PERSPECTIVE, PATTERNS OF SPREAD, AND PATHOLOGY
The predisposing carcinogenic factors are atrophic gastric mucosa and intestinal metaplasia that transit into neoplasia from Ménétrier disease or hypertrophic gastritis. The predominant cancer is adenocarcinoma. Gastrointestinal stromal tumors (GISTs) are presented for staging in the seventh edition of the AJCC Cancer Staging Manual and is being presented here with stomach cancers, although they can occur elsewhere in the gastrointestinal tract (GIT). GISTs are the most common mesenchymal tumors in the GIT.
PERSPECTIVE AND PATTERNS OF SPREAD
Gastric cancers have undergone a decline in deaths and incidence since the 1950s; however, their status as aggressive and highly malignant neoplasms has not changed. In the United States and the Western world, although they have steadily declined in incidence. There is a tremendous variation worldwide; Japan has the highest incidence, accounting for 20% to 30% of all stomach cancers. The predisposing factors remain atrophic gastric mucosa and intestinal metaplasia that transit into neoplasia from Ménétrier disease or hypertrophic gastritis. Fundic and adenomatous polyps as in Gardner and Peutz–Jeghers syndromes tend to undergo carcinogenic change. Because of the large, saclike nature of the stomach, this part of the digestive system can accommodate large neoplasms before onset of symptoms. Presentations range from fungating and ulcerative process to a widely infiltrative process resulting in a linitis plastica, stomach almost devoid of peristalsis. The patterns of invasion into and through the stomach wall are shown in Fig. 24.2 and Table 24.2.
Early diagnosis is essential to cure, and when camera imaging and frequent endoscopic screens are employed, as in Japan, precancerous and small lesions are found. An Early Gastric Cancer (ECG) classification of minimal microscopic lesions has been introduced. ECG in Japan constitutes 25% to 50% of all gastric adenocarcinomas as compared to 5% to 15% in Western countries. ECG is noted to have three types of presentation: Type I (elevated) protrudes in lumen >5 cm; type II are superficial lesions with elevations or depressions; and type III resembles ulcers or craters and amputate gastric folds. The staging recommendations apply to carcinomas, not lymphomas or sarcomas. A tabulation of cell types reflects the varied surface epithelia and secretory glandular cells. Once the mucosa is breeched, invasion of the muscle cell wall occurs with dissemination along these muscle layers (see Table 24.1).
A unique feature of the stomach is the attachment of suspensory ligaments consisting of two layers of peritoneum, that is, gastrohepatic ligament along the lesser curvature and the gastrocolic ligament along the greater curvature. Thus cancer penetrates the muscular propria and invades the ligaments (subserosally) without breeching the serosa. Gastric cancer invasion of the lesser and greater omentum is T3, not T4. Perforation of the visceral peritoneum is required to be T4.
Likewise, the uniquely high number of nodes invaded also are due to lymph nodes along the lesser and greater curvature and located inside the aforementioned ligaments (subserosal) and not external to the serosa cover as in the small intestine and colon.
Figure 24.1 A,B | Infiltrating gastric carcinoma. A. Numerous signet ring cells (arrows) infiltrate the lamina propria between intact crypts. B. Mucin stains highlight the presence of mucin within the neoplastic cells.
Figure 24.2 | Patterns of spread. The patterns of spread and the primary tumor classification are similarly color coded: Tis (cancer in situ of mucosa), yellow; T1 (infiltrates the submucosa), green; T2 (penetrates the muscularis externa), blue; T3 (reaches the subserosa), purple; and T4 (invades through the serosa into a neighboring viscera), red. The concept of visualizing patterns of spread to appreciate the surrounding anatomy is well demonstrated by the six-directional pattern, i.e., SIMLAP, Table 24.2.
PATHOLOGY
Patients with familial adenomatus polyposis have gastric adenomas that transform into cancers at a tenfold higher risk than the general population. Patients with hereditary nonpolyposis colorectal cancer have a 10% risk; juvenile polyposis has 15% to 20% risk of cancer. Numerous genetic abnormalities are associated with gastric adenocarcinoma. P53 is the most common association in 60% to 70% of gastric adenocarcinomas.
Cancer syndromes vary with size, location, and cancer progression. Submucosal T1 cancers are usually asymptomatic; T2 patients, muscularis propria, often have dyspepsia and weight loss; T3 patients often ulcerate and bleed and have melena; T4 patients can have feculent emesis or undigested food due to a gastrocolic fistula. More unusual symptoms and syndromes include the following:
• Pyloric outlet obstruction: early satiety and vomiting versus cardiac lesions where dysphagia predominates
• Paraneoplastic syndromes, such as thrombophlebitis (Trousseau's sign), neuropathies, nephritic syndromes, and less often dermatologic changes as hyperpigmented patches in axilla.
