Tap icon
to view sections


The following module was designed to supplement the clinical experience of medical students. It covers the anatomy, epidemiology, screening, presentation, diagnosis, staging, prognosis, management, and follow up care of gastric cancer. Bolded points are adapted from the Oncology Goals and Objectives for Medical Students for gastric cancer.

This module covers the following objectives:

  1. Review the gross anatomy of the stomach and its surrounding structures. 
  2. Describe the layers of the stomach wall and their importance in staging gastric cancer.
  3. Recognize the most common histology of gastric cancer.
  4. Know that gastric cancers can be classified by histology and location, although their value for prognostication is often not clear.
  5. Know the major risk factors of gastric cancer.
  6. Estimate the incidence of gastric cancer.
  7. Understand the role of screening for gastric cancer in asymptomatic adults. Identify which patient populations stand to benefit from screening.
  8. Recognize that gastric cancer is often asymptomatic and that early symptoms are mostly nonspecific. Know some clinical indications for further workup while appreciating that their predictive value is often limited.
  9. Describe the components of a workup for suspected gastric cancer.
  10. List factors affecting the prognosis and treatment of gastric cancer.
  11. Understand that patients treated with curative intent are nonetheless at risk for recurrence and that this risk is mostly front-loaded. 
  12. Understand that surgery, chemotherapy, and radiation therapy are all important in the treatment of gastric cancer. Appreciate that most patients with gastric cancer will benefit from multidisciplinary discussion (e.g. tumor boards).
  13. Know common and serious complications that can arise during and after the treatment of gastric cancer.
  14. Recognize aspects that should be considered in the follow up of gastric cancer after treatment.


The stomach is a hollow intraperitoneal digestive organ situated in the left upper abdomen, usually in the epigastric region. It is bound proximally by the gastroesophageal junction (GEJ) and distally by the pyloric sphincter.

The stomach consists of four main anatomical regions which differ histologically and functionally:

  1. The gastric cardia is a small ill-defined region of the stomach near the GEJ, the exact extent of which is contested [1]. A common classification system for adenocarcinomas near the GEJ, proposed by Siewert and Stein, defines the cardia as a region spanning 1cm above to 2cm below the GEJ [2]. 
  2. The fundus is a part of the stomach located superior to the level of the GEJ. 
  3. The body is the central portion of the stomach below the fundus but proximal to the pylorus.
  4. The pylorus is the most distal portion of the stomach that can be further divided into the pyloric antrum, which is located inferiorly; and the pyloric canal, where the stomach abruptly narrows as it approaches the duodenum. The pyloric sphincter regulates the passage of chyme from the pylorus to the duodenum.

Image 1. Regions of the stomach
Adapted from Anatomy of the Human Body (20th edition). Philadelphia and New York.

The stomach is also described as having lesser and greater curvatures. The lesser curvature, which forms the medial border of the stomach, attaches to the liver by the lesser omentum. At the lateral edge, the greater curvature of the stomach is attached to the diaphragm, spleen, and transverse colon by the greater omentum.

The wall of the stomach is divided into five main layers. From deep to superficial, these are:

  1. Mucosa which consists of simple columnar epithelium, lamina propria, and muscularis mucosa
  2. Submucosa
  3. Muscularis propria arranged in oblique, circular, and longitudinal layers.
  4. Subserosa
  5. Serosa or visceral peritoneum
Image 2. Layers of the stomach

Organs in Close Proximity:

  1. Superior: Esophagus, Left Hemidiaphragm
  2. Anterior: Liver, Gallbladder, Greater Omentum
  3. Posterior: Left Kidney, Left Adrenal Gland, Spleen, Pancreas, Transverse Colon 
Images 3a and 3b. Organs in proximity of stomach

Vascular Supply:

The stomach’s blood supply is derived from branches of the celiac artery, which arises from the aorta at the level of T12/L1:

  1. The left gastric artery supplies the superior right portion of the stomach stomach.
  2. The common hepatic artery branches into the right gastric artery, which supplies the inferior right portion of the stomach, and the right gastroepiploic artery, which supplies the inferior greater curvature.
  3. The splenic artery branches into the short gastric arteries, which supplies the fundus, and left gastroepiploic artery, which supplies the superior greater curvature.
Image 4. Vascular supply to the stomach


The stomach is innervated by the autonomic nervous system:

  1. Vagus Nerve (parasympathetic nerve supply)
  2. T6-9 spinal cord segments, which pass to the Celiac Plexus through the Greater Splanchnic Nerve (sympathetic nerve supply)


Gastric lymphatic vessels can be found along both the greater and lesser curvature of the stomach. The contents of these vessels are drained into surrounding lymph nodes, which then subsequently drain into the celiac lymph nodes found on the posterior abdominal wall.

Lymph nodes of the stomach are defined by their location relative to adjacent structures. The Japanese Gastric Cancer Association describes 33 regional lymph node stations; these have implications in staging and treatment as discussed later in this module.

