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Background
Gastric cancer was once the second most common cancer in the world. In most developed countries, however,
rates of stomach cancer have declined dramatically over the past half century. In the United States, stomach
malignancy is currently the 14th most common cancer.
Decreases in gastric cancer have been attributed in part to widespread use of refrigeration, which has had
several beneficial effects: increased consumption of fresh fruits and vegetables; decreased intake of salt, which
had been used as a food preservative; and decreased contamination of food by carcinogenic compounds arising
from the decay of unrefrigerated meat products. Salt and salted foods may damage the gastric mucosa, leading
to inflammation and an associated increase in DNA synthesis and cell proliferation. Other factors likely
contributing to the decline in stomach cancer rates include lower rates of chronic Helicobacter pylori infection,
thanks to improved sanitation and use of antibiotics, and increased screening in some countries.[1]
Nevertheless, gastric cancer is still the second most common cause of cancer-related death in the world, and it
remains difficult to cure in Western countries, primarily because most patients present with advanced disease.
Even patients who present in the most favorable condition and who undergo curative surgical resection often
die of recurrent disease. However, 2 studies have demonstrated improved survival with adjuvant therapy: a US
study using postoperative chemoradiation[2] and a European study using preoperative and postoperative
chemotherapy.[3]
Anatomic aspects
The molecular biology responsible for carcinogenesis, tumor biology, and response to therapy in stomach
cancer are active areas of investigation but are not addressed in this review. Instead, this article focuses on
clinical management, which first requires a thorough understanding of gastric anatomy.
An image depicting stomach anatomy can be seen below.
Stomach and duodenum, coronal section.

The stomach begins at the gastroesophageal junction and ends at the duodenum. The stomach has 3 parts: the
uppermost part is the cardia; the middle and largest part is the body, or fundus; and the distal portion, the
pylorus, connects to the duodenum. These anatomic zones have distinct histologic features. The cardia contains
predominantly mucin-secreting cells. The fundus contains mucoid cells, chief cells, and parietal cells. The
pylorus is composed of mucus-producing cells and endocrine cells.
The stomach wall is made up of 5 layers. From the lumen out, the layers include the mucosa, the submucosa,
the muscularis layer, the subserosal layer, and the serosal layer. The peritoneum of the greater sac covers the
anterior surface of the stomach. A portion of the lesser sac drapes posteriorly over the stomach. The
gastroesophageal junction has limited or no serosal covering. The right portion of the anterior gastric surface is
adjacent to the left lobe of the liver and the anterior abdominal wall. The left portion of the stomach is adjacent
to the spleen, the left adrenal gland, the superior portion of the left kidney, the ventral portion of the pancreas,
and the transverse colon.
The site of stomach cancer is classified on the basis of its relationship to the long axis of the stomach.
Approximately 40% of cancers develop in the lower part, 40% in the middle part, and 15% in the upper part;
10% involve more than one part of the organ. Most of the decrease in gastric cancer incidence and mortality in
the United States has involved cancer in the lower part of the stomach; the incidence of adenocarcinoma in the
cardia has actually shown a gradual increase.
Next Section: Pathophysiology
Pathophysiology
Ooi et al identified 3 oncogenic pathways that are deregulated in the majority (>70%) of gastric cancers: the
proliferation/stem cell, NF-kappa β, and Wnt/beta-catenin pathways. Their study suggests that interactions
between these pathways may play an important role in influencing disease behavior and patient survival.[4]
Understanding the vascular supply of the stomach allows understanding of the routes of hematogenous spread.
The vascular supply of the stomach is derived from the celiac artery. The left gastric artery, a branch of the
celiac artery, supplies the upper right portion of the stomach. The common hepatic artery branches into the
right gastric artery, which supplies the lower portion of the stomach, and the right gastroepiploic branch, which
supplies the lower portion of the greater curvature.
Understanding the lymphatic drainage can clarify the areas at risk for nodal involvement by cancer. The
lymphatic drainage of the stomach is complex. Primary lymphatic drainage is along the celiac axis. Minor
drainage occurs along the splenic hilum, suprapancreatic nodal groups, porta hepatis, and gastroduodenal areas.
Previous
Next Section: Pathophysiology
Epidemiology
Frequency
United States
The American Cancer Society estimates that 21,130 cases of gastric cancer will be diagnosed in 2009 (12,820
in men, 8,310 in women) and that 10,620 persons will die of the disease.[5] Gastric cancer is the seventh leading
cause of cancer deaths.
International
Once the second most common cancer worldwide, stomach cancer has dropped to fourth place, after cancers of
the lung, breast, and colon and rectum. However, stomach cancer remains the second most common cause of
death from cancer. The American Cancer Society estimates that in 2007 there were an estimated one million
new cases, nearly 70% of them in developing countries, and about 800,000 deaths.[1]
Tremendous geographic variation exists in the incidence of this disease around the world. Rates of the disease
are highest in Asia and parts of South America and lowest in North America.[1] The highest death rates are
recorded in Chile, Japan, South America, and the former Soviet Union.
Mortality/Morbidity
The 5-year survival rate for curative surgical resection ranges from 30-50% for patients with stage II disease
and from 10-25% for patients with stage III disease. Because these patients have a high likelihood of local and
systemic relapse, some physicians offer them adjuvant therapy. The operative mortality rate for patients
undergoing curative surgical resection at major academic centers is less than 3%.