Unusual metastatic manifestations include the following:
• Krukenberg tumors of ovary
• Rectal shelf of Blumer due to pouch of Douglas invasion
• St. Joseph nodule at umbilicus
GIST refers to a wide spectrum of mesenchymal tumors, from leiomyomas to leiomyosarcomas, with varying combinations and permutations that include tumor size, mitotic activity, mitotic rate (mitosis/high-power field [HPF]) and are clustered into a range of prognostic groups. GIST can arise from smooth muscle walls of muscularis propria, which is ubiquitous in the GIT, it is not surprising that they can occur throughout this system. Since the stomach has three layers of smooth muscle, it can be anticipated to be the most common site (60%), followed by small intestine (35%), rectum (3%), colon (1% to 2%), and esophagus (1%).
Lymph nodes and lymphatic spread do not occur as a rule. Metastases tend to be intra-abdominal (omental deposits) and to the liver, but other nonabdominal sites include bone, lung, and skin. Solitary omental and mesenteric tumors can be primaries. Multiple GIST can occur in neurofibromatosis type I (familiar GIST). Symptoms include GIT bleeding, dyspepsia, or obstructions. As a group they represent 1% of gastric tumors.
Gastric cancer can be subdivided into two forms:
• The intestinal form is characterized by tubular gland-like structures mimicking intestinal villi and is declining worldwide.
• The diffuse form is poorly differentiated, infiltrative, and lacks any semblance of glands.
There is evidence that gastric cancers are a multistep process similar to colon cancer. The initiation and progression are attributed to Helicobacter pylori that causes a chronic gastritis and gastric ulcers.
Intestinal metaplasias consist of three types: Type I is similar to normal morphology, Type II lacks enterocytes secretes siglomucins and Type III secretes sulfamucins. Progression to severe cysplasia and cancer is 10-20%, 20–40%, and 75–100% respectively for Types I, II, II. Gastric polyps tend to be hyperplastic and malignancy unlike colon is low: 1% in contrast to gastric adenomas transform in 11%.
GISTs arise from “pacemaker cells” and are so classified based on molecular and immunohistology, specifically express KIT protein, tyrosine kinase receptor, or its gene (PDG FRA). Histologically, the cells are composed of plump spindle cells with permanent cytoplasmic vacuoles enmeshed within a myoid stroma.
TNM STAGING CRITERIA
TNM STAGING CRITERIA
T size is the key factor, not depth of invasion as in epithelial adenocarcinomas, that is, 5, 5 to 10, >10 cm, and is modified by mitotic rate/HPF that assigns a prognostic group (score), which in turn provides a rate of tumor progression. Gastric cancers are confined and accommodated in the stomach and can reach large size as compared with other, narrower parts of the intestine. Bormans originally described the various appearances of advanced cancer, including the criteria to distinguish a malignant versus a benign gastric ulcer: I, polypoid; II, ulcerative; III, infiltrative ulcerated; and IV, linitis plastica.
The major American Joint Committee on Cancer (AJCC) staging criteria are based on depth of invasion of a hollow viscus: T1 (mucosal) invades lamina propria; T2 has been modified as T2a (invades muscularis propria) and T2b (subserosa). Subserosal stage applies to tumors extending into gastrocolic or gastrohepatic ligament or lesser or greater omentum. The omentum consists of two layers of peritoneum. An infiltrating cancer sandwiched between the two layers of omental peritoneum is considered subserosal despite being extragastric because the serosa is not penetrated. T3 means penetration of serosa or visceral peritoneum, and T4 implies invasion of surrounding viscera such as spleen, transverse colon, liver, diaphragm, pancreas, or other structure (Fig. 24.3A).
Intramural extension to esophagus or duodenum follows the depth-of-invasion rules for staging rather than advancing in stage.
Generally, there is no overarching principle or context design for stage groupings in the digestive system (gastrointestinal tract) or major digestive glands. Stages are frequently expanded to six by subdividing stages into A and B. The T and N categories are assigned to a stage grouping, specifically for division of a stage into more (a) versus less (b) favorable groupings. This occurs at different stages for different sites.