Image 5. Lymphatic drainage of stomach


Adenocarcinomas account for 95% of gastric cancers. In fact, the term “gastric cancer” used without qualification is understood to refer to gastric adenocarcinoma [3]. Rarer gastric cancers include lymphomas (second most common), gastrointestinal stromal tumors, carcinoid tumors, adenocanthomas, squamous cell carcinoma, small cell carcinoma, and leiomyosarcoma.

Gastric adenocarcinomas can be classified histologically as either diffuse or intestinal type, as described by Laurén [4]. The intestinal type is named for its tendency to form glands resembling those found in the colon [3]. Intestinal type adenocarcinomas usually develop in the distal stomach and arise from precursor lesions. Risk factors include H. pylori infection, male sex, and older age. In contrast, diffuse type tends to be poorly differentiated and has a greater propensity to invade and spread. They are usually found in the proximal stomach and do not have precursor lesions. Compared to intestinal type, the diffuse type is less strongly linked to H. pylori and more prevalent in women and younger patients [4, 5]. The prognostic value of Laurén classification independent of TNM stage is uncertain [6].

Tumor site is also important in the discussion of gastric cancer because it affects lymphatic drainage and treatment. A common distinction is cardia versus noncardia gastric cancer. Adenocarcinoma near the cardia are further grouped by Siewert classification [2]:

  1. Type I: tumor epicenter located 1-5cm above the GEJ
  2. Type II: tumor epicenter located 1cm above to 2cm below the GEJ. These are the true tumors of the cardia.
  3. Type III: tumor epicenter located 2-5cm below the GEJ.

Siewert types I and II adenocarcinomas are staged as esophageal cancer while Siewert type III adenocarcinomas are staged as gastric cancer [7]. Only Siewert type III is covered in this module. Please refer to the module on esophageal cancer for Siewert types I and II cancer.


Gastric cancer is the 11th most commonly diagnosed cancer in Canada with 3500 new cases and 2100 deaths in 2017 [8]. Worldwide, gastric cancer ranked 6th in total diagnoses with 1,034,000 new cases in 2018. It was responsible for 783,000 deaths, making it the second-leading cause of death after lung cancer [9].

The incidence of gastric cancer is in steady decline in Canada and worldwide, a trend attributed to improved hygiene, dietary changes, and the eradication of H. pylori [10, 11]. A notable exception is gastric cancer originating from the cardia, whose incidence has remained stable or increased in the US and Europe against the overall trend [12, 13, 14].

Risk factors

We summarize the risk factors for gastric cancer in the table below.

Gastric Cancer Risk Factors


H. pylori and EBV infections
Alcohol consumption
Salt consumption
H. Pylori and EBV infections
Radiation exposure


Race/ethnicity (East Asians and Eastern Europeans are at elevated risk)
Male sex
Increased age
Family history of gastric cancer
Genetic conditions including hereditary diffuse gastric cancer, Lynch syndrome, familial adenomatous polyposis, Li-Fraumeni syndrome, and Peutz-Jeghers syndrome

H. Pylori Infection

Infection by H. pylori is strongly linked to non-cardia gastric cancer and gastric lymphoma, increasing risk by around sixfold [14, 15]. Once infected, the lifetime risk of developing gastric cancer is 1% [16]. Importantly, the eradication of H. pylori reduces this risk [17].

EBV infection

Worldwide, 10% of gastric cancers are associated with EBV. The incidence of EBV-associated gastric cancers are highest in the USA and Germany, where it accounts for 16-18% of all gastric cancers [55]. EBV infection is associated with PD-L1 overexpression [56]. EBV-associated gastric cancer has a relatively favorable prognosis compared to other gastric cancers [55].


Obesity increases the risk of gastric cancer of the cardia, but its association with non-cardia gastric cancer is weaker [18, 19].

Tobacco smoking

Smokers are more likely to develop gastric cancer, with dose and duration both contributing to risk [20, 21]. The association is especially strong in intestinal type gastric cancer and gastric cancer involving the cardia [21]. After quitting, the risk of developing gastric cancer decreases over time, with an incidence approaching that of non-smokers after 10 years [20].

Alcohol consumption

Heavy alcohol consumption has consistently been shown to increase the risk of gastric cancer, but the effects of lighter use are less clear [22, 23]. A nonlinear dose-response relationship may explain this finding [24].


It appears that high salt intake increases the risk of gastric cancer. In contrast, fruits and vegetables may have a protective role, possibly mediated by vitamin C [25].


Adjusted for age, men are approximately twofold more likely to develop gastric cancer [10, 26]. Men are projected to account for 2200 of the 3500 annual cases of gastric cancer in Canada [8].


The incidence of gastric cancer increases with age. Among those newly diagnosed with gastric cancer, 93% are at least 45 years old [26].

Race and Ethnicity

Geographically, the incidence of gastric cancer is highest in East Asia and Eastern Europe [9]. Some of this risk persists in the offspring of parents who migrate to the West [16].

Family history and genetics

Positive family history appears to increase the risk of gastric cancer by 1.5 to 3.5 fold in most studies, independent of H. pylori infection and dietary contributions [27]. However, fewer than 3% of gastric cancers are considered hereditary. The most common of the hereditary gastric cancers is hereditary diffuse gastric cancer, in which germline mutations of the CDH-1 gene are most strongly implicated. Rarer hereditary causes of gastric cancer include Lynch syndrome, familial adenomatous polyposis, Li-Fraumeni syndrome, and Peutz-Jeghers syndrome [28].