A review of 8 trials by Rothwell et al found allocation to aspirin reduced death caused by cancer. Individual
patient data were available from 7 of the 8 trials. Benefit was apparent after 5 years of follow-up. The 20-year
risk of cancer death was also lower in the aspirin group for all solid cancers. A latent period of 5 years was
observed before risk of death was decreased for esophageal, pancreatic, brain, and lung cancers. A more
delayed latent period was observed for stomach, colorectal, and prostate cancer. Benefit was only seen for
adenocarcinomas in lung and esophageal cancers. The overall effect on 20-year risk of cancer death was
greatest for adenocarcinomas.[6]
Race
The rates of gastric cancer are higher in Asian and South American countries than in the United States. Japan,
Chile, and Venezuela have developed a very rigorous early screening program that detects patients with early
stage disease (ie, low tumor burden). These patients appear to do quite well. In fact, in many Asian studies,
patients with resected stage II and III disease tend to have better outcomes than similarly staged patients treated
in Western countries. Some researchers suggest that this reflects a fundamental biologic difference in the
disease as it manifests in Western countries.
In the United States, Asian and Pacific Islander males and females have the highest incidence of stomach
cancer, followed by black, Hispanic, white, American Indian, and Inuit populations.
Sex
In the United States, gastric cancer affects slightly more men than women; the American Cancer Society
estimates that in 2009, 12,820 new cases will occur in men and 8,310 in women.[5] Worldwide, however, gastric
cancer rates are about twice as high in men as in women.[1]
Age
Most patients are elderly at diagnosis. The median age for gastric cancer in the United States is 70 years for
males and 74 years for females. The gastric cancers that occur in younger patients may represent a more
aggressive variant or may suggest a genetic predisposition to development of the disease.
In the United States, about 25% of stomach cancer patients present with localized disease, 31% present with
regional disease, and 32% present with distant metastatic disease; the remainder of cases surveyed were listed
as unstaged.
Early disease has no associated symptoms; however, some patients with incidental complaints are diagnosed
with early gastric cancer. Most symptoms of gastric cancer reflect advanced disease. Patients may complain of
indigestion, nausea or vomiting, dysphagia, postprandial fullness, loss of appetite, melena, hematemesis, and
weight loss.
Late complications include pathologic peritoneal and pleural effusions; obstruction of the gastric outlet,
gastroesophageal junction, or small bowel; bleeding in the stomach from esophageal varices or at the
anastomosis after surgery; intrahepatic jaundice caused by hepatomegaly; extrahepatic jaundice; and inanition
resulting from starvation or cachexia of tumor origin.
Next Section: Physical
Physical
All physical signs are late events. By the time they develop, the disease is almost invariably too far advanced
for curative procedures.
Signs may include a palpable enlarged stomach with succussion splash; hepatomegaly; periumbilical metastasis
(Sister Mary Joseph nodule); and enlarged lymph nodes such as Virchow nodes (ie, left supraclavicular) and
Irish node (anterior axillary). Blumer shelf (ie, shelflike tumor of the anterior rectal wall) may also be present.
Some patients experience weight loss, and others may present with melena or pallor from anemia.
Paraneoplastic syndromes such as dermatomyositis, acanthosis nigricans, and circinate erythemas are poor
prognostic features.
Other associated abnormalities also include peripheral thrombophlebitis and microangiopathic hemolytic
anemia.
Previous
Next Section: Physical
Causes
Gastric cancer may often be multifactorial, involving both inherited predisposition and environmental factors.[7]
Environmental factors implicated in the development of gastric cancer include diet, Helicobacter pylori
infection, previous gastric surgery, pernicious anemia, adenomatous polyps, chronic atrophic gastritis, and
radiation exposure.
Diet
A diet rich in pickled vegetables, salted fish, salt, and smoked meats correlates with an increased incidence of
gastric cancer.[7]
A diet that includes fruits and vegetables rich in vitamin C may have a protective effect.[8]
Smoking
Smoking is associated with an increased incidence of stomach cancer in a dose-dependent manner, both for
number of cigarettes and for duration of smoking.
Smoking increases the risk of cardiac and noncardiac forms of stomach cancer.[9] Cessation of smoking reduces
the risk.
A meta-analysis of 40 studies estimated that the risk was increased by approximately 1.5- to 1.6-fold and was
higher in men.[10]
Helicobacter pylori infection
Chronic bacterial infection with H pylori is the strongest risk factor for stomach cancer.
H pylori may infect 50% of the world's population, but many fewer than 5% of infected individuals develop
cancer. It may be that only a particular strain of H pylori is strongly associated with malignancy, probably
because it is capable of producing the greatest amount of inflammation. In addition, full malignant
transformation of affected parts of the stomach may require that the human host have a particular genotype of
interleukin (IL) to cause the increased inflammation and an increased suppression of gastric acid secretion. For
example, IL-17A and IL-17F are inflammatory cytokines that play a critical role in inflammation. Wu et al
found that carriage of IL-17F 7488GA and GG genotypes were associated with an increased risk of gastric
cancer.[11]
H pylori infection is associated with chronic atrophic gastritis, and patients with a history of prolonged gastritis
have a sixfold increased risk of developing gastric cancer. Interestingly, this association is particularly strong
for tumors located in the antrum, body, and fundus of the stomach but does not seem to hold for tumors
originating in the cardia.[12]
Previous gastric surgery
Previous surgery is implicated as a risk factor. The rationale is that surgery alters the normal pH of the
stomach, which may in turn lead to metaplastic and dysplastic changes in luminal cells.[13]
Retrospective studies demonstrate that a small percentage of patients who undergo gastric polyp removal have
evidence of invasive carcinoma within the polyp. This discovery has led some researchers to conclude that
polyps might represent premalignant conditions.
