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Objectives: Long‐term outcomes of gastric subepithelial lesions have not been elucidated. To reveal the natural history, we initiated a prospective, 10‐year follow‐up of patients with small (≤20 mm) gastric subepithelial lesions in September 2014. Here, we report the results of an interim analysis of a prospective observational study. Methods: In total, 567 patients with 610 lesions were prospectively registered between September 2014 and August 2016. The location, size, morphology, and number of subepithelial lesions were recorded on a web‐based case report form. This study has been conducted as an Academic Committee Working Group of the Japan Gastroenterological Endoscopy Society. Results: The endoscopic follow‐up period was 4.60 ± 1.73 years (mean ± standard deviation), and survival data were investigated for 5.28 ± 1.68 years. This interim analysis revealed that the estimated cumulative incidence of a size increase ≥5 mm, after accounting for patients' death and resection of the tumor as competing risk events, was 4.5% at 5 years. In addition, the estimated cumulative incidence of lesion size increase ≥5 mm or resection of lesions was 7.9% at 5 years, and that of size increase ≥10 mm or resection of lesions was 4.5% at 5 years. Conclusion: These results indicate that approximately one in 13 patients with small (≤20 mm) gastric subepithelial lesions may require resection or further investigation for increased tumor size (≥5 mm) within 5 years. [ABSTRACT FROM AUTHOR]

Background and Aim: Anticoagulant users with nonvalvular atrial fibrillation (NVAF) sometimes suffer from gastrointestinal bleeding (GIB) and have difficulty continuing the medication. Left atrial appendage closure (LAAC) has been developed for such situations. We aimed to clarify the clinical significance of a history of GIB in comparison to other factors in patients who had undergone LAAC. Methods: From October 2019 to September 2023, patients with NVAF who underwent LAAC at our hospital were enrolled. We investigated the percentage of patients with a history of GIB who underwent LAAC and compared the incidence of post‐LAAC bleeding in these patients compared to those with other factors. Results: A total of 45 patients were included. There were 19 patients (42%) with a history of GIB who underwent LAAC. In a Kaplan–Meier analysis, the cumulative incidence of bleeding complications after LAAC was significantly higher in patients with a history of GIB in comparison to patients with other factors. There were eight cases of post‐LAAC bleeding in total, and seven cases had GIB. Conclusions: We need to recognize that GIB is a significant complication in patients who undergo LAAC. The management of GIB by gastroenterologists is essential to the success of LAAC. [ABSTRACT FROM AUTHOR]

Background and Aim Methods Results Conclusions The 2017 Japanese guidelines recommend continuing warfarin therapy during the perioperative period or discontinuing direct oral anticoagulants (DOACs) only on the day of endoscopic submucosal dissection for early gastric cancer. However, their safety has not been sufficiently explored. This study aimed to validate this management method.This retrospective, multicenter study analyzed the characteristics and outcomes of patients who underwent gastric endoscopic submucosal dissection between July 2017 and June 2019. The patients were categorized according to the use of warfarin or DOACs.Among the 62 eligible patients, 53 (85%) were male (median age, 76 years). Warfarin was used in 10 patients (16%) and DOACs in 52 patients (84%). Fourteen patients taking DOACs (27%) used concomitant antiplatelet agents, with seven patients (13%) continuing treatment at the time of the endoscopic procedure. No postprocedural bleeding occurred in patients receiving warfarin (0%), whereas 10 cases (19%) of bleeding occurred in patients receiving DOACs: rivaroxaban, 0% (0/22); dabigatran, 0% (0/2); edoxaban, 43% (6/14); and apixaban, 29% (4/14). The type of anticoagulant (P < 0.01) and continuation of antiplatelet therapy (P = 0.02) were risk factors for postprocedural bleeding in patients receiving DOACs. Intraprocedural bleeding requiring transfusion or symptomatic thromboembolic events were not reported.Continuous warfarin therapy is preferred. DOAC withdrawal 1 day before a procedure is associated with a high bleeding rate, which may differ for different types of anticoagulants. The continuation of antiplatelet medications in patients receiving DOACs carries a high risk of bleeding and is a future challenge. [ABSTRACT FROM AUTHOR]