The two primary screening modalities for gastric cancer are:

  1. Upper endoscopy with biopsy of any suspicious lesions
  2. Radiography including barium radiographs with either photofluorography or digital radiography

Between the two, it appears that upper endoscopy is more effective in reducing mortality from gastric cancer [29].

Owing to the low incidence of gastric cancer in Western populations and the uncertain value of screening on health outcomes in the West, screening for gastric cancer in average-risk asymptomatic patients is generally discouraged [30]. 

Screening programs exist in areas where gastric cancer is more endemic, and they appear to reduce gastric cancer mortality; however, the effect on overall survival is less established [29]. Endoscopic screening may be considered on this basis for recent immigrants from high-risk areas [30].

Patients at risk for hereditary cancer syndromes should be considered for confirmatory testing and screen on a case by case basis. A hereditary cancer program can be helpful in the management of these patients.

Presentation and Diagnosis

Early stage gastric cancer is usually asymptomatic, and its symptoms are usually nonspecific even when present. As a result, only 28% of patients in the US are diagnosed with localized (N0M0) disease [26].

The most common symptoms at the time of diagnosis are abdominal pain (50-65%) and weight loss (40%) [31]. In addition to weight loss, other so-called alarm symptoms include dysphagia, persistent vomiting, early satiety, and signs of upper GI bleeding. All of these are generally manifestations of advanced disease but still have limited predictive value owing to the rarity of gastric cancer and the prevalence of these symptoms in the general population [32]. On the other hand, positive findings on the physical examination such as organomegaly or lymphadenopathy necessarily require very advanced disease with dismal prognosis.

Diagnosis begins with a complete history and physical examination to determine the merits of further investigations. 



Inquire about warning symptoms associated with gastric cancer:

  1. Predominant epigastric pain
  2. Unexplained weight loss
  3. Dysphagia
  4. Odynophagia
  5. Early satiety
  6. Evidence of GI obstruction
  7. Persistent vomiting
  8. Hematemesis or feculent emesis
  9. Melena or recently-ingested materials in stool
  10. Iron deficiency anemia
  11. Consider additional alarm symptoms of esophageal cancer (see esophageal cancer module)

Review of systems with emphasis on common sites for metastases — nodes, liver, lung, and bone
Smoking history
Alcohol consumption
Past medical history with emphasis on GERD, previous malignancies and their treatment
Family history

Vital signs, weight, and height.

Head and Neck Exam:

  1. Masses
  2. Cervical lymphadenopathy
  3. Consider nasopharyngolaryngoscopy

Cardiorespiratory exam:

  1. Decreased breath sounds, hyporesonance
  2. Pleural effusion
  3. Cardiac dysfunction

Abdominal exam:

  1. Abdominal distension, masses, or ascites
  2. Virchow's node (enlarged left supraclavicular LN)
  3. Irish node (enlarged left axillary LN)
  4. Sister Mary Joseph's node (periumbilical mass)
  5. Hepatomegaly, jaundice
  6. Digital rectal examination

Consider other findings associated with common sites of metastases — liver, lung, and bone.

Deciding on which patients to investigate with endoscopy is challenging given the limited value of the history and physical examination. To aid risk stratification, the patient’s risk factors and past medical history should be considered. Without a clear alternative explanation, any patient with alarm symptoms in Table 1 should undergo further assessment. Workup is also reasonable for patients with persistent or progressive abdominal pain and those over 55 with persistent or progressive dyspepsia [30]. Upper endoscopic examination with biopsy is the diagnostic test of choice for gastric cancer. The value of routinely adding barium swallow to endoscopy is unclear; however, barium swallow is compulsory if there is a suspicion for tracheoesophageal fistula [31].

Post-diagnostic workup

Once the diagnosis of gastric cancer is established, the following tests should beconsidered for staging and to guide management:



1. Laboratory investigations

CBC, extended electrolytes, urea, creatinine, liver function tests, alkaline phosphatase. Consider tumor markers such as CEA and CA 19-9.

2. Endoscopic ultrasound (unless metastatic or known unresectable)

Assess tumor depth and perform fine needle aspiration of any suspicious nodes. For T and N staging.

3. Staging laparoscopy and cytology for surgical candidates for cT1b+M0 or N1+M0 disease

To rule out advanced disease that may affect operative approach or possibly preclude operative management.

4. PET/CT skull base to mid-thigh if no evidence of metastatic disease, may be omitted in select low-risk T1 patients

Staging investigation.

5. CT chest/abdomen/pelvis

Staging investigation.

6. Consider PFTs

Helpful for radiotherapy candidates if there is uncertainty about pulmonary reserves.

7. HER2-neu status for M1 adenocarcinoma

To assess for trastuzumab candidacy.

8. Consider MSI-H/dMMR and PD-L1 status for M1 disease with availability of pembrolizumab for gastric cancer.

Pembrolizumab has received fast-track approval by the FDA; it is not widely available in Canada.