Specifically, this site has the most unorthodox staging with its eight stages. Stage III is divided into A, B, and C. It is the only anatomic site in which positive nodes (T1 N1) are still stage I, assigned to IB. The T and N progression together advances stages II, III, and IV. Adding subscript numbers to T and N categories together correlates with stage; that is, stage IA = 1, stage IB = 2, stage II = 3, stage IIIA = 4, stage IIIB = 5, and stage IV > 5. The nodal categories are unique: N1, 1 to 2 nodes; N2, 3 to 6 nodes; and N3a 7–15 nodes, N3b has × 16 nodes, >15 nodes. In comparison to many digestive system sites where N1 encompasses all nodal categories, the stomach is the most elaborate. Nevertheless, there are survival curve data supporting subdividing I and III into A and B (see last section).
Gastric cancer can be subdivided into two forms:
• The intestinal form is characterized by tubular gland-like structures mimicking intestinal villi and is declining worldwide.
• The diffuse form is poorly differentiated and infiltrative and lacks any semblance of glands.
There is evidence that gastric cancers are a multistep process similar to colon cancers. The initiation and progression are attributed to Helicobacter pylori that causes a chronic gastritis and gastric ulcers.
Intestinal metaplasias consist of three types: Type I is similar to normal morphology, type II lacks enterocytes secreting siglomucins, and type III secretes sulfamucins. Rates of progression to severe cysplasia and cancer are 10% to 20%, 20% to 40%, and 75% to 100%, respectively, for types I, II, and III. Gastric polyps tend to be hyperplastic, and malignancy, unlike those of the colon, is low: 1%, in contrast to gastric adenomas, which transform in 11% of cases.
SUMMARY OF CHANGES SEVENTH EDITION AJCC
Major changes include subdividing T1 into T1a muscularis mucosa T1b submucosa invasion; T2, T3, T4 are the same N categories are major new definitions for N1, N2, N3 (6th edition). N1 1–2 (1–6), N3 3–6 (7–15), N3 ≤ 7 (>15 nodes).
M1 includes positive peritoneal cytology, which differs from staging.
• Tumors arising at the esophagogastric junction, or arising in the stomach ≤5cm from the esophagogastric junction and crossing the esophagogastric junction are staged using the TNM system for esophageal adenocarcinoma.
• T categories have been modified to harmonize with T categories of the esophagus and small and large intestine.
• T1 lesions have been subdivided into T1a and T1b
• T2 is defined as a tumor that invades the muscularis propria
• T3 is defined as a tumor that invades the subserosal connective tissue
• T4 is defined as a tumor that invades the serosa (visceral peritoneum) or adjacent structures
• N categories have been modified, with N1 = 1–2 positive lymph nodes, N2 = 3–6 positive lymph nodes, N3 = 7 or more positive lymph nodes
• Positive peritoneal cytology is classified as M1
• Stage groupings have been changed
The TNM Staging Matrix is color coded for identification of stage group once T and N stages are determined (Table 24.3).
STOMACH ADENOCARCINOMA
Figure 24.3A | TNM staging diagram presents a vertical arrangement with color bars encompassing TN combinations showing progression. The stomach has the most elaborate nodal staging categories, and despite 15 or >15 regional nodes (N2/N3), resections allow for 20% versus 8% 5-year survival, that is, IIIA ≠ B versus IV or purple versus red lane, respectively. Stage 0, yellow; I, green; II, blue; III, purple; IV, red; and IV (metastatic), black. Definitions of TN on left, and stage grouping on right.
GASTROINTESTINAL STROMAL TUMORS
Perspective and Patterns of Spread
Gastrointestinal stromal tumors (GIST) had been regarded as an obscure entity, but with uncovering of its molecular mechanism and improved diagnosis and reporting, a dramatic increase in incidence after 2000 has been found. In the United States, the annual reported incidence of 15 cases increased after 2000 to approximately 5000 cases per year. The majority of GISTs arise in the stomach (60% to 70%), and so it is presented and discussed at this anatomic site. The other site of some incidence is the small intestine (20% to 30%); for the rest of the digestive system, it is only 10%. Even more uncommon are extraintestinal sites, that is, omentum, mesentery, and retroperitoneum.
Clinical presentations vary with site of occurrence and tumor size, that is, >5 cm, with palpable mass, abdominal pain, and altered digestive peristalsis manifesting as nausea, anorexia, or vomiting. Most frightening is acute hemorrhage, which can occur in 40% of patients. Rupture can lead to peritoneal irritation and acute abdominal pain with splinting.
