Approach Considerations
Studies for staging of stomach cancer may include the following [4] :
-
Upper gastrointestinal (GI) tract endoscopy and biopsy
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Chest/abdomen/pelvic computed tomography (CT) with oral and intravenous contrast
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Positron emission tomography (PET) – CT evaluation if no evidence of M1 disease is found, and if clinically indicated
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Complete blood cell count (CBC) and comprehensive chemistry profile
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Endoscopic ultrasound if no evidence of M1 disease is found
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Endoscopic resection for early-stage cancers
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Biopsy of metastatic disease as clinically indicated
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Microsatellite instability (MSI) and deficient mismatch repair (dMMR) testing if metastatic disease is documented/suspected
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HER2-neu and programmed death ligand 1 (PD-L1) testing if metastatic adenocarcinoma is documented or suspected
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.
In a study of peritoneal cancer (PC) diagnosis, investigators found that the administration of carbonated water for dual-time point imaging may improve the accuracy of FDG PET/CT scanning for PC in patients previously diagnosed with colorectal cancer (CRC). [26]
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. [3]
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.
In 2013, researchers identified a possible third type of gastric adenocarcinoma. In an analysis of 248 gastric tumors using microarray-based gene-expression profiling, Lei et al found that this third subtype of gastric adenocarcinoma (which they termed the "metabolic" subtype; the other 2 subtypes are mesenchymal and proliferative) preferentially responds to 5-fluorouracil (5-FU). The researchers validated their findings in an independent set of 70 gastric tumors. [27, 28, 29] They believe that the preferential sensitivity of metabolic-subtype gastric cancers to 5-FU may be due to their significantly lower expression of thymidylate synthase and dihydropyrimidine dehydrogenase relative to the other 2 subtypes. [27]
Staging
The 2017 American Joint Committee on Cancer (AJCC) Cancer Staging Manual presents the following TNM classification system for staging gastric carcinoma [30] :
Primary tumor (T)
See the list below:
-
TX - Primary tumor cannot be assessed
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T0 - No evidence of primary tumor
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Tis - Carcinoma in situ, intraepithelial tumor without invasion of lamina propria
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T1 - Tumor invades lamina propria, muscularis mucosae, or submucosa
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T1a - Tumor invades lamina propria or muscularis mucosae
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T1b - Tumor invades submucosa
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T2 - Tumor invades muscularis propria
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T3 - Tumor penetrates subserosal connective tissue without invasion of visceral peritoneum or adjacent structures
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T4 - Tumor invades serosa (visceral peritoneum) or adjacent structures
-
T4a - Tumor invades serosa (visceral peritoneum)
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T4b - Tumor invades adjacent structures/organs
Regional lymph nodes (N)
See the list below:
-
NX - Regional lymph node(s) cannot be assessed
-
N0 - No regional lymph node metastases
-
N1 - Metastases in 1-2 regional lymph nodes
-
N2 - Metastases in 3-6 regional lymph nodes
-
N3 - Metastases in 7 or more regional lymph nodes
-
N3a - Metastases in 7-15 regional lymph nodes
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N3b - Metastases in 16 or more regional lymph nodes
Distant metastasis
See the list below:
-
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. [31]
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, [32] 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. [33]
Clinical Staging
See the list below:
-
Stage 0 - Tis, N0, M0
-
Stage I - T1-2, N0, M0
-
Stage IIA - T1-2, N1-3, M0
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Stage IIB - T3, N0, M0 or T4a, N0, M0
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Stage III - T3, N0, M0 or; T4a, N1-3, M0
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Stage IVA - T4b, any N, M0
-
Stage IVB - Any T, any N, M1
For pathologic and post-neoadjuvant therapy stage grouping, see Gastric Cancer Staging
Survival rates
See the list below:
-
Stage IA - 94%
-
Stage IB - 88%
-
Stage IIA - 82%
-
Stage IIB - 68%
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Stage IIIA - 54%
-
Stage IIIB - 36%
-
Stage IIIC - 18%
-
Stage IV - 5%
Spread patterns
Cancer of the stomach can spread directly, via lymphatics, or hematogenously. Features of spread include the following:
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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
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The abundant lymphatic channels within the submucosal and subserosal layers of the gastric wall allow for easy microscopic spread
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The submucosal plexus is prominent in the esophagus and the subserosal plexus is prominent in the duodenum, allowing proximal and distal spread
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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
Laboratory Studies
The goal of obtaining laboratory studies is to assist in determining optimal therapy. Useful studies may include the following:
-
A complete blood cell count (CBC) can identify anemia, which is present in approximately 30% of patients and may be caused by bleeding, liver dysfunction, or poor nutrition
-
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
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Cancer antigen (CA) 19-9 is elevated in about 20% of cases
Distinctive serum glycan patterns may have the potential to serve as markers for gastric cancer risk. In a study of 72 serum samples from patients with gastric cancer, nonatrophic gastritis, or duodenal ulcer, Ozcan and colleagues found that abnormal patterns of serum glycans (sugars attached to proteins) may be useful as a screening tool for identifying patients with Helicobacter pylori infection who are at risk for stomach cancer. [34, 35]
A total of 19 significant differences in serum glycan expression were found between gastric cancer patients and individuals with asymptomatic nonatrophic gastritis. High-mannose–type glycans, glycans with 1 complex type antenna, and bigalactosylated biantennary glycans tended to be lower in gastric cancer patients, whereas levels of nongalactosylated biantennary glycans were higher. Altered serum glycan levels were also seen in study patients with ulcers. [34, 35]
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Stomach and duodenum, coronal section.
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Early gastric cancer in the gastric body. Courtesy of Wikimedia Commons (author Med_Chaos).
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