TX: primary tumor cannot be assessed
T0: no evidence of primary tumor
Tis: tumor confined to mucosa without lamina propria invasion
T1a: tumor invades lamina propria or muscularis mucosa
T1b: tumor invades submucosa
T2: tumor invades muscularis propria
T3a: tumor penetrates subserosa but not serosa or adjacent organs
T4a: tumor invades serosa
T4b: tumor invades adjacent structures

NX: lymph nodes cannot be assessed
N0: no regional* or common iliac lymph node metastases
N1: 1-2 positive regional lymph nodes
N2: 3-6 positive regional lymph nodes
N3a: 7-15 positive regional lymph nodes
N3b: 16+ positive regional lymph nodes

*regional lymph nodes refer to left/right paracardial, perigastric, celiac axis, left gastric artery, common hepatic artery, splenic, and hepatoduodenal nodes

M0: no distant metastases
M1: distant metastases are present


Stage 0: Tis N0 M0
Stage I: T1-2 N0 M0
Stage IIA: T1-2 N1-3 M0
Stage IIB: T3-4a N0 M0
Stage III: T3-4a N1-3 M0
Stage IVA: T4b N0-3 M0
Stage IVB: M1 disease


Stage I: T1-2 N0 M0 or T1 N1 M0
Stage II: T3-4a N0 M0 or T2-3 N1 M0 or T1-2 N2 M0 or T1 N3 M0
Stage III: T4b N0 M0 or T4a-b N1 M0 or T3-4b N2 M0 or T2-4b N3 M0
Stage IV: M1 disease


Stage 0: Tis N0 M0
Stage IA: T1 N0 M0
Stage IB: T2 N0 M0 or T1 N1 M0
Stage IIA: T3 N0 M0 or T2 N1 M0 or T3 N0 M0
Stage IIB: T4a N0 M0 or T3 N1 M0 or T2 N2 M0 or T1 N3a M0
Stage IIIA: T4b N0 M0 or T4a N1 M0 or T3-4a N2 M0 or T2 N3a M0
Stage IIIB: T4b N1-2 M0 or T3-4a N3a M0 or T1-2 N3b M0
Stage IVA: T4b N3a M0 or T3-4b N3b M0
Stage IVB: M1 disease


Surgery, radiotherapy, and systemic therapy are all routinely used in the management of gastric cancer. Treatment plans should be tailored to each patient and benefit from multidisciplinary discussion.

Treatment summary

Recommendations on the treatment of gastric cancer are summarized below. 

We discuss briefly the treatment of gastric cancer depending surgical resectability and the presence of distant metastases.

Surgically Resectable Disease


Surgery is the mainstay of gastric cancer treatment with curative intent, with the procedure of choice depending on patient and tumor characteristics.

Endoscopic mucosal resection or endoscopic submucosal dissection is appropriate for the treatment of favorable early-stage gastric cancer based on depth of invasion (Tis or T1a), size (2cm maximum), pathology (well or moderately-well differentiated), and the absence of ulceration or lymphovascular invasion [37]. Patients meeting these criteria have a <5% chance of LN metastases, so LN dissection may be omitted [16]. Those with less favorable early-stage disease who are unfit for surgery are also candidates for endoscopic resection [37].

Because gastric cancers are usually more advanced at the time of diagnosis in Western countries, gastrectomy with lymph node dissection is far more commonly offered to those treated with curative intent. Multimodal therapy should be considered for T2+ or node-positive disease.

For distal tumors that are at least 6cm removed from the gastric cardia, distal gastrectomy is preferred for being less morbid while maintaining similar survival rates to total gastrectomy [38]. The morbidity benefits of proximal gastrectomy for more proximal tumors over total gastrectomy are less established. As such, proximal tumors are typically managed with total gastrectomy, although proximal gastrectomy may be considered in select patients [37]. Regardless of technique, an attempt should be made to achieve negative margins at least 4cm from the gross tumor.

The optimal extent of lymph node dissection during gastrectomy is controversial. A discussion of the merits of the various levels of lymph node dissection is beyond the scope of this module. Readers interested in details are referred to the guidelines published by the National Comprehensive Cancer Network (NCCN) and the Japanese Gastric Cancer Association, as well as original literature on the topic. The number of nodes that are dissected is important for accurate staging and possibly survival, with a recommended minimum of 15-16 lymph nodes [7, 37, 39].

Multimodal therapy

The effectiveness of multimodal therapy has been demonstrated across multiple trials. Supplementing surgery with chemotherapy or radiation therapy should be strongly considered for all T2+ or node-positive disease [37]. Regimens that have shown superiority to surgery alone include:

  1. Perioperative epirubicin, cisplatin, and fluorouracil (ECF) [40]
  2. Perioperative cisplatin and fluorouracil (CF) [41]
  3. Adjuvant S-1 [42]
  4. Adjuvant capecitabine and oxaliplatin (CAPOX) [43]
  5. Adjuvant fluorouracil and leucovorin-based chemoradiotherapy [44, 45]

Neoadjuvant chemoradiotherapy, whose use was extrapolated from esophageal cancer, has also shown promising early results for gastric cancer [37, 46]. Recently, perioperative fluorouracil, leucovorin, oxaliplatin, and docetaxel (FLOT) has gained traction after it was demonstrated to improve survival over ECF [47]. Finding the optimal sequence and combination of multimodal therapy remains an area of active research, with many variations currently under investigation.