Abstract: A 72‐year‐old Japanese woman presented with a fever, diarrhea, intermittent spotting, and constant fluid discharge from the vagina. Imaging studies revealed an enterovaginal fistula. She underwent radical hysterectomy and radiotherapy 35 years previously. She also had a surgical history of nephrostomy, nephrectomy, ileoascending anastomosis, and colostomy. As bleeding from the enterovaginal fistula was uncontrollable, ileocecal resection was performed. However, a colovesical fistula with urinary tract infection occurred 3 months later. The present case indicates that fistula formation occurs and causes various symptoms in patients who underwent postpelvic radiotherapy, particularly in those with prior surgeries in the irradiated field. [ABSTRACT FROM AUTHOR]

Abstract: Background and Aim: The safety of gastric endoscopic submucosal dissection (ESD) in the antithrombotic drug users remains controversial. Methods: Patients who underwent gastric ESD at Okayama University Hospital between March 2006 and February 2016 were enrolled. This study investigated the risk of post‐ESD bleeding according to the management of the antithrombotic drugs. Results: One thousand twenty lesions (872 patients) were enrolled. In a multivariate analysis, heparin replacement (odds ratio [OR] 5.0, 95% confidence interval [CI] 1.8–14), multiple antithrombotic drug use (OR 2.9, 95% CI 1.1–6.9), a resected specimen of ≥ 33 mm in diameter (OR 2.7, 95% CI 1.5–5.4), Helicobacter pylori negativity (OR 2.2, 95% CI 1.3–3.7), and tumors located in the lower third of the stomach (OR 1.7, 95% CI 1.0–2.9) were significant risk factors for post‐ESD bleeding, while the continuation of aspirin or cilostazol was not (OR 2.6, 95% CI 0.72–7.8). The bleeding rate of the continuation group was comparable with that of the all cessation group among single antithrombotic drug users (4.5% vs 4.4%, P = 1.0); however, the rate of the continuation group was significantly higher than that of the all cessation group among multiple antithrombotic drug users (67% vs 15%, P = 0.020). Conclusions: The risk of post‐ESD bleeding differed according to the management of the antithrombotic drugs. The gastric ESD under the cessation or continuation of aspirin or cilostazol monotherapy was acceptable. However, multiple antithrombotic drug use or heparin replacement was associated with a higher risk of post‐ESD bleeding. [ABSTRACT FROM AUTHOR]

The gastrointestinal (GI) tract is the most commonly involved site of extranodal follicular lymphoma (FL). GI-FL shows very indolent clinical behavior and localized at GI tract without any progression or transformation compared to nodal FL. The most frequently involved site of the GI tract was the duodenum followed by the jejunum and ileum, and only 15% of FL arising in the second part of the duodenum were localized there without scattered very small daughter lesions in other GI tract examined by double-balloon endoscopy. The typical macroscopic appearance of GI-FL was multiple white nodules. Microscopically, neoplastic cells were small- to medium-sized lymphoid cells and formed neoplastic follicles. Most of the cases (>95%) were histologically Grade 1 to 2 (low grade). Several pathological and molecular characteristics were seen in GI-FL (especially duodenal FL) compared with nodal FL: immunoglobulin heavy chain deviation to VH4 and VH5; memory B-cell immunophenotype; and molecular features shared by mucosa-associated lymphoid tissue lymphoma. Considering the pathological and molecular uniqueness of this disease, GI-FL should be separately managed from nodal FL. [ABSTRACT FROM AUTHOR]

