Esophageal cancer (EC) is rapidly increasing in incidence in the United States. Genetic changes associated with the development of EC involve the p16, p53, and APC genes. Human epidermal growth factor 2 (HER-2) overexpression is seen in gastroesophageal junction carcinoma and a subset gastric carcinoma (GC). Interestingly, up to 50% cases of GC are related to Helicobacter pylori infection and up to 16% are related to EBV infection. Microsatellite instability is observed in up to 39% of GC and cell free nucleic acid analysis provides additional opportunities for diagnosis and prognosis of disease.

Gastric Cancer is one of the most common types of cancer. And the occurrence of gastric carcinoma is an evolutionary histopathological stage. As a result, further research of GPL, which is a borderline of gastric cancer, is indispensable for preventing the formation and development of gastric carcinoma. Several studies have demonstrated a correlation between the expression of autophagy, apoptosis and Gastric cancer (GC). However, the effects of autophagy and apoptosis on human gastric cancer progression, particularly on gastric precancerous lesions (GPL), have not totally been investigated. At present, Astragaloside IV(AS-IV) is a saponin purified from Astragalus membranaceous Bge, a traditional Chinese herb that has been widely used for more than 2000 y in the treatment of cancer, cardiovascular and immune disorders. This study was designed to investigate the mechanism of AS-IV protecting gastric mucosa in N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced GPL rats. The lesions of GIM and GED were significantly ameliorated compared with the model rats, especially crowded tubular glandular and back-to-back tubular structure, which were the dangerous borderline between GPL and GC. Western Blot analysis showed that the ratio of Bcl-2/Bax and the protein expression of Bcl-XL, p53, Beclin1, p62, ATG5 and ATG12 were decreased and the level of Caspase3 was increased in the group of AS-IV compared with the model group; RT-PCR analysis showed that the gene expression Ambra1, Beclin1, ATG5, LC3 and p62 were decreased in the group of AS-IV compared with the model group. This research manifested that the occurrence of gastric cancer was preceded by a prolonged precancerous stage, which could be ameliorated by the AS-IV. Meanwhile, the mild and moderate stage of precancerous lesions is similar with gastric adenocarcinoma in critical biological processes, including inflammation, cell proliferation, differentiation. But this lesion is very different from cancer, because it does not appear obvious invasion and malignant lesions in this pathologic stag. Further, AS-IV could regulate p53 expression to activate the Ambra1/Beclin1 complex in GPL, and it will protect the gastric mucosal injury, prevent and cure gastric mucosal atrophy, intestinal metaplasia and atypical hyperplastic lesions. It provided a potential therapeutic strategy in reversing intestinal metaplasia and dysplasia of gastric precancerous lesions and protecting the gastric mucosa in GPL rats.

Gastric stump cancer was first defined as cancer occurring in the remnant stomach 5 years or later following distal subtotal gastrectomy of a benign stomach tumor. This definition was expanded to include malignant gastric cancer recurrence following distal gastrectomy and heterochronous gastric adenocarcinoma. Evidence regarding whether patients with gastric stump cancer had the same prognosis as those with primary gastric cancer has been inconsistent. Nonetheless, considering the notable differences regarding risk factors, treatment strategies, and lymph node metastasis status, gastric stump cancer should be differentiated from primary stomach cancer. Overall, the prognosis of gastric stump cancer is influenced by clinicopathological characteristics such as primary tumor features, location of gastric stump cancer, histological type, invasion depth, lymph node metastasis, and distant metastasis, as well as treatment factors such as treatment strategy, dissection range, and lymph node resection range. In previous studies on gastric stump cancer, the sample size was limited, and future studies with larger sample size are needed to further validate the prognostic factors of gastric stump cancer.

Signet-ring cell carcinoma (SRCC) is an adenocarcinoma characterized by mucin-producing cells and most commonly arises in the stomach. Colonic SRCC can share features of colitis, including long segments of concentric bowel wall thickening and ulcerated mucosa with regions of sparing. We describe a rare case of metastatic gastric SRCC mimicking Crohn's disease. Our patient underwent 2 colonoscopies, and biopsies revealed chronic active inflammation with no evidence of malignancy. The diagnosis of SRCC was only made after colectomy was performed for recurrent bowel obstruction.