Genetic factors
Some 10% of stomach cancer cases are familial in origin.
Genetic factors involved in gastric cancer remain poorly understood, though specific mutations have been
identified in a subset of gastric cancer patients. For example, germline truncating mutations of the E-cadherin
gene (CDH1) are detected in 50% of diffuse-type gastric cancers, and families that harbor these mutations have
an autosomal dominant pattern of inheritance with a very high penetrance.[14]
Other hereditary syndromes with a predisposition for stomach cancer include hereditary nonpolyposis
colorectal cancer, Li-Fraumeni syndrome, familial adenomatous polyposis, and Peutz-Jeghers syndrome.
Epstein-Barr virus
The Epstein-Barr virus may be associated with an unusual (< 1%) form of stomach cancer, lymphoepithelioma-
like carcinoma.
Pernicious anemia
Pernicious anemia associated with advanced atrophic gastritis and intrinsic factor deficiency is a risk factor for
gastric carcinoma.
Gastric ulcers
Gastric cancer may develop in the remaining portion of the stomach following a partial gastrectomy for gastric
ulcer.
Benign gastric ulcers may themselves develop into malignancy.
Obesity
Obesity increases the risk of gastric cardia cancer.
Radiation exposure
Survivors of atomic bomb blasts have had an increased rate of stomach cancer. Other populations exposed to
radiation may also have an increased rate of stomach cancer.
Bisphosphonates
A large cohort study examined whether use of oral bisphosphonates was associated with an increased risk of
esophageal or gastric cancers. No significant difference was observed for increased risk of esophageal or
gastric cancers between the bisphosphonate cohort and the control group.[15]
Previous
Proceed to Differential Diagnoses
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Contributor Information and Disclosures
Author
Elwyn C Cabebe, MD Adjunct Clinical Faculty, Department of Internal Medicine, Division of Medical
Oncology, Stanford University School of Medicine
Elwyn C Cabebe, MD is a member of the following medical societies: American Association for Cancer
Research, American Society of Clinical Oncology, and Philippine Medical Society of Northern California
Disclosure: Nothing to disclose.

Coauthor(s)
Vivek K Mehta, MD Radiation Oncologist, Director, Center for Advanced Targeted Radiotherapies,
Department of Radiation Oncology, Swedish Cancer Institute, Seattle, Washington
Vivek K Mehta, MD is a member of the following medical societies: American Society for Therapeutic
Radiology and Oncology, Phi Beta Kappa, and Sigma Xi

George Fisher, MD, PhD Associate Professor, Department of Internal Medicine, Division of Medical
George Fisher, MD, PhD is a member of the following medical societies: American Cancer Society and
American Medical Association

Specialty Editor Board
Michael Perry, MD, MS, MACP Nellie B Smith Chair of Oncology Emeritus, Professor, Department of
Internal Medicine, Division of Hematology and Oncology, University of Missouri/Ellis Fischel Cancer Center
Michael Perry, MD, MS, MACP is a member of the following medical societies: Alpha Omega Alpha,
American Association for Cancer Research, American College of Physicians, American College of Physicians-
American Society of Internal Medicine, American Medical Association, American Society of Clinical
Oncology, American Society of Hematology, International Association for the Study of Lung Cancer, and
Missouri State Medical Association

Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Benjamin Movsas, MD Vice-Chairman, Department of Radiation Oncology, Fox Chase Cancer Center
Benjamin Movsas, MD is a member of the following medical societies: American College of Radiology,
American Radium Society, and American Society for Therapeutic Radiology and Oncology

Rajalaxmi McKenna, MD, FACP Southwest Medical Consultants, SC, Department of Medicine, Good
Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical
Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis

Chief Editor
Jules E Harris, MD Clinical Professor of Medicine, Division of Hematology/Medical Oncology, Department
of Internal Medicine, University of Arizona College of Medicine; Consulting Staff, Arizona Cancer Center
Jules E Harris, MD is a member of the following medical societies: American Association for Cancer
Research, American Association for the Advancement of Science, American Association of Immunologists,
American Society of Hematology, and Central Society for Clinical Research
Disclosure: GlobeImmune Salary Consulting

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Differentials
• Esophageal Cancer
• Esophageal Stricture
• Esophagitis
• Gastric Ulcers
• Gastritis, Acute
• Gastritis, Atrophic
• Gastritis, Chronic
• Gastroenteritis, Bacterial
• Gastroenteritis, Viral
• Lymphoma, Non-Hodgkin
• Malignant Neoplasms of the Small Intestine
Proceed to Workup
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Author

Coauthor(s)






Chief Editor

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References
19, 2009.
[Medline].
Gut. Jan 2010;59(1):39-48. [Medline].
