Stomach cancer overview: Difference between revisions
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==Screening== | ==Screening== | ||
The two main modalities for gastric cancer screening are [[upper endoscopy]] and [[Contrast medium|contrast]] radiography. In countries with a high [[incidence]] of gastric cancer such as east asia countaries, universal screening is recommended. In areas of low gastric cancer [[incidence]], [[screening]] for gastric cancer with '''[[upper endoscopy]]''' should be reserved for specific high-risk subgroups. The [[Sensitivity (tests)|sensitivity rates]] for [[upper endoscopy]] were 69 % and [[Upper gastrointestinal series|upper GI series]] were 37%. Both studies had a [[Specificity (tests)|specificity]] of 96%. | |||
==Natural history, Complications and Prognosis== | ==Natural history, Complications and Prognosis== | ||
Revision as of 03:06, 28 November 2017
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Parminder Dhingra, M.D. [2]
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Overview
Stomach cancer (also called gastric cancer) can develop in any part of the stomach and may spread throughout the stomach and to other organs; particularly the esophagus and the small intestine. Stomach cancer causes nearly one million deaths worldwide per year.
Classification
Stomach cancer may be classified into adenocarcinoma, lymphoma, gastrointestinal stromal tumor, and carcinoid tumor.
Pathophysiology
There are many molecular causes of gastric cancer; H. pylori and gastric cancer have strong correlation. This is related to nitric oxides accumulation produced by inflammatory cells responding to H. pylori infection. The pathophysiology of stomach cancer depends on histologic subtypes. K-ras mutations is found in invasive cancers and intestinal metaplasia. Inactivation of p53 in gastric epithelial cells reduce their ability to undergo apoptosis. DNA methylation of gene promoters can silence the expression of CDH1. Beta-catenin mutation is a frequent cause of Wnt pathway activation in gastric cancer. Diffuse gastric carcinomas do not have a precancerous lesion. They are highly metastatic with a poorer prognosis than intestinal cancers. When the entire stomach wall is infiltrated, it results in a rigid thickened stomach wall called linitis plastica. There are many associated diseases to gastric cancer; Hereditary diffuse gastric cancer, Gastric Adenocarcinoma and Proximal Polyposis of the Stomach, Lynch syndrome, Familial adenomatous polyposis, Li-Fraumeni syndrome, Peutz Jeghers syndrome, Juvenile polyposis, Hereditary breast and ovarian cancer syndrome, Cowden's syndrome. There are five gross pathology types of gastric cancer; Superficical, ulcerative, infiltrative ulcerative, diffuse infiltrative, and unclassified. There are two major histological classifications for gastric cancer; Japanesse classification and WHO classification. Generally, the main two types are; Intestinal type adenocarcinoma and diffuse type adenocarcinoma.
Differential diagnosis
Stomach cancer must be differentiated from gastric lymphoma, gastric metastasis, gastritis, benign gastric ulcer, menetrier disease.
Epidemiology and Demographics
Stomach cancer is the fifth most common cancer worldwide.[1] In the United States, stomach cancer represents roughly 1.3% of all new cancer cases yearly[2]. In 2011, the age-adjusted prevalence of stomach cancer was estimated to be 23.5 cases per 100,000 individuals in the United States.[3] Stomach cancer is two times more common in men than in women, and the incidence increases with age.
Risk Factors
Common risk factors in the development of stomach cancer are helicobacter pylori infection, cigarette smoking, family history of stomach cancer, and a diet high in salted smoked or preserved foods.
Screening
The two main modalities for gastric cancer screening are upper endoscopy and contrast radiography. In countries with a high incidence of gastric cancer such as east asia countaries, universal screening is recommended. In areas of low gastric cancer incidence, screening for gastric cancer with upper endoscopy should be reserved for specific high-risk subgroups. The sensitivity rates for upper endoscopy were 69 % and upper GI series were 37%. Both studies had a specificity of 96%.
Natural history, Complications and Prognosis
If left untreated, the five-year survival rates of gastric cancer range from almost no survival for patients with disseminated disease to almost 50% survival for patients with localized distal gastric cancers confined to resectable regional disease. Higher recurrence rates are seen with those who have piecemeal or incomplete resections. Depending on the extent of the tumor at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as poor. Complications of gastric cancer are ascites, gastrointestinal bleeding, distant metastasis to other organs, weight loss, recurrence, and treatment complications. The prognosis of patients with gastric cancer is related to tumor extent that includes direct tumor extension and lymph nodes involvement. The five-year survival rate for treated early gastric cancer is over 90 percent: nearly 100 percent for mucosal tumors, and 80 to 90 percent for submucosal tumors.