Aim: Low circulating vitamin D levels are associated with gastric adenocarcinoma, but whether vitamin D levels are associated with premalignant gastric mucosal changes is unknown. Here, we determined associations between vitamin D levels and gastric incomplete intestinal metaplasia, a known gastric adenocarcinoma risk factor. Methods: This was a retrospective, unmatched, case-control study comparing serum 25-hydroxyvitamin D levels among subjects with gastric incomplete intestinal metaplasia (cases; n = 103) and those without gastric incomplete intestinal metaplasia (controls; n = 216). The 25-hydroxyvitamin D levels were categorized as normal (30–100 ng/dL), vitamin D insufficiency (VDi; 20–29 ng/dL), and vitamin D deficiency (VDd; <20 ng/dL). Using multivariable logistic regression, odds ratios (ORs) were calculated and adjusted to age, gender, ethnicity, body mass index, history of hypertension or diabetes mellitus, and timing of vitamin D collection to assess associations between 25-hydroxyvitamin D levels and gastric incomplete intestinal metaplasia. Results: A majority of case subjects were male, Hispanic, and did not have hypertension or diabetes mellitus. The average serum 25-hydroxyvitamin D level was significantly lower in the intestinal metaplasia group than the control group (19.7 ng/dL vs. 34.7 ng/dL; p < 0.001). Hypovitaminosis D was more common in subjects with incomplete intestinal metaplasia in a multivariable regression model (OR 54.1, 95% CI 21.8–134.3; p < 0.001). VDd (OR 129.0, 95% CI 43.7–381.2; p < 0.001) and VDi (OR 31.0, 95% CI 11.9–80.3; p < 0.001) were more common in patients with incomplete intestinal metaplasia than healthy subjects, with VDd slightly more prevalent than VDi (OR 4.0, 95% CI 1.7–9.6; p < 0.001). Conclusions: Vitamin D deficiency and insufficiency are more common in patients with gastric incomplete intestinal metaplasia than healthy subjects and may play a role in the development of premalignant phenotypes related to gastric adenocarcinoma.

Helicobacter pylori (H. pylori) infection is the most important risk factor for gastric cancer (GC) development through the Correa's gastric carcinogenesis cascade. However, H. pylori eradication alone does not eliminate GC, as pre-neoplastic lesions (atrophic gastritis, intestinal metaplasia and dysplasia) may have already developed in some patients. It is therefore necessary to identify patients at high-risk for gastric cancer after H. pylori eradication to streamline the management plan. If the patients have not undergone endoscopy with histologic assessment, the identification of certain clinical risk factors and non-invasive testing (serum pepsinogen) can predict the risk of atrophic gastritis. For those with suspected atrophic gastritis, further risk stratification by endoscopy with histologic assessment according to validated histologic staging systems would be advisable. Patients with higher stages may require long-term endoscopic surveillance. Apart from secondary prevention to reduce deaths by diagnosing GC at an early stage, identifying medications that could potentially modify the GC risk would be desirable. The potential roles of a number of medications have been suggested by various studies, including proton pump inhibitors (PPIs), aspirin, statins and metformin. However, there are currently no randomized clinical trials to address the impact of these medications on GC risk after H. pylori eradication. In addition, most of these studies failed to adjust for the effect of concurrent medications on GC risk. Recently, large population-based retrospective cohort studies have shown that PPIs were associated with an increased GC risk after H. pylori eradication, while aspirin was associated with a lower risk. The roles of other agents in reducing GC risk after H. pylori eradication remain to be determined.

Gastric cancer (GC) remains one of the main causes of cancer-related death worldwide. There are two distinct histological types of GC: diffuse and intestinal. The latter is characterized by the presence of pre-neoplastic lesions. One of the most frequently altered enzymes in intestinal GC is COX-2, an important lesion marker. This work aimed to study COX-2 methylation and expression in N-methyl-N-Nitrosurea (MNU)-induced intestinal GC in six Sapajus apella animals. The partial promoter sequence of S. apella COX-2 gene was obtained and used to identify transcription factors and cis-regulatory element binding sites. The COX-2 methylation pattern was assessed using Methylation-Specific PCR (MSP), and expression was analyzed by immunohistochemistry (IHQ). A total of 20 samples were obtained. A 675 bp fragment of the S. apella COX-2 promoter region was obtained, and it was 99.2% and 68.2% similar to H. sapiens and S. boliviensis, respectively. Similar to humans, several transcription factors and cis-regulatory element binding sites were identified in the S. apella sequence. MSP revealed that all samples were methylated. However, IHQ results demonstrated positive COX-2 expression in all pre-neoplastic and tumoral samples. The results suggest that the analyzed fragment is not crucial in COX-2 regulation of GC in S. apella.