20 2003;107(4):629-34. [Medline].
[Medline].
2002;21:166a.
Oct 2009;209(4):461-7. [Medline].
2010;97(5):643-9. [Medline].
28 1994;343(8909):1309-12. [Medline].
[Medline].
[Medline].
2009;374(9688):477-90. [Medline].
2003;40(2):114-7. [Medline].
2007;357(3):283-91. [Medline].
Surg. Feb 2004;187(2):270-3. [Medline].

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Laboratory Studies
The goal of obtaining laboratory studies is to assist in determining optimal therapy.
A CBC count can identify anemia, which may be caused by bleeding, liver dysfunction, or poor nutrition.
Approximately 30% of patients have anemia.
Electrolyte panels and liver function tests also are essential to better characterize the patient's clinical state.
Carcinoembryonic antigen (CEA) is increased in 45-50% of cases.
Cancer antigen (CA) 19-9 is elevated in about 20% of cases.
Next Section: Imaging Studies
Imaging Studies
Esophagogastroduodenoscopy has a diagnostic accuracy of 95%. This relatively safe and simple procedure
provides a permanent color photographic record of the lesion. This procedure is also the primary method for
obtaining a tissue diagnosis of suspected lesions. Biopsy of any ulcerated lesion should include at least 6
specimens taken from around the lesion because of variable malignant transformation. In selected cases,
endoscopic ultrasound may be helpful in assessing depth of penetration of the tumor or involvement of adjacent
structures.
Double-contrast upper GI series and barium swallows may be helpful in delineating the extent of disease when
obstructive symptoms are present or when bulky proximal tumors prevent passage of the endoscope to examine
the stomach distal to an obstruction (more common with gastroesophageal [GE]-junction tumors). These
studies are only 75% accurate and should for the most part be used only when upper GI endoscopy is not
feasible.
Chest radiograph is done to evaluate for metastatic lesions.
CT scan or MRI of the chest, abdomen, and pelvis assess the local disease process as well as evaluate potential
areas of spread (ie, enlarged lymph nodes, possible liver metastases).
Endoscopic ultrasound allows for a more precise preoperative assessment of the tumor stage. Endoscopic
sonography is becoming increasingly useful as a staging tool when the CT scan fails to find evidence of T3, T4,
or metastatic disease. Institutions that favor neoadjuvant chemoradiotherapy for patients with locally advanced
disease rely on endoscopic ultrasound data to improve patient stratification.
Previous
Histologic Findings
Adenocarcinoma of the stomach constitutes 90-95% of all gastric malignancies. The second most common
gastric malignancies are lymphomas. Gastrointestinal stromal tumors formerly classified as either leiomyomas
or leiomyosarcomas account for 2% of gastric neoplasms (see Gastric Stromal Tumors). Carcinoids (1%),
adenoacanthomas (1%), and squamous cell carcinomas (1%) are the remaining tumor histologic types.
Adenocarcinoma of the stomach is subclassified according to histologic description as follows: tubular,
papillary, mucinous, or signet-ring cells, and undifferentiated lesions.
Pathology specimens are also classified by gross appearance. In general, researchers consider gastric cancers
ulcerative, polypoid, scirrhous (ie, diffuse linitis plastica), superficial spreading, multicentric, or Barrett ectopic
adenocarcinoma.
Researchers also employ a variety of other classification schemes. The Lauren system classifies gastric cancer
pathology as either Type I (intestinal) or Type II (diffuse). An appealing feature of classifying patients
according to the Lauren system is that the descriptive pathologic entities have clinically relevant differences.
Intestinal, expansive, epidemic-type gastric cancer is associated with chronic atrophic gastritis, retained
glandular structure, little invasiveness, and a sharp margin. The pathologic presentation classified as epidemic
by the Lauren system is associated with most environmental risk factors, carries a better prognosis, and shows
no familial history.
The second type, diffuse, infiltrative, endemic cancer, consists of scattered cell clusters with poor
differentiation and dangerously deceptive margins. Margins that appear clear to the operating surgeon and
examining pathologist often are determined retrospectively to be involved. The endemic-type tumor invades
large areas of the stomach. This type of tumor is also not recognizably influenced by environment or diet, is
more virulent in women, and occurs more often in relatively young patients. This pathologic entity is
associated with genetic factors (such as E-cadherin), blood groups, and a family history of gastric cancer.
Previous
Staging
The 2006 American Joint Committee on Cancer (AJCC) Cancer Staging Manual presents the following TNM
classification system for staging gastric carcinoma:[16]
Primary tumor
• TX - Primary tumor (T) cannot be assessed
• T0 - No evidence of primary tumor
• Tis - Carcinoma in situ, intraepithelial tumor without invasion of lamina propria
• T1 - Tumor invades lamina propria or submucosa
• T2 - Tumor invades muscularis propria or subserosa
• T3 - Tumor penetrates serosa (ie, visceral peritoneum) without invasion of adjacent structures
• T4 - Tumor invades adjacent structures
Regional lymph nodes
• NX - Regional lymph nodes (N) cannot be assessed
• N0 - No regional lymph node metastases
• N1 - Metastasis in 1-6 regional lymph nodes
• N2 - Metastasis in 7-15 regional lymph nodes
• N3 - Metastasis in more than 15 regional lymph nodes
Distant metastasis
• MX - Distant metastasis (M) cannot be assessed
• M0 - No distant metastasis
• M1 - Distant metastasis
Prognostic features
Two important factors influencing survival in resectable gastric cancer are depth of cancer invasion through the
gastric wall and presence or absence of regional lymph node involvement.