Staging
According to the American Joint Committee on Cancer, there are 4 stages of stomach cancer based on the tumor spread.
Symptoms
Symptoms of stomach cancer include abdominal pain, bloating, weight loss, hematemesis and melena.
Physical Examination
Patients with stomach cancer generally appear healthy. Common physical examination findings include abdominal distention, palpation of an abdominal mass, and pallor. Leser-Trelat sign and presence of Virchow's node (left supraclavicular lymphadenopathy), Sister Mary Joseph nodule (visible periumbilical nodule), Blumer's shelf (rectal mass/shelf on rectal exam) and/or Trousseau's syndrome (migratory phlebitis) on physical examination are highly suggestive of stomach cancer.
Endoscopy and Biopsy
Biopsy may be helpful in the diagnosis of stomach cancer.
CT
Abdominal CT scan may be helpful in the diagnosis of stomach cancer.
Other imaging findings
Fluoroscopy may be diagnostic of stomach cancer.
Medical therapy
The optimal therapy for stomach cancer depends on the stage at diagnosis. It is indicated for; patients with unresectable or recurrent disease, after non-curative R2 resection, patients with unresectable T4b disease, extensive nodal disease, Hepatic metastases, Peritoneal dissemination or other M1 disease. Response to the treatment should be evaluated by examinations that may include CT, endoscopy and contrast radiography. Adjuvant therapy includes one cycle of fluorouracil (425 mg/m2) + leucovorin calcium (20 mg/m2) for five days followed by radiation therapy for one month given with the same chemotherapy regimen on days 1 through 4 and the last three days of the month. For patients with potientially resectable diseae not yet resected, neoadjuvant therapy is prefered over initial surgery. Another benefit of neoadjuvant chemotherapy is that patients who are at high risk of developing distant metastases may be spared the morbidity of unnecessary gastrectomy if evidence of distant metastases emerges after chemotherapy. Preoperative combined chemotherapy and radiation therapy is more commonly used for esophageal, esophagogastric junction, and gastric cardia cancers than for potentially resectable adenocarcinomas. For locally advanced unresectable and metastatic tumors, goals of chemotherapy include palliation of symptoms, improvement in quality of life, and prolongation of survival. Patients with the presence of human epidermal growth factor receptor 2 (HER2) overexpression are potential candidates for trastuzumab.
Surgery
Surgery is the mainstay of treatment for stomach cancer. Endoscopic resection is suggested for early gastric cancer. There are criteria for endoscopic resection of ealry gastric cancer. Methods for endoscopic resection include endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD). Side effects of endoscopy includes bleeding and perforation. For T1 tumors, a gross resection margin of 2 cm should be obtained. Proximal margin of at least 3 cm is recommended for T2 or deeper tumors with an expansive growth pattern and 5 cm for those with an infiltrative growth pattern. For tumors invading the esophagus, a 5-cm margin is not necessarily required, but frozen section examination of the resection line is desirable to ensure a R0 resection. There is a debate about optimal lymph nodes removal. D1 lymphadenectomy refers to a dissection of only the perigastric lymph nodes. D2 lymphadenectomy is an extended lymph node dissection, includes removal of nodes along the hepatic, left gastric, celiac, and splenic arteries, as well as those in the splenic hilum. D3 dissection is a superextended lymphadenectomy. The surgery includes D2 lymphadenectomy plus the removal of nodes within the porta hepatis and periaortic regions.
Primary prevention
Effective measures for the primary prevention of stomach cancer include smoking cessation, helicobacter pylori infection eradication, and having a balanced diet rich in fruits and vegetables.
References
- ↑ Stomach cancer incidence statistics. Cancer research UK
- ↑ SEER stat fact sheets: stomach cancer
- ↑ Howlader N, Noone AM, Krapcho M, Garshell J, Miller D, Altekruse SF, Kosary CL, Yu M, Ruhl J, Tatalovich Z,Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2011, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2011/, based on November 2013 SEER data submission, posted to the SEER web site, April 2014.