Several clinical syndromes have been described in association with GIST, characterized by multifocal tumors in other organs, for example, lung or adrenal gland, and linkages to neurofibromatosis.
Histopathology
Typically, GISTs were lumped with leiomyomas and, if mitotic activity was high, leiomyosarcomas, before availability of molecular markers. It was recognized that these tumors had similarities to “pacemaker cells” of the digestive system, that is, interstitial cells of Cajal, which coordinates peristalsis. This led to the observation of the role played by KIT receptor tyrosine kinase (RTK). GISTs express CD117, and immunochemical staining distinguishes them from leiomyosarcomas and desmoid tumors.
TNM Staging Criteria
According to consensus by pathologists, two important criteria are the hallmark for staging: size and number of mitosis. Less important are cell phenotype and cell pleomorphism. The AJCC TN categories are illustrated in Table 24.4.
Detection and Diagnosis
Most symptomatic lesions are identified endoscopically as a smooth protrusion of the mucosa. To establish a diagnosis, deep biopsy often is required but may be deferred to avoid tumor rupture. Endoscopic ultrasonograms are useful, revealing a hypoechoic mass contiguous with either muscularis mucosa or, more often, the muscularis propria. If margins are irregular or cystic degeneration is present, these signs suggest malignancy; lesions >4 cm also are most often malignant. Computed tomography (CT) imaging is superior to magnetic resonance imaging (MRI) and more accurately provides tumor extent. Positron emission tomography (PET) scans with 18-fluorodeoxyglucose can provide functional imaging to supplement CT and is believed due to overactive KIT/RTK. PET is also effective in finding metastasis foci in the liver and peritoneal cavity.
Management
Surgical resection is advised for accessible GIST tumors. Radiation therapy is not advised because of the dose-limiting tolerance of stomach, intestine, and liver. Cytotoxic chemotherapy is universally futile. Most intriguing and exciting are the use and effectiveness of molecular targeted therapy with imatinib mesylate for unresectable and metastatic foci. Numerous clinical trials have shown clinical benefit and response in 45% to 89% of cases. PET scanning can demonstrate decrease in tumor avidity in 24 hours, predicting CT responses months later. The optimal dose of imatinib remains to be determined in future clinical trials.
GASTRIC STROMAL SARCOMA
Figure 24.3B | TNM staging criteria are color-coded bars for T advancement: Tis, yellow; T1, green; T2, blue; T3, purple; T4, red.
T-ONCOANATOMY
ORIENTATION OF THREE-PLANAR ONCOANATOMY
The isocenter for the three-planar anatomy is to the left of the midline anteriorly and at the T10/T11 level posteriorly (Fig. 24.4).
T-oncoanatomy
The T-oncoanatomy is displayed in three planar views. A. Coronal, B. Sagittal, C. Transverse axial (Figure 24.5).
The stomach is divided into three regions: upper, middle, and lower third. To delineate these regions, the lesser and greater curves of the stomach are divided; the upper third is the cardia and the fundus, the middle third is the body, and the lower third is the antrum.
The stomach is an organ with numerous metamorphic shapes: Hypertonic contracted stomach is often high in the upper quadrant; hypotonic to atonic viscus drops into the pelvis; and normal orthotonic viscus reaches to the umbilicus. The stomach mucosa begins at the zigzag line of the cardia defined by the pinkish glandular mucosa with its chief and parietal cells (Fig. 24.6).
• Coronal: The body of the stomach has a lesser and a greater curvature, a fundus superior to the body, and a pyloric region divided into an antrum and a pyloric canal. Extensions into adjacent or contiguous structures such as esophagus or duodenum are staged according to the depth of invasion in their wall. Gastric rugae or Magenstrasse are the villous mucosal folds with their secretory epithelia with parietal (HCl), chief (pepsinogen), and mucous (mucin) cells, which constitute them and their varied secretions. In addition to an inner circular layer and an outer longitudinal layer, there is a middle zone of both circular and oblique muscle layers. The cardia and pylorus have sphincteric activity and control the entry and departure of swallowed food.
• Sagittal: The arrow passes from the greater sac into the omental foramen into the lesser sac or omental bursa (Fig. 24.5C).
• Transverse: The gastrosplenic and splenorenal ligaments tether the spleen in place between the stomach and the kidney; the ligaments form a pedicle (stalk), through which blood vessels run to and from the hilum of the spleen. These ligaments are double layers of peritoneum that form the left boundary of the omental bursa (lesser sac); the inner layer consists of peritoneum lining the omental bursa, and the outer layer consists of peritoneum lining the peritoneal cavity (greater sac).