In about 5% of primary gastric cancers, a broad region of the gastric wall or even the entire stomach is
extensively infiltrated by malignancy, resulting in a rigid thickened stomach, termed linitis plastica. Patients
with linitis plastica have an extremely poor prognosis.[17]
Margins positive for presence of cancer are associated with a very poor prognosis.
The greater the number of involved lymph nodes, the more likely the patient is to develop local and systemic
failure after surgery.
In a study by Shen and colleagues,[18] the depth of tumor invasion and gross appearance, size, and location of the
tumor were 4 pathologic factors independently correlated with the number of metastatic lymph nodes
associated with gastric cancer.
Lee and colleagues found that surgical stage, as estimated during curative resection for gastric cancer,
complemented the pathologically determined stage for determining prognosis. Survival was significantly
poorer among patients with pathologic Stages II, IIIa, and IIIb disease in whom intraoperative staging
overestimated the extent of pathological stage.[19]
Staging
• Stage 0 - Tis, N0, M0
• Stage IA - T1, N0 or N1, M0
• Stage IB - T1, N2, M0 or T2a/b, N0, M0
• Stage II - T1, N2, M0 or T2a/b, N1, M0 or T2, N0, M0
• Stage IIIA - T2a/b, N2, M0 or T3, N1, M0 or T4, N0, M0
• Stage IIIB - T3, N2, M0
• Stage IV - T1-3, N3, M0 or T4, N1-3, M0, or any T, any N, M1
Survival rates
• Stage 0 - Greater than 90%
• Stage Ia - 60-80%
• Stage Ib - 50-60%
• Stage II - 30-40%
• Stage IIIa - 20%
• Stage IIIb - 10%
• Stage IV - Less than 5%.
Spread patterns
Cancer of the stomach can spread directly, via lymphatics, or hematogenously.
Direct extension into the omenta, pancreas, diaphragm, transverse colon or mesocolon, and duodenum is
common.
If the lesion extends beyond the gastric wall to a free peritoneal (ie, serosal) surface, then peritoneal
involvement is frequent.
The visible gross lesion frequently underestimates the true extent of the disease.
The abundant lymphatic channels within the submucosal and subserosal layers of the gastric wall allow for
easy microscopic spread.
The submucosal plexus is prominent in the esophagus and the subserosal plexus is prominent in the duodenum,
allowing proximal and distal spread.
Lymphatic drainage is through numerous pathways and can involve multiple nodal groups (eg, gastric,
gastroepiploic, celiac, porta hepatic, splenic, suprapancreatic, pancreaticoduodenal, paraesophageal, and
paraaortic lymph nodes).
Hematogenous spread commonly results in liver metastases.
Previous
Proceed to Treatment & Management
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References
19, 2009.
[Medline].
Gut. Jan 2010;59(1):39-48. [Medline].
20 2003;107(4):629-34. [Medline].
[Medline].
2002;21:166a.
Oct 2009;209(4):461-7. [Medline].
2010;97(5):643-9. [Medline].
28 1994;343(8909):1309-12. [Medline].
[Medline].
[Medline].
2009;374(9688):477-90. [Medline].
2003;40(2):114-7. [Medline].
2007;357(3):283-91. [Medline].
Surg. Feb 2004;187(2):270-3. [Medline].

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Surgical Care
Type of surgery
In general, most surgeons in the United States perform a total gastrectomy (if required for negative margins),
an esophagogastrectomy for tumors of the cardia and gastroesophageal junction, and a subtotal gastrectomy for
tumors of the distal stomach.
A randomized trial comparing subtotal with total gastrectomy for distal gastric cancer revealed similar
morbidity, mortality, and 5-year survival rates.[20]
Because of the extensive lymphatic network around the stomach and the propensity for this tumor to extend
microscopically, traditional teaching is to attempt to maintain a 5-cm surgical margin proximally and distally to
the primary lesion.
Lymph node dissection
The extent of the lymph node dissection is somewhat controversial.
Many studies demonstrate that nodal involvement indicates a poor prognosis, and more aggressive surgical
approaches to attempt to remove involved lymph nodes are gaining popularity.
Two randomized trials compared D1 (perigastric lymph nodes) with D2 (hepatic, left gastric, celiac, and
splenic arteries, as well as those in the splenic hilum) lymphadenectomy in patients who were treated for
curative intent. In the largest of these trials, postoperative morbidity (43% versus 25%) and mortality (10%
versus 4%) were higher in the D2 group.[21, 22]
Most critics argue that these studies were underpowered and overestimated benefit. In addition, a recent
randomized trial found a much lower rate of complications than those earlier trials. Degiuli et al reported
complication rates of 17.9% and 12% with D2 and D1 dissections, respectively — a statistically insignificant
difference — and postoperative mortality rates of 2.2% and 3%, respectively.[23]
D2 dissections are recommended by the National Comprehensive Cancer Network over D1 dissections. A
pancreas- and spleen - preserving D2 lymphadenectomy is suggested, as it provides greater staging
information, and may provide a survival benefit while avoiding its excess morbidity when possible.