In this patient, the large hyperplastic polyps and swollen fundic gland polyps in the stomach prompted vonoprazan discontinuation, resulting in significant gastric polyps regression. A gastric hyperplastic polyp (A, arrow, same polyp in Figure 1) and fundic gland polyps (A, arrowhead) are seen. Keywords: esophagogastroduodenoscopy; fundic gland polyp; hyperplastic polyp EN esophagogastroduodenoscopy fundic gland polyp hyperplastic polyp 358 359 2 09/07/22 20220901 NES 220901 Esophagogastroduodenoscopic examination shows a large, reddish polyp in the gastric cardia. [Extracted from the article]

Background and Aim Reduced expression in immortalized cells (REIC)/dickkopf-3 (Dkk-3) is a tumor suppressor gene that is downregulated in various cancers. In our previous study of prostate cancer, the REIC/Dkk-3-expressing adenoviral vector (Ad-REIC) was found to induce cancer-selective apoptosis. This study recently developed a novel super gene expression (SGE) system and used this system to re-construct an Ad-REIC vector, termed the Ad-SGE-REIC, to achieve more effective therapeutic outcomes. In this study, the therapeutic effects of Ad-SGE-REIC on hepatocellular carcinoma (HCC) was assessed. Methods Human HCC cell lines (HLE, Huh7, HepG2, HLF, SK-Hep1, and PLC), human HCC tissues, and mouse HCC cell line (Hepa1-6) were used in this study. REIC/Dkk-3 expression was assessed by immunoblotting and immunohistochemistry. The relative cell viability and the apoptotic effect were examined in vitro, and the anti-tumor effects of Ad-SGE-REIC treatment were analyzed in the mouse xenograft model. This study additionally assessed anti-tumor immunological effects on the immunocompetent mice. Results REIC/Dkk-3 expression was decreased in HCC cell lines and HCC tissues. Ad-SGE-REIC reduced cell viability and induced apoptosis in HCC cell lines (HLE and Huh7), inhibited tumor growth in the mouse xenograft model, and demonstrated in vivo anti-cancer immunostimulatory effects on the HCC cell line (Hepa1-6). Conclusions Ad-SGE-REIC treatment not only enhanced cell killing effects in vitro but also elicited significant therapeutic effects, with tumor growth suppression, in vivo. REIC/Dkk-3 gene therapy using Ad-SGE-REIC potentially represents an innovative new therapeutic tool for HCC. [ABSTRACT FROM AUTHOR]

Follicular lymphoma ( FL) shows co-expression of B-cell lymphoma 2 ( BCL2) and CD10, whereas downexpression of CD10 is occasionally experienced in gastrointestinal ( GI) FL with unknown significance. Gastrointestinal FL is a rare variant of FL, and its similarity with mucosa-associated lymphoid tissue lymphoma was reported. We investigated the clinicopathological and genetic features of CD10 downexpressed ( CD10down) GI- FL. The diagnosis of CD10down FL was carried out with a combination of pathological and molecular analyses. The incidence of CD10down GI- FL was shown in 35/172 (20.3%) cases, which was more frequent than nodal FL (3.5%, P < 0.001). The difference was additionally significant between GI- FL and nodal FL when the analysis was confined to primary GI- FL (55.2% vs 3.5%, P < 0.001). Compared to CD10+ GI- FL, CD10down GI- FL significantly involved the stomach or large intestine ( P = 0.015), and additionally showed the downexpression of BCL6 ( P < 0.001). The follicular dendritic cell meshwork often showed a duodenal pattern in the CD10down group ( P = 0.12). Furthermore, a lymphoepithelial lesion was observed in 5/12 (40%) gastric FL cases, which indicated caution in the differentiation of mucosa-associated lymphoid tissue lymphoma. Molecular analyses were undertaken in seven cases of CD10down GI- FL, and an identical clone was found between CD10down follicles and CD10+ BCL2+ neoplastic follicles. In the diagnosis of cases with CD10down BCL2+ follicles, careful examination with molecular studies should be carried out. [ABSTRACT FROM AUTHOR]