Nonmetastatic unresectable or medically inoperable patients

Literature on the treatment of locally advanced disease is limited. Fluorouracil-based chemoradiotherapy appears to be more effective than either chemotherapy or radiotherapy alone in two older trials [48, 49]. For medically fit patients, chemoradiation may increase the likelihood of conversion to resectable disease [37]. The alternative is combination chemotherapy alone, as with metastatic disease discussed henceforth.

Metastatic Disease

Chemotherapy is the cornerstone of treatment for patients with advanced gastric cancer. Compared to supportive care, chemotherapy has been found to improve quality of life and prolong survival from 4.3 to 11 months [50]. Two-agent chemotherapy, which extends survival compared to single-agent chemotherapy, is recommended for most patients [37, 50]. The combination of a fluoropyrimidine (e.g. 5-fluorouracil or capecitabine) and a platinum agent (e.g. cisplatin or oxaliplatin) is considered first line, although several alternative regimens have also shown promising results [37]. Combination chemotherapy with three cytotoxic drugs further prolongs survival and increases response rates, albeit with greater toxicity; these regimens may be appropriate as first-line treatment for select medically fit patients with good performance status [37, 50].

A number of targeted therapies have emerged with encouraging results in specific patient populations over the past decade [51, 52, 53]. Health Canada has approved trastuzumab and ramucirumab for HER2-overexpressing and previously-treated patients with advanced gastric cancer, respectively. Other targeted therapies are also showing promising early results, including FDA-approved pembrolizumab for select MSI-H/dMMR tumors [37].

There is conflicting evidence on the aggressive management of oligometastatic gastric cancer with surgery or radiotherapy directed at either the primary or metastatic deposits [56-62]. The only phase III trial completed to date, conducted in East Asia, did not find benefit in adding gastrectomy to chemotherapy [61]. Ongoing RCTs will hopefully shed further light on this subject (RENAISSANCE, NCT03161522) [63]. The management of oligometastatic gastric cancer is dependent on center of practice. A comprehensive discussion on this subject is beyond the scope of the module; however, relevant features include:

  1. Patient’s age, health, performance status
  2. Number and volume of metastases
  3. Location of metastases (para-aortic nodes, lung, liver are some potential candidates considered more amenable to surgery)
  4. Timeline: metachronous versus synchronous
  5. Basis of diagnosis
  6. Primary tumor status (controlled versus uncontrolled)
  7. T and N stage
  8. Local expertise and resources
  9. Palliative Treatment

Radiotherapy is effective for local palliation, with more than two-thirds of patients experiencing bleeding, pain or obstruction responding to therapy. Concurrent chemoradiotherapy is associated with significantly higher toxicity than radiotherapy alone, but there is a lack of evidence comparing local outcomes [55]. The benefits to chemotherapy on survival are, however, well established. Other options used to control local symptoms include endoscopic treatment, interventional radiology, medical therapy (e.g. proton pump inhibitors), stenting, and stenting [37]. In view of the significant heterogeneity in this population, there are unsurprisingly few studies comparing the effectiveness of different modalities. A multidisciplinary approach is especially critical for this diverse group of patients.

Treatment Toxicity

Radiation toxicity

Side effects to gastric radiation are common and sometimes necessitate breaks or discontinuation of therapy, with deleterious effects on survival [16]. Concurrent chemotherapy appears to compound toxicity [54]. For example, in the landmark INT-0116 trial which established the use of adjuvant chemoradiation, 54% of patients undergoing adjuvant chemoradiatiotherapy experienced grade 3+ hematologic toxicity and 33% experienced grade 3+ gastrointestinal toxicity. A total of 17% stopped chemoradiotherapy altogether as a result of unacceptable toxicity [44]. IMRT, which has the potential to lower the dose delivered to end organs, is especially preferable in cases where there is a concern for high-grade toxicity. We list some common and serious complications below [16].

Acute toxicities
  1. Nausea +/- vomiting 
  2. Anorexia and malnutrition (nutritional support, enteral feeding as needed)
  3. Fatigue
  4. Dehydration
  5. Esophagitis (proton pump inhibitors)
  6. Epidermitis
  7. Changes in gastric motility 
  8. Prolonged gastric emptying
  9. Myelosuppression with chemoradiation (follow CBC weekly or more frequently as indicated)

These complications often resolve within 1-2 weeks of completing therapy but demand close follow up and aggressive management. 

Late toxicities
  1. Dyspepsia
  2. Radiation gastritis
  3. Gastric ulcer
  4. Gastric perforation
  5. Gastric obstruction
  6. Liver toxicity
  7. Renal toxicity
  8. Cardiac toxicity


Overall survival

SEER [26] reports that the 5-year survival rates for gastric cancer are 68% for localized disease, 31% for regional disease, and 5% for distant metastatic disease for patients diagnosed between 2009-2015. 

