The next speaker is Sawani Namgang Ruafang, who is an assistant professor of medicine at Johns Hopkins, is an outstanding therapeutic endoscopist, and is here to discuss gastric cancer, particularly who and how to screen. Thank you, Sawani. Good morning, everyone. I would like to thank ASGE, Dr. M. Monser, and Dr. Lennon for an opportunity to talk to you today on this topic, gastric cancer, who and how to screen. Gastric cancer is one of the most common cancers, according to over one million new cases annually, and is the third leading cause of cancer death worldwide. There's a significant geographic variations in incidence of gastric cancer, and high-risk regions are in East Asia, like in Japan, Korea, and certain part of China, in former Soviet Union, Eastern Europe, Central and South America. In the US, overall incidence of gastric cancer is low, but the number of new cases are actually higher than cases of esophageal cancer. So this is not an uncommon cancer, and there's an early lesion that we can target for early detection and treat, similar to esophageal cancer. As mentioned, although overall incidence of gastric cancer is low in the US, but there's a significant variation in incidence across different ethnicity. The incidence of gastric cancer in white American is about half of that of African American, Hispanic, and Asian. And if we look at the Asian subgroup, the Japanese American and Korean American have a very high risk of gastric cancer. So if we look at the incidence of male Korean American, the incidence is 50 in 100,000 cases a year. So this is higher than incidence of colorectal cancer in the US. In the study looking at the impact of immigration and risk of gastric cancer, they found that individuals who are the first and first generation immigrant, for example, those from Japan, which is a high incidence country, when they move to the US, their risk of gastric cancer is still high, although lower than people who live in Japan. And the risk become lower in the succeeding generation. And about two generations after that, the risk become similar to that of the American, white American. So it's important to recognize that patients that come from high incidence countries, they still have high risk of developing gastric cancers. In the gastric carcinogenic model proposed by Dr. Correa, intestinal type gastric adenocarcinoma is a sequential progression due to chronic inflammation from chronic gastritis to atrophy to gastric intestinal metaplasia, develop dysplasia, and eventually gastric adenocarcinoma. And the primary factor that's driving this process is H. pylori infection, among other environmental factors. Gastric IM, intestinal metaplasia, is a precursor lesion for gastric cancer and is diagnosed historically by a replacement of gastric mucosa by intestinal epithelium due to chronic gastric inflammation. The overall prevalence of gastric IM is about 5% in the U.S., but the prevalence is higher in the Asian ethnic group and those who have H. pylori infection. There are two main historic subtype of gastric IM. The complete type resembles intestinal, small intestine mucosa with goblet cells and brush border, and incomplete type resembles chronic epithelium. We can also describe gastric IM according to the extent of disease to focal IM, which is the IM that involves only antrum or incisora, and the extensive type means involvement both antrum and body. Atopic gastritis is also a precursor lesion for gastric cancer. This is defined as the replacement of gastric epithelium with either connective tissue or different type of epithelium. So if the biopsy show gastric intestinal metaplasia, this generally imply diagnosis of atopic gastritis as well. And on endoscopy, you can recognize atopic gastritis as pale mucosa and loss of gastric folds and prominent submucosal blood vessels due to thinning of the gastric epithelium. Like in this picture, you can draw the line of atopic gastritis in the antrum. And in this picture, it extends up to the proximal gastric body. So what is the risk of progression to gastric cancer in these patients? In this study, in low-risk Western population in Sweden, they found that approximately one in 50 patients with atopic gastritis and one in 39 patients with gastric intestinal metaplasia will go on and develop gastric cancer over 20 years follow-up period. But if they develop dysplastic lesions, then the risk become much higher, one in 19 patients. And not all gastric IM has equal risk of progression to gastric cancer. So these are main risk factors. Patients that have first-degree family history of gastric cancer, incomplete gastric IM, or extensive involvement of gastric IM, these are the main risk factors to progress to gastric cancer. So when we have patients with biopsies show gastric IM, we need to check H. pylori and treat if the patient have H. pylori infection because H. pylori eradication increase likelihood of regression of gastric IM in the non-severe cases. And this also decrease risk of gastric cancer incidence and gastric cancer mortality. After eradication of H. pylori, then assess the patient risk of developing gastric cancer. Do they have incomplete IM? Do they have extensive involvement in the stomach? Or do they have a family history of gastric cancers? If they have any of these, then consider repeat endoscopy for surveillance every three to five years after discussion pros and cons of endoscopy. But if the patient doesn't have any of these risk factors, then look at the index endoscopy. Do we have enough information to determine the patient risk? If yes, then there's no need for follow-up endoscopy. But if not, then consider repeat short interval endoscopy in a year and do biopsy and determine extent and histologic subtype of gastric IM. And the HEA guidelines recommend against routine endoscopy in everyone with gastric IM without assessing their risk and the patient's understanding about benefit and risk of endoscopy. For individuals who are first and second generations immigrants from high-incident countries that we mentioned, like Japan, Korea, from Russia, or Chile, Peru, or they have family history of gastric cancers, there's a recommendation that published in GIE some years ago to consider upper endoscopy at age 50. And it's cost-effective if we do it at the same time with screening colonoscopy. This is to assess their risk. Do they have H. pylori, atopic gastritis, intestinal metoplasia, or any other risk factor? If not, then their risk of developing gastric cancer is similar to general population. There's no need for follow-up endoscopy. But if they have H. pylori, then treat and repeat endoscopy in three to five years to see if they have progression to atopic gastritis or intestinal metoplasia. If they have these precursor lesions or they have family history of gastric