Outcome
The 5-year survival rate for a curative surgical resection ranges from 60-90% for patients with stage I, 30-50%
for patients with stage II disease, and 10-25% for patients with stage III disease.
Because these patients have a high likelihood of local and systemic relapse, some physicians offer adjuvant
therapy.
Next Section: Consultations
Consultations
Specialists recommend obtaining consultations freely in the management of most malignancies, and gastric
carcinoma is no exception. The gastroenterologist, surgical oncologist, radiation oncologist, and medical
oncologist work closely as a team.
Deterrence/Prevention
A diet that includes fruits and vegetables rich in vitamin C may have a protective effect.
Next Section: Complications
Complications
Direct mortality rate within 30 days after a surgical procedure for gastric cancer has been reduced substantially
over the last 40 years. Most major centers report a direct mortality rate of 1-2%.
Early postoperative complications include anastomotic failure, bleeding, ileus, transit failure at the
anastomosis, cholecystitis (often occult sepsis without localizing signs), pancreatitis, pulmonary infections, and
thromboembolism. Further surgery may be required for anastomotic leaks.
Late mechanicophysiologic complications include dumping syndrome, vitamin B-12 deficiency, reflux
esophagitis, and bone disorders, especially osteoporosis.
Postgastrectomy patients often are immunologically deficient, as measured by blastogenic and delayed
cutaneous hypersensitivity responses.
Previous
Prognosis
Unfortunately, only a minority of patients with gastric cancer who undergo a surgical resection will be cured of
their disease. Most patients have a recurrence.
Patterns of failure
Several studies have investigated the patterns of failure after surgical resection alone. Studies that depend
solely on the physical examination, laboratory studies, and imaging studies may overestimate the percentage of
patients with distant failure and underestimate the incidence of local failure, which is more difficult to detect.
A reoperation series from the University of Minnesota may offer a more accurate understanding of the biology
of the disease. In this series of patients, researchers surgically reexplored patients 6 months after the initial
surgery and meticulously recorded the patterns of disease spread. The total local-regional failure rate
approached 67%. The gastric bed was the site of failure in 54% of these cases, and the regional lymph nodes
were the site of failure in 42%. Approximately 26% of patients had evidence of distant failure. The patterns of
failure included local tumor regrowth, tumor bed recurrences, regional lymph node failures, and distant failures
(ie, hematogenous failures and peritoneal spread). Primary tumors involving the gastroesophageal junction
tended to fail in the liver and the lungs. Lesions involving the esophagus failed in the liver.[24]
Adjuvant therapy
The pattern of failure prompted a number of investigations into adjuvant therapy. The rationale behind
radiotherapy is to provide additional local-regional tumor control. Adjuvant chemotherapy is used either as a
radiosensitizer or as definitive treatment for presumed systemic metastases.
Adjuvant radiotherapy
Moertel and colleagues randomized postoperative patients with advanced gastric cancer to receive 40 Grays
(Gy) of radiotherapy or 40 Gy of radiotherapy with 5-FU as a radiosensitizer and demonstrated improved
survival associated with the combined-modality therapy.[25]
The British Stomach Cancer Group reported lower rates of local recurrence in patients who received
postoperative radiotherapy than in those who underwent surgery alone.[26]
The update of the initial Gastrointestinal Tumor Study Group series revealed higher 4-year survival rates in
patients with unresectable gastric cancer who received combined-modality therapy than in those who received
chemotherapy alone (18% vs 6%).[27]
In a series from the Mayo Clinic, patients were randomized to receive postoperative radiotherapy with 5-FU or
surgery alone, and improved survival was demonstrated in patients receiving adjuvant therapy (23% vs 4%).[28]
Intraoperative radiotherapy
Some authors suggest that intraoperative radiotherapy (IORT) shows promising results.
This alternative method of delivering radiotherapy allows for a high dose to be given in a single fraction while
in the operating room so that other critical structures can be avoided.
The National Cancer Institute randomized patients with grossly resected stage III/IV gastric cancer to receive
either 20 Gy of IORT or 50 Gy of postoperative external beam radiation. Local failure was delayed in the
patients treated with IORT (21 mo vs 8 mo). Although the median survival duration also was higher (21 mo vs
10 mo), this figure did not reach statistical significance.[29]
Adjuvant chemotherapy
Numerous randomized clinical trials comparing combination chemotherapy in the postoperative setting to
surgery alone did not demonstrate a consistent survival benefit.
Recent meta-analyses have shown a hint of statistical benefit. In one meta-analysis of 13 randomized trials,
adjuvant systemic chemotherapy was associated with a significant survival benefit (odds ratio for death, 0.80;
95% CI, 0.66-0.97). In subgroup analysis, there was a trend toward a larger magnitude of effect for trials in
which at least two thirds of the patients had node-positive disease.[30]
A postoperative chemoradiation study was prompted in part by the patterns of local failure often preceding
systemic spread.
Adjuvant chemoradiotherapy
A randomized phase III study performed in the United States, Intergroup 0116, demonstrated a survival benefit
associated with postoperative chemoradiotherapy compared with surgery alone.[2]
In this study, patients underwent an en bloc resection.