The gastrointestinal (GI) tract is the most common primary site of extranodal diffuse large B-cell lymphoma (DLBCL), with approximately one-third of extranodal DLBCL occurring in the GI tract. We investigated the clinicopathological features and immunohistochemically-assessed cell-of-origin of 49 GI DLBCL cases (stomach, 24; small intestine, 10; colon, 15) and also examined the presence of MYD88 L265P as recently this mutation has been frequently identified in ABC-like DLBCL, particularly in extranodal sites. Small intestinal DLBCL was characterized by the preponderance of women ( P = 0.041) and elevated LDH ( P = 0.002) and soluble interleukin-2 receptor ( P = 0.033). Small intestinal DLBCL more frequently showed anemia ( P = 0.031) and elevated CRP ( P = 0.029) than gastric DLBCL. ABC-like phenotype was seen in 71.4 % cases (stomach, 79 %; small intestine, 70 %; colon, 60 %). MYD88 L265P was detected in 6.1 % cases; all were primary gastric DLBCL with ABC-like phenotype but had no distinct clinicopathological features. In conclusion, GI DLBCL had different clinicopathological features according to the primary site especially in the small intestine. Also, MYD88 L265P had little involvement in GI DLBCL compared with other extranodal DLBCLs, suggesting that its pathogenesis might be different from that of organs with a high frequency of MYD88 L265P. [ABSTRACT FROM AUTHOR]

Background and Aim Reduced expression in immortalized cells/dickkopf-3 (REIC/DKK3) is a reported tumor suppressor gene and has potential to become an innovative therapy for various cancers. We examined the antitumor immunological effects of human REIC/DKK3 protein against pancreatic cancer. Methods Activation of extracellular signal-regulated kinases 1 and 2, mammalian target of rapamycin, and signal transducer and activator of transcription 3 by REIC/DKK3 protein was assessed in human peripheral blood mononuclear cells using immunoblotting. Pancreatic cancer cell lines (AsPC-1 and MIA Paca-2) were cocultured with peripheral blood mononuclear cells, and the anticancer effects of REIC/DKK3 protein were assessed using the methyl thiazole tetrazolium, cytotoxicity, and enzyme-linked immunospot assays. The antitumor immunological effects of the combined treatment with REIC/DKK3 protein and peripheral blood mononuclear cells were also assessed in a pancreatic cancer model using non-obese diabetic/severe combined immunodeficiency mice. Results The REIC/DKK3 protein activated extracellular signal-regulated kinases 1 and 2, mammalian target of rapamycin, and signal transducer and activator of transcription 3 in peripheral blood mononuclear cells. REIC/DKK3 protein inhibited in vitro cancer cell viability and enhanced cytotoxicity when incubated with peripheral blood mononuclear cells. REIC/DKK3 protein induced significant production of interferon gamma from lymphocytes incubated with pancreatic cancer cells, indicating that CD8+ T cells were activated in the peripheral blood mononuclear cells when cocultured with AsPC-1 and MIA Paca-2 in the presence of REIC/DKK3 protein. Combined treatment with REIC/DKK3 protein and peripheral blood mononuclear cells produced in vivo anticancer immunostimulatory effects on pancreatic cancer cells. Conclusions The REIC/DKK3 protein and peripheral blood mononuclear cells synergistically enhanced anticancer immunological effects against pancreatic cancer cells. The observed immunomodulatory effect of combined treatment likely occurs in adenovirus-mediated REIC/DKK3 gene therapy and provides important clues to the therapeutic mechanisms involving immune cells. [ABSTRACT FROM AUTHOR]