Factors that affect prognosis aside from disease stage include performance status, ALP level, and race [16]. Asians in particular appear to have more favorable outcomes than Caucasians, Blacks, and Hispanics regardless of tumor location [33]. Histologic grade and tumor location have not consistently been found to affect prognosis independent of stage [7, 34, 35]. 

Recurrence risk

Approximately 30% of patients treated surgically with curative intent will experience recurrence (with follow-up varying from 2-14 years) . Recurrence is usually early with a median duration to failure of 10.8 months. The failure pattern is predominantly distant [36]. 

Follow up care

There is a lack of prospective studies guiding follow up and no expert consensus on what constitutes best practice. In view of the recurrence trends, surveillance should be concentrated in the early years, at which time the risk for recurrence is highest.  

Follow up visits should include history and physical examination, in addition to endoscopic surveillance for those who have received endoscopic resection. Particular emphasis should be placed on nutrition. Further investigations should generally be performed based on clinical presentation.

An example of a surveillance schedule for patients treated curatively, depending on the stage of disease and selected treatment, is below [25]. Follow up should be tailored to each patient based on their unique circumstances.

Tis and pathologic stage I treated with endoscopic resection

  1. History and physical every 3-6 months for 1-2 years, then every 6-12 months for 3-5 years. Followed annually afterward.
  2. CBC and chemistry as clinically indicated.
  3. EGD every 6 months for 1 year, then annually for 3-5 years.
  4. CT chest, abdomen, and pelvis with oral and IV contrast as clinically indicated.
Pathologic stage I treated with gastrectomy
  1. History and physical every 3-6 months for 1-2 years, then every 6-12 months for 3-5 years. Followed annually afterward.
  2. CBC and chemistry as clinically indicated.
  3. EGD as clinically indicated.
  4. CT chest, abdomen, and pelvis with oral and IV contrast as clinically indicated.
  5. Monitor nutrition including B12 and iron. Treated as indicated
Pathologic stage II-III treated with gastrectomy OR stages I-III treated with neoadjuvant therapy 
  1. History and physical every 3-6 months for 1-2 years, then every 6-12 months for 3-5 years. Followed annually afterward.
  2. CBC and chemistry as clinically indicated.
  3. EGD as clinically indicated.
  4. CT chest, abdomen, and pelvis with oral and IV contrast every 6-12 months for 2 years, then annually for up to 5 years. PET/CT can also be considered on the same schedule.
  5. Monitor nutrition including B12 and iron. Treated as indicated

Virtual Patient Case

Use your mouse to click through the slides and answer each question in the text box provided.
Note: This case can be completed on an iPad. To do this download the (free) Articulate Mobile Player for the iPad by clicking here.