Figure 24.4 | Orientation and overview of oncoanatomy. The anatomic isocenter for stomach cancers is at T10/T11. A. Coronal. B. Sagittal.
Figure 24.5 | T-oncoanatomy. Connecting the dots. Structures are color coded for cancer stage progression. The color code for the anatomic sites correlates with the color code for the stage group (Fig. 24.3) and patterns of spread (Fig. 24.2) and SIMLAP tables (Table 24.2). Connecting the dots in similar colors will provide an appreciation for the 3D oncoanatomy.
N-ONCOANATOMY AND M-ONCOANATOMY
N-ONCOANATOMY
Regional Lymph Nodes
Several groups of regional lymph nodes drain the wall of the stomach. These perigastric nodes are found along the lesser and greater curvatures. Other major nodal groups follow the main arterial and venous vessels from the aorta and the portal circulation. Adequate nodal dissection of these regional nodal areas is important to ensure appropriate designation of the pN determination. Although it is suggested that at least 16 regional nodes be assessed pathologically, a pN0 determination may be assigned on the basis of the actual number of nodes evaluated microscopically (Table 24.5, Fig. 24.6).
Involvement of other intra-abdominal lymph nodes, such as the hepatoduodenal, retropancreatic, mesenteric, and paraaortic, is classified as distant metastasis. The specific nodal areas are as follows:
• Greater curvature of stomach: Greater curvature, greater omental, gastroduodenal, gastroepiploic, pyloric, and pancreaticoduodenal
• Pancreatic and splenic area: Pancreaticolienal, peripancreatic, splenic
• Lesser curvature of stomach: Lesser curvature, lesser omental, left gastric, cardioesophageal, common hepatic, celiac, and hepatoduodenal
• Distant nodal groups: Retropancreatic, para-aortic, portal, retroperitoneal, mesenteric.*
*Preceding passage from Edge SB, Byrd DR, and Compton CC, et al, AJCC Cancer Staging Manual, 7th edition. New York, Springer, 2010, p. 119.
M-ONCOANATOMY
The entire portal circulation should be considered as a unit in regard to the venous anatomy of the gastrointestinal tract below the diaphragm (Fig. 24.6B). The two major trunks are the inferior mesenteric and superior mesenteric veins. The inferior mesenteric vein drains the left colon and sigmoid colon tributaries, which covers the vascular drainage to the left of the midline originating from the superior rectal veins. On the right side, the superior mesenteric vein originates from the tributaries draining the ileum, jejunum, and the ileocolic and right middle colic veins. The inferior mesenteric vein usually joins the splenic vein, which coalesces with the superior mesenteric vein and forms the portal vein. The splenic vein, which is a major tributary of the portal system, also drains much of the stomach along its greater curvature and includes the short gastric veins and left and right gastric epiploic veins. The right gastric epiploic also flows into the superior mesenteric vein. The entire drainage of the lesser curvature of the stomach including the left and right gastric veins drains directly into the portal vein. Because the portal vein then drains directly into the liver, it is the target metastatic organ and the most commonly involved organ in hematogenous spread pattern from the venous system of the gastrointestinal tract, as compared with other parts of the body, where the drainage is directly into the lung by way of the caval system.
The incidence of liver metastases exceeds that of other sites. According to a variety of reports in the literature, the range is 38% to 100% at autopsy. Other sites are mainly bone metastases, 20% to 35%, and lung metastases, 40% to 60%, with only occasional metastases to brain.
Figure 24.6 | A. N-oncoanatomy. Sentinel nodes of stomach are along the lesser and greater curvatures. B. M-oncoanatomy. The left and right gastric veins drain into the portal venous system, leading to liver metastases predominantly.
STAGING WORKUP
RULES FOR CLASSIFICATION AND STAGING
Clinical Staging and Imaging
The stomach, as are all digestive tract viscera, when involved with cancer can be detected by endoscopy and double-contrast studies. The challenge is accurate delineation of gastric cancer, which penetrates the many layers composing the stomach wall. Endoscopic ultrasound (EUS) is the most favored method of determining the cancer's extent in and through the stomach wall. CT is excellent for diagnosing both extragastric extension and distant metastases. MRI is not helpful because of organ motion. Single photon emission CT scans of liver and bone are useful, but CT is better for assessing liver and lung metastases (Fig. 24.7), and MRI is superior for brain foci (Table 24.6).
