eMedicine Specialties > Oncology > Carcinomas of the Gastrointestinal Tract

Gastric Gastrointestinal Stromal Tumors

Author: Michael A Choti, MD, MBA, Jacob C Handelsman Professor of Surgery, Professor of Oncology and Engineering, Johns Hopkins University School of Medicine
Coauthor(s): Matthew Hueman, MD, Fellow in Surgical Oncology, The Johns Hopkins Hospital; Instructor, Department of Surgery, The Johns Hopkins School of Medicine
Contributor Information and Disclosures

Updated: Jun 4, 2009

Introduction

Background

Gastrointestinal stromal tumors (GISTs) are mesenchymal neoplasms of the gastrointestinal (GI) tract and are thought to develop from the interstitial cells of Cajal, innervated cells associated with the Auerbach plexus. GISTs are typically defined by the expression of c-KIT (CD117) in the tumor cells, as these activating KIT mutations are seen in 85-95% of GISTs. About 3-5% of the remainder of KIT -negative GISTs contain PDGFR alpha mutations.1,2,3

The PDGFR alpha mutation seems to leave the PDGFR a-receptor constitutively active and may represent an alternate pathway with activation of similar downstream signaling as the KIT receptor. The recent discovery of these receptor mutations has redefined the classification and management of the disease. With only about 5000 new cases expected annually in the United States, GISTs are rare and constitute only 1% of all malignant tumors of the GI tract but are the most common mesenchymal neoplasm of the GI tract.

Shown here is a gastric gastrointestinal stromal ...

Shown here is a gastric gastrointestinal stromal tumor (GIST). This is a gross specimen following partial gastrectomy. Note the submucosal tumor mass with the classic features of central umbilication and ulceration.

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Shown here is a gastric gastrointestinal stromal ...

Shown here is a gastric gastrointestinal stromal tumor (GIST). This is a gross specimen following partial gastrectomy. Note the submucosal tumor mass with the classic features of central umbilication and ulceration.


The discovery in 2000 of the efficacy of imatinib, an inhibitor of the BCR-ABL oncoprotein used in the treatment of chronic myeloid leukemia (CML), in treating metastatic gastrointestinal stromal tumor has revolutionized the care of patients with GISTs.4  Prior to the advent of immunohistochemical methods enabling the specific identification of c-KIT positive tumors, these tumors were inaccurately classified as gastric or intestinal smooth muscle tumors (leiomyomas or leiomyosarcomas).

The identification of the clinical efficacy of imatinib in c-KIT- positive metastatic GIST has led to the further discovery of imatinib as a clinically effective tyrosine-kinase inhibitor targeting KIT and PDGFR alpha in KIT receptor-positive GIST.5,6,7,8,9 This discovery has been celebrated as the example of the power of targeted, individualized therapy and has helped focus a great deal of attention on this orphan disease. As of December 19, 2008, the FDA has now approved imatinib mesylate for the adjuvant therapy of primary resected GIST,10 in addition to the initial approval for metastatic GIST in 2002.

While GISTs can occur at any point along the GI tract, the focus of this article is on gastric GISTs. In the spectrum of cancers of the stomach, gastric GISTs constitute only 1-3% of all malignant gastric tumors. GISTs are most commonly found in the stomach (47-60% of cases)11  as compared to small bowel (30%) and esophagus and rectum (10%).

Histologically, GISTs can be distinguished from cellular spindle cell (70%) tumors to epithelioid (20%) or pleomorphic/mixed morphology tumors, but such histologic distinction does not carry clear prognostic significance. While GISTs are typically CD117-positive (85-95%), positivity for CD34 (60-70%), nestin, ACAT2, S100 (10%), and DES may be helpful in establishing the diagnosis.

Characteristics of GISTs that are predictive of aggressive behavior are mitotic rate greater than 5 per 10 high-power fields (HPF), size larger than 5 cm and 10 cm, and location (small bowel GISTs of comparable size and mitotic rate are generally more aggressive than gastric GISTs). However, tumors with low mitotic index (<5 per 50 HPF) and smaller size (2-5 cm) can also metastasize. So while gastric GISTs are commonly less aggressive than those of nongastric intestinal origin, they still maintain the propensity for distant spread.

Pathophysiology

GISTs are typically diagnosed as solitary lesions, although in rare cases, multiple lesions can be found. These tumors can grow intraluminally or extraluminally toward adjacent structures. When the growth pattern is extraluminal, patients can harbor the disease symptom free for an extended period and present with very large exogastric masses.

Distant metastases tend to appear late in the course of the disease in most cases. In contrast to other soft tissue tumors, the common metastatic sites of GISTs are the liver and peritoneum. Lymph node involvement is rare, occurring in only 0-8% of cases.

