Endoscopic submucosal dissection for gastrointestinal neoplasms

Kakushima, Naomi; Fujishiro, Mitsuhiro

doi:10.3748/wjg.14.2962

Cited by 160 publications

(149 citation statements)

References 57 publications

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“…The identification of useful markers of GC risk is thus hoped for. Evaluating HPrelated chronic gastritis and determining which subjects are at high risk for developing GC is very important, and would likely increase the efficacy of GC screening by endoscopic or other examinations (Enomoto et al, 2010a;Mukoubayashi et al, 2007;Ohata et al, 2005), and strategic approaches to metachronous multiple GC after endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) performed as minimally invasive treatment for early GC (Gotoda, 2007;Kakushima & Fujishiro, 2008;Nakajima et al, 2006). In addition, in terms of GC prevention, it has become clear that HP-related chronic gastritis cannot be ignored as an origin of carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

Gastric Cancer Risk Diagnosis and Prevention in Subjects with Helicobacter pylori-related Chronic Gastritis

Enomoto¹,

Watanabe²,

Mukoubayashi³

et al. 2011

Gastritis and Gastric Cancer - New Insights in Gastroprotection, Diagnosis and Treatments

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GC risk diagnosis based on the natural history of HP-related chronic gastritisNovel risk markers to identify GC high-risk groups based on a detailed natural history of HP-related chronic gastritis have long been awaited. In this section, we discuss the emerging significance of serum PG as a GC risk marker for more precise identification of GC high-risk groups. Serum PG testHP-related chronic gastritis usually starts in the antrum and expands proximally towards the body of the stomach (Kimura, 1972;Tatsuta et al., 1973). As several studies dealing with endoscopic biopsies or chromoendoscopic testing have found that progression of chronic atrophic gastritis (CAG) increases the risk of cancer (Meister et al., 1979;Sipponen et al., 1985;Siurala et al., 1966;Tatsuta et al., 1993;Testoni et al., 1987), accurate and reliable evaluation of the extent of CAG is considered important for identifying individuals at high risk of cancer. However, accurately diagnosing the extent of CAG based on a few biopsy samples is difficult, because CAG together with intestinal metaplasia is a multifocal process. Furthermore, histological diagnosis of gastric atrophy depends on subjective judgment without a gold standard (Guarner et al., 1999;Plummer et al., 1997). A test for CAG progression that is more convenient, free of discomfort or risk, economical and based on objective parameters is needed. PG is the inactive precursor of pepsin, a digestive enzyme specifically produced in the stomach. Immunologically, two isozymes exist (Kageyama, 2003). PGI is produced by chief cells and mucus neck cells of the gastric fundic glands. In contrast, PGII is produced not only by chief cells and mucus neck cells, but also in cardiac glands, pyloric glands, and Brunner's glands, with localization of producing cells in a wide range from the stomach to the duodenum. The majority of PG produced (about 99%) is secreted in the stomach lumen and functions as a digestive enzyme. However, a small amount of PG (about 1%) is also present in blood and can be evaluated by measuring serum PG levels. Serum PG levels are generally agreed to reflect the morphological and functional status of the stomach mucosa (Hirschowitz, 1957;Samloff et al., 1982). In an endoscopic study with Congo red staining, we have shown a strong correlation between an increase in glandular boundary, associated with diagnosed progression of gastric mucosal atrophy, and stepwise reductions in serum PGI levels and the PGI/PGII ratio ( Fig. 1) (Miki et al., 1987). In other words, by measuring serum PGI and the PGI/II ratio, the progression of CAG, which is involved in GC carcinogenesis, can be objectively evaluated (Ichinose et al., 2001). In addition, during HP infection, serum PGI and PGII increase, and the PG I/II ratio decreases. These findings are improved after eradication treatment (Furuta et al., 1997) and are useful as gastric mucosal inflammatory markers. Several criteria are used in the serum PG test. As criteria for GC screening, the combination of PGI ≤70 ng/ml and PGI/II ratio ≤3.0...