cancers, this is considered high risk, then consider endoscopy every one to two years in this group of patients. So how do we recognize gastric IM on endoscopy? You can see it's as a whitish patch or patches, homogeneous discoloration on white light endoscopy. But you can only see it when it's severe. And white light endoscopy is not a very sensitive test to diagnose or detect gastric IM. The narrowband imaging improves detection of gastric IM. So for example, in this picture, it looks very normal on white light. But under NBI, you can see the whitish-bluish area of gastric IM. And in the closer view, you see the tuberculous and reshapular mucosal pattern. This is suggestive of gastric IM. And how do we do biopsy for these patients? We still do the Sydney system biopsy mapping protocol the way we do for diagnosis of H. pylori infection, which is at least five non-targeted biopsy. One from the antrum, laser curvature. One from antrum, greater curvature, about two to three centimeter, both pylolas. And one from incisora. And this put in one jar. One biopsy from laser curvature body and greater curvature body and put in the separate jar. And if you see abnormal lesion, discrete lesions, then biopsy that and place in another separate jar. Don't put them all together. So how good are these modalities in detecting gastric IM? Both NBI and mapping biopsy have higher detection rate of gastric IM compared with high definition white light alone. And if we combine modalities of this, which one is best, we find that combined NBI and mapping biopsy give you the highest diagnostic yield of gastric IM. So what important to know is that high definition white light alone is insufficient for detection of gastric IM. We should use NBI with targeted biopsy and mapping biopsy for these patients. When examine stomach for gastric IM, we not only looking for gastric IM, but looking for this place here, an early gastric cancer, in order to treat these lesions before it progress to advanced cancer. So important to prepare stomach the way we do for screening colonoscopy. Adequately distance the stomach wall, clean the mucous and bubbles. We have to ensure mucosal visibility before we examine. We have to clean until there's no bubbles or mucous left or very minimum thin layers of mucous that do not obscure view. So if you still see thick layers of mucous like this, we need to clean more before we start examine the stomach. And systematic examination that done recommended by the expert Japanese, we should spend some time looking at every area of the stomach, start from the forward view in the antrum, look at full quadrant, slowly pull endoscope back. And you can see here, this is diffuse atrophy. We also take a lot of pictures, although it may be difficult to do here, but at least taking picture help you have the pinpoint of the area you already examine. So after pull the endoscope back and look carefully to the proximal stomach, then retroflex. Make sure that we look behind the scope at the cardiac. And I'm going to make this a little bit faster. And lesser curvature, which you don't see well on a forward view. And push the scope in to the incisor level, make sure that we see both side of the incisor. How long we should spend time examine for gastric lesions? In this study from Singapore, they found that the endoscopist that spend longer than seven minutes has almost three times increase in detection of gastric lesions, plastic lesion, or early gastric cancers than endoscopist that spend less than seven minutes. So it's recommended to at least spend seven minutes examination time for high risk patient. In order to detect dysplasia or early gastric cancer, we need to know what it look like. It doesn't look like a big mess like you see in advanced gastric cancer. So we have to pay attention to clues during endoscopy like some changes in the color, a loss of blood vessels, or thinning of the mucosal for spontaneous bleeding. These lesions can present as protrude lesions, can present as focal redness. These are cancers, depressed lesions, erosions, full convergence, this is also cancer, or look like only scar. The only clue here is this appearance of blood vessels, this is a cancer here, or spontaneous bleeding, this thing is cancer. So this is a quiz, can you find cancer in this picture? So the cancer is here, how about this? There's a cancer here, yeah, so yes, this also cancer. So this is a case we saw not long ago. The patient underwent upper endoscopy at outside institution, and the random biopsy in the antrum shows severe dysplasia and gastric intestinal metaplasia on two separate endoscopy. So the patient was referred to gastrectomy because of the endoscopically invisible lesion. So we repeat endoscopy, and we found 13 millimeter depressed lesion at the pre-pyloric antrum. So this lesion was resected by ESD, and the patient did not require surgery. So once you diagnose dysplastic lesions or early gastric cancers, what are treatment options? It can be endoscopic resections, either EMR or ESD, or surgery. For endoscopic options, ESD is superior to EMR for early gastric neoplasia because it's associated with higher on-block resection rate, higher histologically complete resection, and lower risk of local recurrence. Although it takes longer time to do and has higher risk of perforation, but given the overall benefit of ESD over EMR, ESG guidelines recommend that ESD is the treatment of choice for early gastric neoplasia. And EMR is an acceptable option for small lesion with very low risk of advanced histology, for example, the flat 2A region. So this is early gastric cancer, flat elevated with depressed component here. After marking, you perform mucosal incision and submucosal dissection. You can see the separation of muscle and submucosal layer, and continue dissection until you remove the entire lesion in on-block fashion. So in summary, gastric IM is a common condition seen about 5% in the US, and it's a risk factor for gastric cancer. We need to assess the risk of progression to gastric cancer according to the location, extent of gastric IM, histologic subtype, and family history of gastric cancer. For individuals who's considered high risk based on their family history and their ethnicity, consider screening endoscopy at age 50. The upper endoscopy, when you perform for these patients, make sure that we clean the stomach well. Distend the stomach. Spend some time, at least seven minutes. Use both white light and NBI for examination and do systematic mapping biopsy. And if you identify dysplastic lesion or laryngostic cancer, most often an ESD is preferred to EMR. Thank you very much for your attention.

gastric cancer screening

incidence of gastric cancer

ethnicities and gastric cancer

gastric intestinal metaplasia

screening methods for gastric cancer