Frequency

United States

An estimated 5000 new cases are diagnosed annually in the United States, as compared to about 150,000 new cases of colorectal cancer.

International

GISTs are rare, and data concerning its worldwide prevalence are lacking. In general, it constitutes 1-3% of all gastric malignancies.

Mortality/Morbidity

Long-term survival is typically correlated inversely with tumor size and mitotic rate. Gastric GISTs carry a better prognosis than small bowel GISTs of similar size and mitotic rate. In general, gastric GISTs portend a much better prognosis than adenocarcinoma of the stomach.

Even after complete resection of primary GIST, at least 50% of patients develop recurrence or metastasis, at a median time to recurrence of 2 years. This high rate of recurrence is in the setting of an overall 5-year survival rate of 50%.

Patients with advanced GIST on tyrosine-kinase inhibitor therapy may develop tumor-related intraluminal or intraperitoneal hemorrhage, rupture, fistula, or obstruction requiring emergent surgery.

Race

No racial predilection exists.

Sex

No sex predilection exists.

Age

Onset can occur at any age but occurs most commonly in the sixth and seventh decades of life.

Clinical

History

  • Upper GI bleeding is the most common clinical manifestation of gastrointestinal stromal tumors (GISTs), manifesting as hematemesis or melena in 40-65% of patients. Bleeding occurs because of an ulcer forming in the gastric mucosa overlying the tumor.
  • Other symptoms are generally associated with an enlarging abdominal mass and may include abdominal pain, anorexia, nausea, vomiting, weight loss, epigastric fullness, and early satiety.
  • Not uncommonly, GISTs can be found incidentally, at endoscopy or even at the time of surgery. In Japan, mass screening for gastric adenocarcinoma with upper endoscopy has led to an increase in incidental findings of asymptomatic GISTs.

Physical

Physical examination rarely demonstrates any significant findings. In some cases, examination may identify a palpable abdominal mass in the abdomen. Palpable masses are typically detected in patients with an exogastric tumor growth.

Causes

No risk factors have been identified.12

More on Gastric Gastrointestinal Stromal Tumors

Overview: Gastric Gastrointestinal Stromal Tumors
Differential Diagnoses & Workup: Gastric Gastrointestinal Stromal Tumors
Treatment & Medication: Gastric Gastrointestinal Stromal Tumors
Follow-up: Gastric Gastrointestinal Stromal Tumors
Multimedia: Gastric Gastrointestinal Stromal Tumors
References
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Further Reading

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Keywords

gastric gastrointestinal stromal tumors, gastric GISTs, malignant gastric stromal tumors, gastric leiomyosarcomas, gastrointestinal stromal tumors, GISTs, gastric GIST, fibrosarcoma, angiosarcoma, hemangiopericytoma, gastric smooth muscle tumors, intestinal smooth muscle tumors

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Contributor Information and Disclosures

Author

Michael A Choti, MD, MBA, Jacob C Handelsman Professor of Surgery, Professor of Oncology and Engineering, Johns Hopkins University School of Medicine
Michael A Choti, MD, MBA is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Surgeons, American Hepato-Pancreato-Biliary Association, American Society of Clinical Oncology, American Surgical Association, Association for Academic Surgery, International Hepato-Pancreato-Biliary Association, Society for Surgery of the Alimentary Tract, Society of Surgical Oncology, and Society of University Surgeons
Disclosure: Nothing to disclose.

Coauthor(s)

Matthew Hueman, MD, Fellow in Surgical Oncology, The Johns Hopkins Hospital; Instructor, Department of Surgery, The Johns Hopkins School of Medicine
Matthew Hueman, MD is a member of the following medical societies: American Association for Cancer Research, American College of Surgeons, American Hepato-Pancreato-Biliary Association, American Society of Clinical Oncology, Association for Academic Surgery, and Society of Surgical Oncology
Disclosure: Nothing to disclose.

Medical Editor

Robert C Shepard, MD, FACP, Associate Professor of Medicine in Hematology and Oncology at University of North Carolina at Chapel Hill; Vice President of Scientific Affairs, Therapeutic Expertise, Oncology, at PRA International
Robert C Shepard, MD, FACP is a member of the following medical societies: American Association for Cancer Research, American College of Physician Executives, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Medical Association, American Medical Informatics Association, American Society of Hematology, Association of Clinical Research Professionals, Eastern Cooperative Oncology Group, European Society for Medical Oncology, Massachusetts Medical Society, and Society for Biological Therapy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

CME Editor

Rajalaxmi McKenna, MD, FACP, Consulting Staff, Department of Medicine, Southwest Medical Consultants, SC, 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
Disclosure: Nothing to disclose.

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 at Tucson; 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; Amplimed Consulting fee Consulting; FibroGen Consulting fee Consulting

 
 
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