Background and Aim The reduced expression in immortalized cells REIC/the dickkopf 3 ( Dkk-3) gene, tumor suppressor gene, is downregulated in various malignant tumors. In a prostate cancer study, an adenovirus vector carrying the REIC/ Dkk-3 gene ( Ad-REIC) induces apoptosis. In the current study, we examined the effects of REIC/ Dkk-3 gene therapy in pancreatic cancer. Methods REIC/ Dkk-3 expression was assessed by immunoblotting and immunohistochemistry in the pancreatic cancer cell lines ( ASPC1, MIAPaCa2, Panc1, BxPC3, SUIT-2, KLM1, and T3M4) and pancreatic cancer tissues. The Ad-REIC agent was used to investigate the apoptotic effect in vitro and antitumor effects in vivo. We also assessed the therapeutic effects of Ad-REIC therapy with gemcitabine. Results The REIC/ Dkk-3 expression was lost in the pancreatic cancer cell lines and decreased in pancreatic cancer tissues. Ad-REIC induced apoptosis and inhibited cell growth in the ASPC1 and MIAPaCa2 lines in vitro, and Ad-REIC inhibited tumor growth in the mouse xenograft model using ASPC1 cells. The antitumor effect was further enhanced in combination with gemcitabine. This synergistic effect may be caused by the suppression of autophagy via the enhancement of mammalian target of rapamycin signaling. Conclusions Ad-REIC induces apoptosis and inhibits tumor growth in pancreatic cancer cell lines. REIC/ Dkk-3 gene therapy is an attractive therapeutic tool for pancreatic cancer. [ABSTRACT FROM AUTHOR]

Follicular lymphoma ( FL) of the gastrointestinal tract, particularly duodenal follicular lymphoma ( DFL), is a rare variant of FL with indolent clinical behavior, and this disease is included in the 2008 World Health Organization classification system. In contrast to nodal follicular lymphoma ( NFL), DFL occurs most frequently in the second part of the duodenum, lacks follicular dendritic cell meshworks and has memory B-cell characteristics. However, its molecular pathogenesis is still unclear. In the present study, we examined 10 DFL, 18 NFL and 10 gastric MALT lymphoma samples using gene expression analysis. Quantitative RT- PCR experiments and immunohistochemical analysis for 72 formalin-fixed, paraffin-embedded tissues from an independent series, including 32 DFL, 19 gastric MALT lymphoma and 27 NFL samples, were performed for validation of microarray data. Gene expression profiles of the three lymphoma types were compared using 2918 differentially expressed genes ( DEG) and results suggested that DFL shares characteristics of MALT lymphoma. Among these DEG, CCL20 and MAd CAM-1 were upregulated in DFL and MALT but downregulated in NFL. In contrast, protocadherin gamma subfamily genes were upregulated in DFL and NFL. Quantitative RT- PCR and immunohistochemical studies demonstrated concordant results. Double immunofluorescence studies revealed that CCL20 and CCR6 were co-expressed in both DFL and MALT. We hypothesize that increased expression of CCL20 and MAd CAM-1 and co-expression of CCL20 and CCR6 may play an important role in tumorigenesis. [ABSTRACT FROM AUTHOR]