  1. Giuli R. Barretts Esophagus Columnar Lined Esophagus ; 250 Questions - 250 Answers. Montrouge: Libbey Eurotext; 2003. 
  2. Siewert JR, Stein HJ. Adenocarcinoma of the gastroesophageal junction: classification, pathology and extent of resection. Dis Esoph. 1996;9(3):173–182.
  3. DeVita VT Jr, Lawrence TS, Rosenberg SA. Devita, Hellman, and Rosenberg's Cancer Principles & Practice of Oncology. 11th ed. Philadelphia: Wolters Kluwer Lippincott Williams & Wilkins; 2018.
  4. Lauren P. The two histological main types of gastric carcinoma: diffuse and so-called intestinal-type carcinoma. An attempt at a histo-clinical classification. Acta Pathol Microbiol Scand 1965;64:31–49.
  5. Hristov B, Lin SH, Christodouleas JP. Radiation Oncology: A Question-Based Review. 3rd ed. Philadelphia: Wolters Kluwer Lippincott Williams & Wilkins; 2018.
  6. Berlth F, Bollschweiler E, Drebber U, Hoelscher AH, Moenig S. Pathohistological classification systems in gastric cancer: diagnostic relevance and prognostic value. World J Gastroenterol. 2014;20(19):5679-84.
  7. Amin MB, Edge SB, Greene FL, et al, eds. AJCC cancer staging manual. 8th ed. New York: Springer-Verlag; 2017.
  8. Canadian Cancer Statistics Advisory Committee. Canadian Cancer Statistics 2018. Toronto, ON: Canadian Cancer Society; 2018. cancer.ca/Canadian-Cancer-Statistics-2018-EN. Accessed June 15, 2019.
  9. Bray F, Ferlay J, Soerjomataram I, Siegel R, Torre L, Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2018;68(6):394-424.
  10. Canadian Cancer Statistics Advisory Committee. Canadian Cancer Statistics 2017. Toronto, ON: Canadian Cancer Society; 2017.
  11. Sitarz R, Skierucha M, Mielko J, Offerhaus GJA, Maciejewski R, Polkowski WP. Gastric cancer: epidemiology, prevention, classification, and treatment. Cancer Manag Res. 2018;10:239-248.
  12. Devesa SS, Blot WJ, Fraumeni JF. Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer. 1998;83(10):2049-53.
  13. Botterweck AA, Schouten LJ, Volovics A, Dorant E, Van den brandt PA. Trends in incidence of adenocarcinoma of the oesophagus and gastric cardia in ten European countries. Int J Epidemiol. 2000;29(4):645-54.
  14. Gastric cancer and Helicobacter pylori: a combined analysis of 12 case control studies nested within prospective cohorts. Gut. 2001;49(3):347-53.
  15. Parsonnet J, Hansen S, Rodriguez L, et al. Helicobacter pylori infection and gastric lymphoma. N Engl J Med. 1994;330(18):1267-71.
  16. Halperin EC, Wazer DE, Perez CA, Brady LW. Perez and Brady's Principles and Practice of Radiation Oncology. 7th ed. Philadelphia: Wolters Kluwer Lippincott Williams & Wilkins; 2018.
  17. Lee YC, Chiang TH, Chou CK, et al. Association Between Helicobacter pylori Eradication and Gastric Cancer Incidence: A Systematic Review and Meta-analysis. Gastroenterology. 2016;150(5):1113-1124.e5.
  18. Chen Y, Liu L, Wang X, et al. Body mass index and risk of gastric cancer: a meta-analysis of a population with more than ten million from 24 prospective studies. Cancer Epidemiol Biomarkers Prev. 2013;22(8):1395-408.
  19. Yang P, Zhou Y, Chen B, et al. Overweight, obesity and gastric cancer risk: results from a meta-analysis of cohort studies. Eur J Cancer. 2009;45(16):2867-73.
  20. Nomura AM, Wilkens LR, Henderson BE, Epplein M, Kolonel LN. The association of cigarette smoking with gastric cancer: the multiethnic cohort study. Cancer Causes Control. 2012;23(1):51-8.
  21. Praud D, Rota M, Pelucchi C, et al. Cigarette smoking and gastric cancer in the Stomach Cancer Pooling (StoP) Project. Eur J Cancer Prev. 2018;27(2):124-133.
  22. Ma K, Baloch Z, He TT, Xia X. Alcohol Consumption and Gastric Cancer Risk: A Meta-Analysis. Med Sci Monit. 2017;23:238-246.
  23. Tramacere I, Negri E, Pelucchi C, et al. A meta-analysis on alcohol drinking and gastric cancer risk. Ann Oncol. 2012;23(1):28-36.
  24. Wang PL, Xiao FT, Gong BC, Liu FN. Alcohol drinking and gastric cancer risk: a meta-analysis of observational studies. Oncotarget. 2017;8(58):99013-99023.
  25. Tsugane S, Sasazuki S. Diet and the risk of gastric cancer: review of epidemiological evidence. Gastric Cancer. 2007;10(2):75-83.
  26. Howlader N, Noone AM, Krapcho M, Miller D, Brest A, Yu M, Ruhl J, Tatalovich Z, Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2016, National Cancer Institute. Bethesda, MD, seer.cancer.gov/csr/1975_2016/, based on November 2018 SEER data submission, posted to the SEER web site, April 2019.
  27. Yaghoobi M, Bijarchi R, Narod SA. Family history and the risk of gastric cancer. Br J Cancer. 2010;102(2):237-42.
  28. Sereno M, Aguayo C, Ponce CG, et al. Gastric tumours in hereditary cancer syndromes: clinical features, molecular biology and strategies for prevention. Clin Transl Oncol. 2011; 13: 599-610
  29. Zhang X, Li M, Chen S, et al. Endoscopic Screening in Asian Countries Is Associated With Reduced Gastric Cancer Mortality: A Meta-analysis and Systematic Review. Gastroenterology. 2018;155(2):347-354.e9.
  30. Family Practice Oncology Network. Upper Gastrointestinal Cancer (Suspected) Part 1. BC Cancer Agency; 2016.
  31. Kufe DW, Pollock RE, Weichselbaum RR, et al., eds. Holland-Frei Cancer Medicine. 6th ed. Hamilton: BC Decker; 2003.
