed with FAP. Notably, the morphology and location of GNs differed between patients with and without FGPsis. Endoscopic treatment and outcomes require more attention in cases of FGPsis.

The Inhibitory Effect of Eupatilin on Helicobacter Pylori-Induced Release of Leukotriene $D_4$ in the Human Neutrophils and Gastric Mucosal Cells

  • Lee, Jung-Jin;Han, Bok-Gee;Kim, Mal-Nam;Chung, Myung-Hee
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.5
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    • pp.573-580
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    • 1997
  • In this report, the inhibitory action of eupatilin was investgated by using leukotriene $D_4$ in the human neutrophils and Kato III cells (Gastric adenoma cells as a substitute for gastric mucosal cells) stimulated by Helicobacter pylori. Leukotriene $D_4$ ($LTD_4$) was released from both neutrophils and Kato III cells when these cells were incubated with H. pylori. The release of $LTD_4$ increased time-dependently and the maximum release of $LTD_4$ was $2.3{\sim}2.5$ pmol. But in the presence of eupatilin, the release of $LTD_4$ from these cells was inhibited in a dose-dependent manner. In the neutrophils, the release of $LTD_4$ was suppressed to 70% and 50% of the control levels when neutrophils was incubated with 0.01 and 0.1 mM of eupatilin. In the Kato III cells, the release of $LTD_4$ was suppressed to 59% and 27% of the control levels by adding 0.01 and 0.1 mM of eupatilin. We estimated the intracellular $Ca^{2+}$ levels when Kato III cells and neutrophils were stimulated by H. pylori using $^{45}Ca$. But the suppressive effect of eupatilin on $Ca^{2+}$ influx into these cells was not significant. We also obtained the results that H. pylori induced $Ca^{2+}$ influx into these cells by confocal microscopy, however there was no differences in the dose level of eupatilin. These results were confirmed by 1H Nuclear Magnetic Resonance(NMR) spectroscopy. The NMR patterns of eupatilin in the absence of $Ca^{2+}$ was changed compare with when $Ca^{2+}$ was present, but its effect was not strong.

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Chemoprevention of Helicobacter pylori-associated Gastric Carcinogenesis in a Mouse Model; Is It Possible?

  • Hahm, Ki-Baik;Song, Young-Joon;Oh, Tae-Young;Lee, Jeong-Sang;Surh, Young-Joon;Kim, Young-Bae;Yoo, Byung-Moo;Kim, Jin-Hong;Ha, Sang-Uk;Nahm, Ki-Taik;Kim, Myung-Wook;Kim, Dae-Yong;Cho, Sung-Won
    • BMB Reports
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    • v.36 no.1
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    • pp.82-94
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    • 2003
  • Although debates still exist whether Helicobacter pylori infection is really class I carcinogen or not, H. pylori has been known to provoke precancerous lesions like gastric adenoma and chronic atrophic gastritis with intestinal metaplasia as well as gastric cancer. Chronic persistent, uncontrolled gastric inflammations are possible basis for ensuing gastric carcinogenesis and H. pylori infection increased COX-2 expressions, which might be the one of the mechanisms leading to gastric cancer. To know the implication of long-term treatment of antiinflammatory drugs, rebamipide or nimesulide, on H. pylori-associated gastric carcinogenesis, we infected C57BL/6 mice with H. pylori, especially after MNU administration to promote carcinogenesis and the effects of the long-term administration of rebamipide or nimesulide were evaluated. C57BL/6 mice were sacrificed 50 weeks after H. pylori infection. Colonization rates of H. pylori, degree of gastric inflammation and other pathological changes including atrophic gastritis and metaplasia, serum levels and mRNA transcripts of various mouse cytokines and chemokines, and NF-${\kappa}B$ binding activities, and finally the presence of gastric adenocarcinoma were compared between H. pylori infected group (HP), and H. pylori infected group administered with long-term rebamipide containing pellet diets (HPR) or nimesulide mixed pellets (HPN). Gastric mucosal expressions of ICAM-1, HCAM, MMP, and transcriptional regulations of NF-${\kappa}B$ binding were all significantly decreased in HPR group than in HP group. Multi-probe RNase protection assay showed the significantly decreased mRNA levels of apoptosis related genes and various cytokines genes like IFN-$\gamma$, RANTES, TNF-$\alpha$, TNFR p75, IL-$1{\beta}$ in HPR group. In the experiment designed to provoke gastric cancer through MNU treatment with H. pylori infection, the incidence of gastric carcinoma was not changed between HP and HPR group, but significantly decreased in HPN group, suggesting the chemoprevention of H. pylori-associated gastric carcinogenesis by COX-2 inhibition. Long-term administration of antiinflammatory drugs should be considered in the treatment of H. pylori since they showed the molecular and biologic advantages with possible chemopreventive effect against H. pylori-associated gastric carcinogenesis. If the final concrete proof showing the causal relationship between H. pylori infection and gastric carcinogenesis could be obtained, that will shed new light on chemoprevention of gastric cancer, that is, that gastric/cancer could be prevented through either the eradication of H. pylori or lessening the inflammation provoked by H. pylori infection in high risk group.