Background & Aim: Runt‐related transcription factor 3 (RUNX3) is a tumor suppressor gene that is expressed in gastric and other cancers including pancreatic cancer. However, the precise function of RUNX3 in pancreatic cancer has not been fully elucidated. In this study, we aimed to determine the effect of decreased RUNX3 expression in pancreatic cancer. Methods: This study included 36 patients with primary pancreatic cancer, who had undergone pancreaticoduodenectomy. All patients were treated with 1000 mg/m2 gemcitabine after the surgery. The pancreatic cancer cell lines PANC‐1, MIAPaCa‐2, BxPC‐3, SUIT‐2, and KLM‐1 were used for immunoblotting analysis of RUNX3 and multidrug resistance protein (MRP) expressions. Ectopic RUNX3 expression was achieved by cDNA transfection of the cells, and small interfering RNA (siRNA) against RUNX3 was used to knock down endogenous RUNX3. Cell growth in the presence of gemcitabine was assessed using the MTT assay. Results: Patients with RUNX3‐positive and RUNX3‐negative pancreatic cancer had a median survival of 1006 and 643 days, respectively. Exogenous RUNX3 expression reduced the expression of MRP1, MRP2, and MRP5 in endogenous RUNX3‐negative cells, whereas RUNX3 siRNA increased the expressions of these genes in endogenous RUNX3‐positive cells. Exogenous RUNX3 expression decreased gemcitabine IC50 in RUNX3‐negative cells. Conclusion: Loss of RUNX3 expression contributes to gemcitabine resistance by inducing MRP expression, thereby resulting in poor patient survival. Highlights: We categorized pancreatic cancer into 2 groups by RUNX3 expression.We defined the staining grade as low or high by using 30% staining area as cutoff.The prognosis was significantly poor in RUNX3‐negative subjects.RUNX3 protein expression reduced the expression of multidrug‐resistant proteins.RUNX3 expression increased gemcitabine sensitivity in pancreatic cancer cells. [ABSTRACT FROM AUTHOR]

Loss or decreased expression of runt-related transcription factor 3 (RUNX3), a tumor suppressor gene involved in gastric and other cancers, has been frequently observed in hepatocellular carcinoma (HCC). The objective of this study was to identify the regulatory mechanism of the epithelial-mesenchymal transition (EMT) by RUNX3 in HCC. Human HCC cell lines, Hep3B, Huh7, HLF and SK-Hep1, were divided into low- and high-EMT lines, based on their expression of TWIST1 and SNAI2, and were used in this in vitro study. Ectopic RUNX3 expression had an anti-EMT effect in low-EMT HCC cell lines characterized by increased E-cadherin expression and decreased N-cadherin and vimentin expression. RUNX3 expression has previously been reported to reduce jagged-1 (JAG1) expression; therefore, JAG1 ligand peptide was used to reinduce EMT in RUNX3-expressing low-EMT HCC cells. Immunohistochemical analyses were performed for RUNX3, E-cadherin, N-cadherin and TWIST1 in 33 human HCC tissues, also divided into low- and high-EMT HCC, based on TWIST1 expression. E-cadherin expression was correlated positively and N-cadherin expression was correlated negatively with RUNX3 expression in low-EMT HCC tissues. Correlations between EMT markers and RUNX3 mRNA expression were analyzed using Oncomine datasets. Similarly, mRNA expression of E-cadherin was also significantly correlated with that of RUNX3 in low-EMT HCC, while mRNA expression of JAG1 was negatively correlated with that of RUNX3. These results suggest a novel mechanism by which loss or decreased expression of RUNX3 induces EMT via induction of JAG1 expression in low-EMT HCC. [ABSTRACT FROM AUTHOR]

Background and Aim: Hepatocellular carcinoma (HCC) is a hypervascular tumor, and angiogenesis plays an important role in its development. Previously, we demonstrated that des-γ-carboxyl prothrombin (DCP) promotes both cell proliferation and migration of human umbilical vein endothelial cells (HUVECs) by inducing the autophosphorylation of kinase insert domain receptor (KDR). In the present study, DCP-associated tumor angiogenesis was assessed by comparing hypovascular and common hypervascular HCC. Methods: The solitary HCCs of 827 patients were classified into two groups according to the tumor density at the arterial phase of a dynamic computed tomography scan; the initial clinical data of patients with the hyper- and hypovascular types were compared. The HCC tissues from 95 tumors were analyzed by immunohistochemical staining for DCP and phosphorylated KDR, and intratumoral microvessel density (MVD) was analyzed to evaluate microvessel angiogenesis. Results: The serum DCP levels (320 ± 3532 mAU/mL) and tumor size (18.4 ± 9.0 mm) of patients with hypervascular HCC were significantly greater than those with hypovascular HCC (38.7 ± 80 mAU/mL and 14.6 ± 5.2 mm, P < 0.001). Immunohistochemical analysis revealed that the expressions of DCP and phospho-KDR were significantly greater in hypervascular HCC (71.4% and 31.0%, respectively) than in hypovascular HCC (7.6% and 5.7%, respectively). Intratumoral MVD was significantly correlated with DCP (r = 0.48, P < 0.0001). Conclusions: des-γ-carboxyl prothrombin production is associated with tumor angiogenesis in HCC. [ABSTRACT FROM AUTHOR]