  32. Vakil N, Moayyedi P, Fennerty MB, Talley NJ. Limited value of alarm features in the diagnosis of upper gastrointestinal malignancy: systematic review and meta-analysis. Gastroenterology. 2006;131(2):390-401.
  33. Kim J, Sun CL, Mailey B, et al. Race and ethnicity correlate with survival in patients with gastric adenocarcinoma. Ann Oncol. 2010;21(1):152-60.
  34. Asplund J, Kauppila JH, Mattsson F, Lagergren J. Survival Trends in Gastric Adenocarcinoma: A Population-Based Study in Sweden. Ann Surg Oncol. 2018;25(9):2693-2702.
  35. Zhao J, Zhao J, Du F, et al. Cardia and Non-Cardia Gastric Cancer Have Similar Stage-for-Stage Prognoses After R0 Resection: a Large-Scale, Multicenter Study in China. J Gastrointest Surg. 2016;20(4):700-7.
  36. Spolverato G, Ejaz A, Kim Y, et al. Rates and patterns of recurrence after curative intent resection for gastric cancer: a United States multi-institutional analysis. J Am Coll Surg. 2014;219(4):664-75.
  37. National Comprehensive Cancer Network. Gastric Cancer (Version 2.2019). https://www.nccn.org/professionals/physician_gls/pdf/gastric.pdf. Accessed June 15, 2019.
  38. Bozzetti F, Marubini E, Bonfanti G, Miceli R, Piano C, Gennari L. Subtotal versus total gastrectomy for gastric cancer: five-year survival rates in a multicenter randomized Italian trial. Italian Gastrointestinal Tumor Study Group. Ann Surg. 1999;230(2):170-8.
  39. Hundahl SA, Phillips JL, Menck HR. The National Cancer Data Base Report on poor survival of U.S. gastric carcinoma patients treated with gastrectomy: Fifth Edition American Joint Committee on Cancer staging, proximal disease, and the "different disease" hypothesis. Cancer. 2000;88(4):921-32.
  40. Cunningham D, Allum WH, Stenning SP, et al. Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer. N Engl J Med. 2006;355(1):11-20.
  41. Ychou M, Boige V, Pignon JP, et al. Perioperative chemotherapy compared with surgery alone for resectable gastroesophageal adenocarcinoma: an FNCLCC and FFCD
  42. Sakuramoto S, Sasako M, Yamaguchi T, et al. Adjuvant chemotherapy for gastric cancer with S-1, an oral fluoropyrimidine. N Engl J Med. 2007;357(18):1810-20.
  43. Bang YJ, Kim YW, Yang HK, et al. Adjuvant capecitabine and oxaliplatin for gastric cancer after D2 gastrectomy (CLASSIC): a phase 3 open-label, randomised controlled trial. Lancet. 2012;379(9813):315-21.
  44.  Macdonald JS, Smalley SR, Benedetti J, et al. Chemoradiotherapy after surgery compared with surgery alone for adenocarcinoma of the stomach or gastroesophageal junction. N Engl J Med. 2001;345(10):725-30. 
  45. Smalley SR, Benedetti JK, Haller DG, et al. Updated analysis of SWOG-directed intergroup study 0116: a phase III trial of adjuvant radiochemotherapy versus observation after curative gastric cancer resection. J Clin Oncol. 2012;30(19):2327-33.
  46. Newton AD, Datta J, Loaiza-bonilla A, Karakousis GC, Roses RE. Neoadjuvant therapy for gastric cancer: current evidence and future directions. J Gastrointest Oncol. 2015;6(5):534-43.
  47. Al-batran SE, Homann N, Pauligk C, et al. Perioperative chemotherapy with fluorouracil plus leucovorin, oxaliplatin, and docetaxel versus fluorouracil or capecitabine plus cisplatin and epirubicin for locally advanced, resectable gastric or gastro-oesophageal junction adenocarcinoma (FLOT4): a randomised, phase 2/3 trial. Lancet. 2019;393(10184):1948-1957.
  48. Moertel CG, Childs DS, Reitemeier RJ, Colby MY, Holbrook MA. Combined 5-fluorouracil and supervoltage radiation therapy of locally unresectable gastrointestinal cancer. Lancet. 1969;2(7626):865-7.
  49. A comparison of combination chemotherapy and combined modality therapy for locally advanced gastric carcinoma. Gastrointestinal Tumor Study Group. Cancer. 1982;49(9):1771-7.
  50. Wagner AD, Syn NL, Moehler M, et al. Chemotherapy for advanced gastric cancer. Cochrane Database Syst Rev. 2017;8:CD004064.
  51. Bang YJ, Van cutsem E, Feyereislova A, et al. Trastuzumab in combination with chemotherapy versus chemotherapy alone for treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer (ToGA): a phase 3, open-label, randomised controlled trial. Lancet. 2010;376(9742):687-97.
  52. Fuchs CS, Tomasek J, Yong CJ, et al. Ramucirumab monotherapy for previously treated advanced gastric or gastro-oesophageal junction adenocarcinoma (REGARD): an international, randomised, multicentre, placebo-controlled, phase 3 trial. Lancet. 2014;383(9911):31-39.
  53. Wilke H, Muro K, Van cutsem E, et al. Ramucirumab plus paclitaxel versus placebo plus paclitaxel in patients with previously treated advanced gastric or gastro-oesophageal junction adenocarcinoma (RAINBOW): a double-blind, randomised phase 3 trial. Lancet Oncol. 2014;15(11):1224-35.
  54. Tey J, Soon YY, Koh WY, et al. Palliative radiotherapy for gastric cancer: a systematic review and meta-analysis. Oncotarget. 2017;8(15):25797-25805.
  55. Iizasa H, Nanbo A, Nishikawa J, Jinushi M, Yoshiyama H. Epstein-Barr Virus (EBV)-associated gastric carcinoma. Viruses. 2012;4(12):3420-39.
  56. Sasaki S, Nishikawa J, Sakai K, et al. EBV-associated gastric cancer evades T-cell immunity by PD-1/PD-L1 interactions. Gastric Cancer. 2019;22(3):486-496.

Whiteboard Videos

Coming soon