Patients with T3 and/or N+ adenocarcinoma of the stomach or gastroesophageal junction were randomized to
receive a bolus of 5-fluorouracil (5-FU) and leucovorin (LV) and radiotherapy or observation.
Patients who received the adjuvant chemoradiotherapy demonstrated improved disease-free survival (from 32%
to 49%) and improved overall survival rates (from 41% to 52%) compared to those who were merely observed.
This regimen is considered the standard of care in the United States.
Neoadjuvant chemotherapy
Neoadjuvant chemotherapy may allow downstaging of disease to increase resectability, decrease
micrometastatic disease burden prior to surgery, allow patient tolerability prior to surgery, determine
chemotherapy sensitivity, reduce the rate of local and distant recurrences, and ultimately improve survival.
A European randomized trial also demonstrated survival benefit when patients were treated with 3 cycles of
preoperative chemotherapy (epirubicin, cisplatin, and 5-fluorouracil) followed by surgery and then 3 cycles of
postoperative chemotherapy compared with surgery alone. The benefit was comparable to that obtained with
postoperative chemoradiation in the US trial.[3] However, the Gastric Chemotherapy Group for Japan did not
demonstrate a significant survival benefit with neoadjuvant chemotherapy.
Choice of preoperative and postoperative chemotherapy versus postoperative chemotherapy and radiation
remains controversial, and an ongoing United States Intergroup study, CALGB 80101, will look more closely
at that question.
Advanced unresectable disease
Many patients present with distant metastases, carcinomatosis, unresectable hepatic metastases, pulmonary
metastases, or direct infiltration into organs that cannot be resected completely.
In the palliative setting, radiotherapy provides relief from bleeding, obstruction, and pain in 50-75% of patients.
The median duration of palliation is 4-18 months.
Surgical procedures such as wide local excision, partial gastrectomy, total gastrectomy, simple laparotomy,
gastrointestinal anastomosis, and bypass also are performed with palliative intent, with a goal of allowing oral
intake of food and alleviating pain.
Platinum-based chemotherapy, in combinations such as epirubicin/cisplatin/5-FU or docetaxel/cisplatin/5-FU,
represents the current first-line regimen. Other active regimens include irinotecan and cisplatin and other
combinations with oxaliplatin and irinotecan.
Results of cisplatin-based chemotherapy have been largely discouraging, with median time to progression of 3-
4 months and overall survival of approximately 6-9 months despite reported response rates of up to 45%. Early
results reported in 2007 by Japanese clinicians suggest some improvement in both response rates and survival
with the oral fluoropyrimidine S-1 used alone or in combination with cisplatin.[31] (S-1 combines 3
investigational drugs: tegafur, a prodrug of 5-FU; gimeracil, an inhibitor of fluorouracil degradation; and
oteracil or potassium oxanate, a GI tract adverse-effect modulator.) These results remain to be confirmed by
ongoing studies in Europe and North America.
Bevacizumab, a monoclonal antibody against vascular endothelial growth factor (VEGF) is currently being
evaluated for use in advanced gastric cancer.[32]
Novel treatment strategies may be guided by the use of gene signatures.[33] Kim et al reported that combined
overexpression of MYC, EGFR, and FGFR2 predicts a poor response of metastatic gastric cancer to treatment
with cisplatin and fluorouracil.[34]
Ishido et al reported that in patients receiving S-1 chemotherapy after gastrectomy for advanced gastric cancer,
intratumoral mRNA expression of thymidylate synthase (TS) is an independent prognostic factor for response
to chemotherapy. In 39 patients who received postoperative S-1, recurrence-free survival and overall survival
were significantly longer in patients with low TS expression than in those with high TS expression (P=0.021
and 0.016, respectively), whereas in 40 patients treated with surgery only, TS expression did not correlate with
survival.[35]
Overexpression of human epidermal growth factor receptor 2 (HER2) is a significant negative prognostic factor
for gastric cancer. In the international ToGA trial (trastuzumab with chemotherapy in HER2-positive advanced
gastric cancer), about 22% of patients with advanced gastric cancer were found to have tumors that
overexpressed HER2. In this phase III trial, 594 patients with HER2-positive advanced gastric cancer were
randomized to receive standard chemotherapy alone or chemotherapy plus trastuzumab (Herceptin). Overall
survival with trastuzumab was 13.8 months, compared with 11.1 months in the chemotherapy group (hazard
ratio, 0.74, P = .0046).[36]
Although modest, this 2.7-month improvement in overall survival is clinically meaningful in this group of
patients, who have a poor prognosis. In addition to the impact on overall survival, trastuzumab improved all of
the secondary end points, including progression-free survival (increased from 5.2 mo to 6.7 mo; P = .002) and
overall response rate (increased from 34.5% to 47%; P =.0017).
Trastuzumab was approved in October of 2010 for the treatment of HER2-overexpressing metastatic gastric or
gastroesophageal junction adenocarcinoma. It is administered in combination with cisplatin and capecitabine or
5-fluorouracil in patients who have not received prior treatment for metastatic disease. The trastuzumab dose
consists of an initial cycle of 8 mg/kg intravenously (IV) infused over 90 minutes, followed by subsequent
cycles of 6 mg/kg IV infused over 30-90 minutes every 3 weeks. Treatment is continued until the disease
progresses.
