An 8-Month History of Vague Systemic Symptoms

Juan Carlos Munoz, MD; Nina Y. Singh, MD; Suraj A. Naik, MD

Disclosures

October 01, 2018

Discussion

The patient's history, ethnic background, physical examination, and abdominal CT scan were concerning for metastatic gastric cancer. The liver MRI (not shown) demonstrated hepatic masses with findings compatible with metastatic disease. The EGD with biopsy revealed a large, submucosal, noncircumferential mass without stigmata of recent bleeding in the gastric fundus (Figure 3).

Figure 3.

Pathologic examination of the biopsy sample revealed a poorly differentiated adenocarcinoma. Colonoscopy was unremarkable. However, the carcinoembryonic antigen level was 36.39 ng/mL (reference range, 0.0-3.8 ng/mL). An ultrasound-guided, core-needle liver biopsy with imprint cytology also revealed a poorly differentiated adenocarcinoma morphologically consistent with gastric adenocarcinoma. The patient was scheduled to receive a combination of capecitabine and oxaliplatin.

Gastric cancer (stomach cancer) is the fifth most common malignancy worldwide and is the third leading cause of cancer-related death each year. In the United States, gastric cancer ranks fifteenth in incidence among the major types of cancer. Estimates of new cases and death in the United States in 2018 were 26,240 and 10,800, respectively. Gastric cancer is more common among men than women and among other races and ethnicities than non-Hispanic white individuals. Most patients are over 60 years of age. Cancer of the distal part of the stomach (body and antrum) has been decreasing since the 1930s; however, in the last 2 decades the incidence of more proximal gastric cancer (fundus and cardia) has increased dramatically.[1] The overall 5-year survival rate of people with gastric cancer in the United States is about 31%. One reason for this is that most gastric cancers are found at an advanced stage. The prognosis is better if the cancer is in the distal stomach.[2]

The exact etiology of gastric cancer is unknown. The risk for gastric cancer varies among regions of the world. East Asia, Southern and Eastern Europe, South America, and Central America are considered high-risk areas for gastric cancer.[3] The geographic and racial variation in the incidence of gastric cancer is most likely due to differences in diet, a major carcinogenic determinant in gastric carcinoma. A diet rich in animal proteins or high in preserved, smoked, salted, pickled, grilled, barbecued, or poorly refrigerated foods increases the risk of developing gastric cancer. Protective factors described in the literature include adequate consumption of fresh fruit, vegetables (in particular brassica vegetables, such as broccoli, cauliflower, and cabbages), and allium vegetables (such as onions and garlic).[4] Obesity also increases the risk of developing gastric cancer.[5]

Studies of Japanese immigrants in the United States have confirmed that early exposure to environmental rather than genetic factors has a great influence on the mortality and incidence rate of gastric cancer. The mortality rate of gastric cancer in the second and third generation of Japanese immigrants tends to decline to that of the native population of the United States.[6] Other risk factors for the development of gastric cancer include persistent inflammation of the gastric lining, such as in Helicobacter pylori infection; pernicious anemia; chronic gastritis, such as in Ménétrier disease; a history of gastric surgery; and a history of smoking.[7,8] Certain genetic disorders, such as hereditary diffuse gastric cancer, hereditary nonpolyposis colorectal cancer (Lynch syndrome), and familial adenomatous polyposis, have been associated with increased risk for stomach cancer.[9,10]

In a small study, Kim et al found a significantly positive correlation between cyclin-dependent kinase (CDK) 8 and β-catenin expression and the oncogenesis and progression of gastric adenocarcinoma, particularly lymph node metastasis.[11] The investigators suggested not only that: (1) the detection of CDK8 and delocalization of β-catenin may indicate a poor prognosis, but also (2) because CDK8 suppresses β-catenin activation in gastric adenocarcinoma, this finding may lead to a potential treatment in this disease.[11]

Comments

3090D553-9492-4563-8681-AD288FA52ACE
Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as:

processing....