Adenocarcinoma of the Stomach - Erler Zimmer 3D anatomy Series MP2080

This dissection model highlighting an Adenocarcinoma of the Stomach is part of the exclusive Monash 3D anatomy series, a comprehensive series of human dissections reproduced with ultra-high resolution color 3D printing.

Clinical History.

An 82-year-old woman presented with an episode of melena (dark tarry stools). She had a 6-month history of dyspepsia and nausea. Recently she had noticed weight loss and early satiety. Immediately after admission she had a major melena episode and died.

Pathology

This is a postmortem specimen sliced to include a sagittal view of the esophagus, stomach, proximal duodenum, and pancreas. A large ulcer measuring 7x5 cm is evident on the lesser curve of the stomach. The ulcer is shallow and wide with raised rolled edges and necrotic debris at the base. There is gastric rust leakage radiating along the mucus from the ulcer. Dissection of the ulcer reveals elevation of the rim by pale homogeneous tumor tissue. Within the crater of the ulcer were two eroded arteries with evidence of recent hemorrhage. The pancreas is adherent to the serous aspect of the ulcer. Histology taken from the lesion (sites visible as regular 3-cm defects) demonstrated an ulcerative, well-differentiated adenocarcinoma of the stomach with direct invasion into the pancreas.

Further Information.

Gastric adenocarcinoma is the most common malignant tumor of the stomach. Incidence varies widely with geography: with much higher incidence in Japan, Chile, and Eastern Europe than in North America, Africa, Southeast Asia, and Northern Europe. Risk factors include smoking, high-salt diets, H. Pylori infection, gastroesophageal reflux disease (GERD), atrophic gastritis, and gastric mucosal intestinal metaplasia.
There are two distinct classifications: intestinal and diffuse gastric adenocarcinoma. Intestinal adenocarcinoma resembles glandular tissue similar to adenocarcinoma of the colon or esophagus. Intestinal types tend to be bulky: they grow like an ulcerated or exophytic tumor. The intestinal type occurs most frequently in endemic areas, has a male predominance and a mean age of 55 years at presentation. The intestinal type may arise from precursor lesions, such as dysplasia and/or adenomas with dysplasia. Diffuse type gastric tumors have an infiltrative growth pattern and are composed of "signet ring" cells, that is, cells that have large mucin-filled vacuoles leading to displacement of the nucleus to the periphery of the cell. The cells appear to have lost adhesion to each other and thus may be widely distributed within the stomach mucosa. A mass may not be appreciated in this diffuse type as a desmoplastic reaction may occur around the tumor cells, causing a thickened and rigid stomach wall with loss of rugae, creating a "skin bottle" appearance knowing also the plastic line. The diffuse type has the same incidence across sexes and countries and has no precursor lesions. Germline mutations in CDH1, which cause loss of E-cadherin function leading to loss of cell adhesion, can lead to increased risk of diffuse gastric cancer, which may be familial. Patients with familial adenomatous polyposis (FAP) with germline mutation in the adenomatous polyposis coli (APC) gene have an increased risk of developing gastric adenocarcinoma of the intestinal type. causing a thickened and rigid stomach wall with loss of rugae, creating a "leather bottle" appearance knowing also the plastic line. The diffuse type has the same incidence across sexes and countries and has no precursor lesions. Germline mutations in CDH1, which cause loss of E-cadherin function leading to loss of cell adhesion, may lead to increased risk of diffuse gastric cancer, which may be familial. Patients with familial adenomatous polyposis (FAP) with germline mutation in the adenomatous polyposis coli (APC) gene have an increased risk of developing gastric adenocarcinoma of the intestinal type. causing a thickened and rigid stomach wall with loss of rugae, creating a "leather bottle" appearance knowing also the plastic line. The diffuse type has the same incidence across sexes and countries and has no precursor lesions. Germline mutations in CDH1, which cause loss of E-cadherin function leading to loss of cell adhesion, can lead to increased risk of diffuse gastric cancer, which may be familial. Patients with familial adenomatous polyposis (FAP) with a germline mutation in the adenomatous polyposis coli (APC) gene have an increased risk of developing gastric adenocarcinoma of the intestinal type. causing loss of E-cadherin function leading to loss of cell adhesion, may lead to an increased risk of diffuse gastric cancer, which may be familial. Patients with familial adenomatous polyposis (FAP) with a germline mutation in the adenomatous polyposis coli (APC) gene have an increased risk of developing gastric adenocarcinoma of the intestinal type. which by causing loss of E-cadherin function leading to loss of cell adhesion, may result in an increased risk of diffuse gastric cancer, which may be familial. Patients with familial adenomatous polyposis (FAP) with germline mutation in the adenomatous polyposis coli (APC) gene have an increased risk of developing intestinal-type gastric adenocarcinoma.

Early symptoms include dyspepsia, dysphagia, and nausea. Later symptoms include weight loss, anorexia, early satiety, fatigue, anemia and hemorrhage. Treatment depends on the stage of the tumor with surgical resection for early tumors and chemotherapy for advanced tumors.

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What advantages does the Monash University anatomical dissection collection offer over plastic models or plastinated human specimens?

• Each body replica has been carefully created from selected patient X-ray data or human cadaver specimens selected by a highly trained team of anatomists at the Monash University Center for Human Anatomy Education to illustrate a range of clinically important areas of anatomy with a quality and fidelity that cannot be achieved with conventional anatomical models-this is real anatomy, not stylized anatomy.
• Each body replica has been rigorously checked by a team of highly trained anatomists at the Center for Human Anatomy Education, Monash University, to ensure the anatomical accuracy of the final product.
• The body replicas are not real human tissue and therefore not subject to any barriers of transportation, import, or use in educational facilities that do not hold an anatomy license. The Monash 3D Anatomy dissection series avoids these and other ethical issues that are raised when dealing with plastinated human remains.