Patients with malignant pancreatobiliary neoplasm sometimes manifest duodenal obstruction and biliary stricture synchronously or metachronously. In this paper, we reviewed our experience with and technique for combined endoscopic duodenal stent placement and endoscopic ultrasonography (EUS)-guided biliary drainage. Between May 2007 and September 2009, this combined technique was performed on seven patients with distal biliary strictures and duodenal obstructions. The clinical success rate of the procedure, complications, patency periods of duodenal stents and patency periods of biliary stents were retrospectively evaluated. Clinical success was achieved in all seven cases for both procedures. Complications related to EUS-biliary drainage, namely localized peritonitis due to bile leakage, occurred in two cases. Both patients recovered without additional interventions. Occlusion of a duodenal stent was observed in one patient, but additional intervention could not be performed due to sepsis. Occlusion of both a duodenal stent and a biliary stent was also observed in one patient, and this was resolved with the insertion of an additional duodenal stent and a biliary stent exchange. In conclusion, combined duodenal stent placement and EUS-guided biliary drainage is a therapeutic option in case of failed endoscopic retrograde cannulation of malignant strictures with a malignant duodenal obstruction. [ABSTRACT FROM AUTHOR]

Background and Aim Methods Results Conclusions As the population ages, the number of elderly patients with superficial esophageal squamous cell carcinoma (ESCC) is increasing. We aimed to clarify the indications for endoscopic resection (ER) in late‐elderly patients with ESCC in terms of life expectancy.Patients aged ≥75 years who underwent ER for ESCC at our institution from January 2005 to December 2018 were enrolled. Clinical data, including the Eastern Cooperative Oncology Group performance status, American Society of Anesthesiologists physical status (ASA‐PS), Charlson comorbidity index, and prognostic nutritional index (PNI), were collected at the time of ER. The main outcome measure was overall survival (OS).Two hundred eight consecutive patients were enrolled. The patients' median age was 78 years (range, 75–89 years). The 5‐year follow‐up rate was 88.5% (median follow‐up period, 6.6 years). The 5‐year OS rate was 79.2% (95% confidence interval [CI], 72.2–84.8), and 5‐year net survival standardized for age, sex, and calendar year was 1.04 (95% CI, 0.98–1.09). In the multivariate analysis, an ASA‐PS of 3 (hazard ratio, 2.45; 95% CI, 1.16–5.17) and PNI of <44.0 (hazard ratio, 2.73; 95% CI, 1.38–5.40) were independent prognostic factors. When neither of these factors was met, the 5‐year OS rate was 87.8% (95% CI, 80.0–92.9), and 5‐year net survival was 1.08 (95% CI, 1.02–1.14).ER for ESCC in late‐elderly patients may improve life expectancy. ER is recommended in patients with a good ASA‐PS and PNI. [ABSTRACT FROM AUTHOR]

We herein present a unique polyp diagnosed as polypoid colonic hamartomatous inverted polyp. Colonoscopic examination revealed a clover-like submucosal tumor about 30 mm in size with a long stalk at the mid-transverse colon. The polyp consisted of elongated crypts with cystic dilatation located in the submucosal layer. To the best of our knowledge, there have been no previous reports of the same type of pedunculated colonic polyp, similar in appearance to inflammatory myoglandular polyps but covered with a layer of normal mucosa possessing the muscularis mucosae at the uppermost surface of the polyp. [ABSTRACT FROM AUTHOR]