Pathologic Staging
The surgically resected stomach and removed associated lymph nodes are assessed. Tumor extension and location of both primary and nodes should be documented. Accurate radial margins should be marked and recorded and are defined “as the surgically dissected surface adjacent to the deepest point of tumor invasion beyond the wall of the stomach.” The completeness of resection depends on the clearing of the deepest point of invasion: R0 (complete), R1 (microscopic), and R2 (macroscopic). This aspect of number of regional nodes involved exceeds most cancer sites, in which a more limited number of nodes determines substages.
Oncoimaging Annotations
• Screening for early gastric cancers is best done using double contrast (barium–air) coupled with endoscopy.
• Staging is performed by endoscopic ultrasound (EUS) and CT for extensions beyond the wall.
• Lymph node invasion is reliably determined in surgical pathologic assessment of excised nodes rather than imaging.
• Distinguishing malignant from benign ulcers depends on features such as the meniscus sign and nodular and irregular folds around the ulcer.
• Dissemination into lesser and greater omentum, peritoneal implants, and ascites is detectable by CT.
• EUS is of value in analyzing cancer invasion of five-layered stomach wall. In linitis plastica, the layers are preserved but the wall is thickened, especially the fourth layer, corresponding to the muscularis externa.
• Correlation of T stage depth of penetration versus EUS:
Tis mucosa—hyperechoic
T1a mucosa muscularis—hypoechoic
T1b submucosa—hyperechoic
T2 muscularis propria—hypoechoic
T3 serosa—hyperechoic
• EUS is 90% to 99% accurate in distinguishing T1 from T2 and determines early gastric cancer amenable to endoscopic resection.
PROGNOSIS AND CANCER SURVIVAL
• EUS and CT have similar diagnostic accuracy of perigastric nodes: 50% to 80%.
• Nodal size > 5 mm rather than 1 cm based on a study that found 55% of lymph nodes 5 mm were positive for tumor deposits.
Endoscopically, mucosal resection is for Tis lesions, 2 cm size if elevated, 1 cm if slightly depressed and is of the intestinal type.
PROGNOSIS
The limited number of prognostic factors are listed in Table 24.7.
DETECTION AND DIAGNOSIS
Endoscopy and biopsy as well as EUS determine size, stage of T.
CANCER STATISTICS AND SURVIVAL
The majority of digestive systems neoplasms are successfully treated with multimodal treatment. The number of new patients with cancers are 275,000 of which 50% (140,000) survive. The incidence is slightly greater in males than females 54% vs. 46% i.e., 150,000 vs. 1260,000. The death rates over the past five decades have most dramatically decreased in stomach and colon rectum cancers and are unchanged for pancreas and liver. The deaths are also greater in males than females: 56% vs. 44% i.e. 80,000 vs. 60,000.
An overview of digestive system cancers and their incidence of new patients and their death rates are tabulated according to ACS Cancer Facts and Figures 2010 (Tables 22.6 and 22.7).
The largest gains in survival are in colon and rectum, followed by stomach. The poorest results are those in pancreas and liver. The gains other sites vary depending on early detection of cancer in a localized stage in esophago-gastric junction or where chemoradiation is very effective i.e. anal cancers.
Figure 24.7 | Axial CTs of T10 and T11 level correlate with the T-oncoanatomy transverse section (Figure 24.5C). Oncoimaging with CT is commonly applied to staging cancers, often combined with PET to determine true extent of primary cancer and involved lymph nodes 1. Middle hepatic vein. 2. Inferior vena cava. AS, ant seg right lobe of liver; LS, lateral seg left lobe of liver; MS, medial seg left lobe of liver; PS, post seg right lobe of liver; Spl, spleen; Stom, stomach.
Specifically, the stomach accounted for 21,000 new cancer cases and 110,590 cancer deaths, with a survival (5-year) rate improvement over the last five decades (1975–2005) of 11%. Currently, relative 5-year survival for all stages is 27%, but, when localized, it improves to 59% (Fig. 24.8). The basis for subdividing stages I and III is supported by American Joint Committee on Cancer survival data. An intergroup trial by a gastrointestinal group has established that chemoradiation postoperatively doubles survival from 20% to 40% at 5 years. Gastrointestinal stromal tumors of the stomach: a clinicopathologic, immunohistochemical, and molecular genetic studies of 1,765 cases with long-term follow-up (Table 24.8).
Figure 24.8 | Five-year observed survival of surgically resected gastric adenocarcinomas. (From Edge SB, Byrd DR, and Compton CC, et al, AJCC Cancer Staging Manual, 7th edition. New York, Springer, 2010, p. 118.)