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Section: Introductionmentioning

confidence: 99%

Gastric Cancer Risk Diagnosis and Prevention in Subjects with Helicobacter pylori-related Chronic Gastritis

Enomoto¹,

Watanabe²,

Mukoubayashi³

et al. 2011

Gastritis and Gastric Cancer - New Insights in Gastroprotection, Diagnosis and Treatments

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“…However, early gastric cancer is defined as adenocarcinoma confined to the mucosa or submucosa of the stomach and can be treated using endoscopic submucosal dissection (ESD), which is an advanced therapeutic technique that can offer extremely promising outcomes. 11,12 Examination of miRNA expression profiles has revealed that specific miRNAs are aberrantly expressed in various human cancers.…”

mentioning

confidence: 99%

The tumor suppressor microRNA‐29c is downregulated and restored by celecoxib in human gastric cancer cells

Saito

Suzuki

Imaeda

et al. 2012

Intl Journal of Cancer

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MicroRNAs (miRNAs) are small noncoding RNAs that function as endogenous silencers of target genes and play critical roles during carcinogenesis. The selective cyclooxygenase-2 (COX-2) inhibitor celecoxib has been highlighted as a potential drug for treatment of gastrointestinal tumors. The aim of this study was to investigate the role of miRNAs in gastric carcinogenesis and the feasibility of a new therapeutic approach for gastric cancer. miRNA expression profiles were examined in 53 gastric tumors including gastric adenomas (atypical epithelia), early gastric cancers and advanced gastric cancers and in gastric cancer cells treated with celecoxib. miRNA microarray analysis revealed that miR-29c was significantly downregulated in gastric cancer tissues relative to nontumor gastric mucosae. miR-29c was significantly activated by celecoxib in gastric cancer cells. Downregulation of miR-29c was associated with progression of gastric cancer and was more prominent in advanced gastric cancers than in gastric adenomas and early gastric cancer. In addition, expression of the oncogene Mcl-1, a target of miR-29c, was significantly increased in gastric cancer tissues relative to nontumor gastric mucosae. Activation of miR-29c by celecoxib induced suppression of Mcl-1 and apoptosis in gastric cancer cells. These results suggest that downregulation of the tumor suppressor miR-29c plays critical roles in the progression of gastric cancer. Selective COX-2 inhibitors may have clinical promise for the treatment of gastric cancer via restoration of miR-29c.

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“…The overall incidence of bleeding and perforation with ESD is 11% and 6% respectively [32][33][34]. Due to the widespread acceptance of gastric and oesophageal ESDs, the number of medical facilities that perform colorectal ESDs grew in recent years [35,36].…”

Section: Endoscopic Mucosal Resection (Emr)/endoscopic Submucosal Dismentioning

confidence: 99%

“…Patients with upper GI resection of tumoral lesions should be treated with intravenous PPI as for Forrest IIa ulcers [5]: High-dose PPI therapy improves healing rates and reduces the risk of delayed bleeding [33]. There are small successful series of over-the-scope-clips (OTSC) use in acute GI bleeding unresponsive to conventional methods, which is becoming a consistent approach [87].…”

Section: Haemorrhagementioning

confidence: 99%

Emergencies after endoscopic procedures

Rolanda

Caetano

Dinis-Ribeiro

2013

Best Practice & Research Clinical Gastroenterology

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Keywords:GI endoscopy adverse events GI emergencies Bleeding Haemorrhage Perforation Infection Embolization Diagnosis and management of severe complications a b s t r a c t Endoscopy adverse events (AEs), or complications, are a rising concern on the quality of endoscopic care, given the technical advances and the crescent complexity of therapeutic procedures, over the entire gastrointestinal and bilio-pancreatic tract. In a small percentage, not established, there can be real emergency conditions, as perforation, severe bleeding, embolization or infection. Distinct variables interfere in its occurrence, although, the awareness of the operator for their potential, early recognition, and local organized facilities for immediate handling, makes all the difference in the subsequent outcome. This review outlines general AEs' frequencies, important predisposing factors and putative prophylactic measures for specific procedures (from conventional endoscopy to endoscopic cholangio-pancreatography and ultrasonography), with comprehensive approaches to the management of emergent bleeding and perforation.

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Endoscopic submucosal dissection for gastrointestinal neoplasms

Cited by 160 publications

References 57 publications

Gastric Cancer Risk Diagnosis and Prevention in Subjects with Helicobacter pylori-related Chronic Gastritis

Gastric Cancer Risk Diagnosis and Prevention in Subjects with Helicobacter pylori-related Chronic Gastritis

The tumor suppressor microRNA‐29c is downregulated and restored by celecoxib in human gastric cancer cells

Emergencies after endoscopic procedures

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