Differentiation between malignant and benign in terms of insurance claims (보험의학적 악성도평가)

  • Lee, Sinhyung
    • The Journal of the Korean life insurance medical association
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    • v.32 no.1
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    • pp.21-27
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    • 2013
  • In case of neoplasm claims, it is important to make a decision of differentiating malignant and benign. In Korean insurance market, there are many insurance products that cover cancer. In the insurance claims adjustment, differentiation between malignant and benign is according to histologic findings. However there are many neoplasms of bad clinical course in spite of benign histopathologic classification. In this article; astrocytoma, thymoma, gastrointestinal stromal tumor, colonic intramucosal carcinoma, gastric high grade adenoma/dysplasia, carcinoid tumor, MALT lymphoma, revision of Korean Classification of Disease-6th edition, and bladder tumors are reviewed in terms of differentiation between malignant and benign in the insurance claims. It may be helpful for claims staff to review important neoplasms in terms of differentiation between malignant and benign.

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The Effect of Rebamipide on Cellular Release of Leukotriene $B_4$ by Helicobacter Pylori (Helicobacter pylori에 의해 호중구 및 위점막 세포로부터 유도되는 Leukotriene $B_4$의 생성에 미치는 Rebamipide의 영향)

  • Lee, Jung-Jin;Han, Bok-Gee;Ro, Jai-Youl;Rhee, Kwang-Ho;Youn, Hee-Shang;Kim, Mal-Nam;Chung, Myung-Hee
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.6
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    • pp.825-830
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    • 1997
  • Leukotrienes(LTs) are hewn to act as a mediator provoking tissue response in inflammation. This finding implicates that LTs also play important roles in the pathogenesis of H, pylori-induced gastritis and gastric ulceration. Rebamipide is being currently used as a therapeutics for gastritis and peptic ulcer, but their mechanisms of action have not been known clearly yet. One possibility is that their therapeutic effects are ascribed to interfering with the H. pylori-induced release of LTs from neutrophils and gastric mucosal cells. In the present study, this possibility was tested using $LTB_4$ as the test material in human neutrophils and Kato III cells(gastric adenoma cells as a substitute for gastric mucosal cells). The release of $LTB_4$ from both neutrophils and Kato III cells was time and H. pylori-dose dependent. The maximum release of $LTB_4$ was induced by neutrophils and Kato III cells when these cells incubated with H. pylori $(4.8{\times}10^8\;cells/ml$ for 30min. But in the presence of rebamipide the release of $LTB_4$ from these cells was suppressed in dose dependent manners. The release was completely suppressed at 1.0 mM of rebamipide in neutrophils and 2.0 mM of this drug in Kato III cells, respectively. We also obtained the results that the release of $LTB_4$ was induced by A23187$(Ca^{2+}\;ionophore)$ and the A23187-induced release was also inhibited by rebamipide. It seems that the machanism of action of rebamipide is through its interaction with the level of intracellular $Ca^{2+}$. In view of the roles of $LTB_4$ in inflammatory reaction and the roles of H. pylori in gastritis and peptic ulcer, the effects of this drug observed in this study may contribute to their therapeutic action in these gastric disorders.

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BRUNNER'S GLAND ADENOMA - Case report, and review of etiopathogenesis and clinical features - (Brunner 씨 선종 - 임상증례 및 임상상적 문헌고찰 -)

  • Lee, Kyung-Chul
    • Journal of Yeungnam Medical Science
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    • v.2 no.1
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    • pp.265-269
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    • 1985
  • Brunner's glands of the duodenum rarely develop proliferative lesions, occasionally in association with gastric hyperchlorhydria or chronic pancreatitis. The clinical presentation can vary from vague upper abdominal symptoms with dyspepsia and nausea to diarrhea, jaundice, obstruction and gastrointestinal bleeding. The diagnosis is usually made by radiological studies followed by upper endoscopy which can also provide definitive treatment. At times surgery is necessary for adequate removal of these lesions, as in the case herein described.

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Upper Gastrointestinal Tract Polyps: What Do We Know About Them?

  • Buyukasik, Kenan;Sevinc, Mert Mahsuni;Gunduz, Umut Riza;Ari, Aziz;Gurbulak, Bunyamin;Toros, Ahmet Burak;Bektas, Hasan
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.7
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    • pp.2999-3001
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    • 2015
  • Background: This study aimed to evaluate upper gastrointestinal polyps detected during esophago-gastroduodenoscopy tests. Materials and Methods: We conducted a retrospective analysis on data regarding 55,987 upper gastrointestinal endoscopy tests performed at the endoscopy unit of Istanbul Education and Research Hospital between January 2006 and June 2012. Results: A total of 66 upper gastrointestinal polyps from 59 patients were analyzed. The most common clinical symptom was dyspepsia, observed in 41 cases (69.5%). The localizations of the polyps were as follows: 29 in the antrum (43.9%), 15 in the corpus (22.7%), 11 in the cardia (16.7%), 3 in the fundus (4.54%), 3 in the second portion of the duodenum (4.54%), 2 in the bulbus (3.03%) and 3 in the lower end of the esophagus (4.54%). Histopathological types of polyps included hyperplastic polyps (44) (66.7%), faveolar hyperplasia (8) (12.1%), fundic gland polyps (4) (6.06%), squamous cell polyps (4) (6.06%), hamartomatous polyps (3) (4.54%), and pyloric gland adenoma (3) (4.54%). Histopathological analysis of the gastric mucosa showed chronic atrophic gastritis in 30 cases (50.84%), HP infection in 33 cases (55.9%) and intestinal metaplasia in 19 cases (32.20%). In 3 cases with multiple polyps, adenocarcinoma was detected in hyperplastic polyps. Conclusions: Among polypoid lesions of the upper gastrointestinal tract, the most common histological type is hyperplastic polyps. Generally, HP infection is associated with chronic atrophic gastritis and intestinal metaplasia. The incidence of adenocarcinoma tends to be higher in patients with multiple hyperplastic polyps.