Previous
Patient Education
For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also,
see eMedicine's patient education article, Stomach Cancer.
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Identifying the Risk Factors Through the Username or Email:
Development of a Predictive Model for Gastric
Cancer in South Korea
Password:
Lee, Dong-Suk PhD, RN; Yang, Han-Kwang MD, PhD; Kim,
Jong-Won MD, PhD; Yook, Jeong-Whan MD, PhD; Jeon,
Seong-Hoon MD, PhD; Kang, Sung-Hak MD, PhD; Kim,
Young-Ju PhD
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Authors' Affiliations: Nursing School, Kangwon National University,
Kangwon (Dr Lee); Surgical Department, Seoul National University
Hospital, Seoul (Drs Yang and J. W. Kim); Surgical Department (Dr Forgot your Password?
Yook); Health Promotion Center (Dr Jeon), Asan Medical Center, Seoul;
and Health Promotion Center, Catholic University Hospital, Kyunggi (Dr
Kang); and Department of Information Statistics, Kangwon National
University, Kangwon, South Korea (Dr Y. J. Kim). Enter and submit the email address
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This research was supported by a grant from the Korea Research instructions to reset your password
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Corresponding author: Young-Ju Kim, PhD, Department of Information Sorry, the specified email address
Statistics, Kangwon National University, 192-1 Hyoja-Dong, ChunCheon, could not be found. Try again.
Kangwon-Do 200-701, Kangwon, South Korea Email:
(ykim7stat@kangwon.ac.kr).
Accepted for publication July 25, 2008.
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Abstract
The objective of this study was to identify the main risk factors for gastric
cancer in Koreans through the development of a predictive model by Forgot your Password?
multivariate logistic regression analysis that could aid the development of
specific guidelines for early detection. We conducted a case control study to
identify the risk factors for gastric cancer. The cohorts comprised 183
patients with gastric cancer and 199 adults without gastric cancer as Link to reset your password has
controls. Risk factors were identified, and a predictive model was been sent to specified email
established by multivariate logistic regression analysis. Major risk factors address.
included in the final predictive model were being older, having a family
history of gastric cancer, a family history of gastric ulcer, a personal history
of gastric ulcer, a poor perceived health status, a low perceived financial
status, being exposed to jobs considered to cause stomach cancer, drinking
tap water, and eating irregularly and rapidly. The accuracy of the final
predictive model was confirmed by its high degrees of sensitivity and Remember me
specificity. The predictive model developed in this study can be used for
classifying high-risk groups and for guiding early-detection screening for
gastric cancer.
Gastric cancer is the fourth most common type of cancer and the second What does "Remember me"
leading cause of cancer death worldwide.1 In South Korea and Japan, the mean?
most prevalent type of cancer is gastric cancer, in contrast to the incidence By checking this box, you'll stay
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and dietary factors such as the consumption of smoked meat, salted meat, To protect your most sensitive data
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early in life can have a long-lasting effect,3 for example, Japanese migrants password), we'll ask you to re-enter
retain their lifetime risks after emigrating from Japan. Several case control your password when you access
studies4-6 performed in South Korea found that living in a rural area before these services.
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that occupational contact is a contributing factor, coming from a lower What if I'm on a computer that I
socioeconomic group (as well as dietary habits in these groups) may play a share with others?
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The 5-year survival rate after the early detection of gastric cancer is 90% to
98%,2 demonstrating the importance of detecting gastric cancer at an early
stage. However, the early detection rate of gastric cancer is relatively low in
South Korea, especially considering its high incidence.1,8 There are several
reasons for this low rate of early detection in South Korea: (1) Most Article Tools
Koreans are unaware of risk factors such as traditional Korean food, which • Article as PDF (1.07 MB)
is very salty. (2) Guidelines published by the Korean National Cancer
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Epidemiologic Analysis of Gastric Carcinoma in the Western Region of Nepal Nepal Journal of Epidemiology
2010;1 (1):27-32 Copyright © 2010 INEA PublEpidemiologic Analysis of Gastric Carcinoma in the Western Region of
Nepal Nepal Journal of Epidemiology 2010;1 (1):27-32 Copyright © 2010 INEA Published online by NepJOL-INASP
www.nepjol.info/index.php/NJE
Epidemiologic Analysis of Gastric Carcinoma in the Western
Region of Nepal Ghosh A1, Sathian B2, Gharti D M3, Narasimhan R4, Talwar O P5 1
Associate Professor, Department of Pathology, Manipal College of Medical Sciences,
Pokhara, Nepal 2 Assistant Professor, Department of Community Medicine, Manipal
College of Medical Sciences, Pokhara, Nepal 3 Lecturer, Department of Pathology, Manipal
College of Medical Sciences, Pokhara, Nepal 4 Professor, Department of Pathology,
Manipal College of Medical Sciences, Pokhara, Nepal 5 Professor & HOD, Department of
Pathology, Manipal College of Medical Sciences, Pokhara, Nepal
• ished online by NepJOL-INASP www.nepjol.info/index.php/NJE
Epidemiologic Analysis of Gastric Carcinoma in the Western Region of Nepal Nepal Journal of Epidemiology
2010;1 (1):27-32 Copyright © 2010 INEA Published online by NepJOL-INASP www.nepjol.info/index.php/NJE
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