eMedicine Specialties > Oncology > Carcinomas of the Gastrointestinal Tract

Intestinal Stromal Tumors: Treatment & Medication

Author: Prashanth Vallabhajosyula, MD, MS, Clinical Fellowship, Oxford Hospital, UK
Coauthor(s): Michael A Choti, MD, MBA, Jacob C Handelsman Professor of Surgery, Professor of Oncology and Engineering, Johns Hopkins University School of Medicine
Contributor Information and Disclosures

Updated: Sep 11, 2007

Treatment

Medical Care

In general, attempts to treat GISTs with cytotoxic chemotherapy or radiation therapy have been unsuccessful. Effects of radiation therapy on survival are unknown. GISTs are not ideal for this modality because of intra-abdominal motility, and for large tumors, the required field of radiation exposure may cause too much morbidity. Postoperative radiation therapy has managed fixed GISTs, but the results have not been exciting. Recurrences are reported both within and outside the radiation field. Most often, radiation therapy is used in the palliative setting for symptomatic, unresectable disease.

Standard cytotoxic chemotherapy has not been helpful in GIST management. One report noted only a 7% response rate (3 of 43 people with GISTs) to doxorubicin and dacarbazine in gastric sarcomas, compared to 22% for leiomyosarcomas. Other chemotherapy combinations have been equally unsuccessful.

Imatinib mesylate (Gleevec), a tyrosine kinase inhibitor, is the first drug that effectively showed response rates against GIST progression. Two important studies support a major role for Imatinib in the treatment of GISTs.

  • Demetri et al (2001) reported a 54% response rate in 147 people with metastatic GISTs upon treatment with 400-600 mg of daily imatinib and at least 6 months of follow-up. A minor response was recorded in 28%, and 14% had resistance to the drug.9
  • van Oosterom et al (2001), in a phase I trial, reported a 53% response rate in 36 people with metastatic GISTs on a minimum 9-month follow-up. Only 11% showed absolute resistance, 11% had stable tumor loads, and 17% showed minor response.10
  • Both these mentioned studies reported approximately 90% improvement in clinical symptoms.
Related CME is available at The Role of Tyrosine Kinase Inhibitors in the Treatment of Gastrointestinal Stromal Tumors.

Although historically, the standard care after surgical resection was observation alone, with the advent of imatinib therapy, trials have been initiated in the United States and in Europe investigating the benefit of adding imatinib therapy in patients undergo complete surgical resection. The efficacy of imatinib has also altered the paradigm in the treatment of patients with inoperable disease related to the difficulty in achieving negative margins or the risk of severe organ dysfunction. In these patients, imatinib therapy may be given in the neoadjuvant setting to shrink the tumor, with later surgical intervention for a complete resection.

Currently, for most cases of metastatic disease, imatinib therapy is considered the first-line treatment. Due to the success of imatinib therapy, 70% of patients with metastatic disease live more than 2 years after starting therapy. In comparison, only 20% patients with metastatic disease treated with doxorubicin had a 2-year survival. Present recommendations are for life-long treatment with imatinib for metastatic disease. In patients with metastatic disease who develop resistance to imatinib therapy, new tyrosine kinase inhibitors are being investigated. Sunitinib malate (SU11248), a tyrosine kinase inhibitor, is being investigated as an alternative treatment of metastatic GIST, especially in imatinib-resistant GIST. Although at this point, imatinib remains the first-line agent for treatment of metastatic disease.

Surgical Care

Surgical resection remains the cornerstone of treatment for localized GISTs. A complete resection offers the only chance for cure. Patients with complete tumor resection have a clear survival benefit over those with less radical or no surgery. Complete resection is associated with approximately 50-65% 5-year survival rate, but more than 50% of patients who undergo primary resection develop tumor recurrence (see Table 1 in Mortality/Morbidity).

For small GISTs, local resection may be adequate, if technically possible and it does not compromise a complete resection. Small intestinal tumors may require segmental resection, and a wedge resection may be used for small gastric GISTs in some cases. Avoid enucleation of small tumors since predicting the preoperative malignant potential of GISTs is difficult, even if the tumor appears benign. Since limited resection is adequate for small malignant GISTs, minimally invasive surgery techniques can be adopted in select cases. Laparoscopic resection of GISTs of the stomach has demonstrated the feasibility and safety of this technique.

Approach all GISTs with an intention of a complete en bloc resection, including resection of any involved organs or structures such as the colon, spleen, kidney, and pancreas. As GISTs rarely metastasize to lymph nodes, routine lymphadenectomy is not indicated and does not show any survival benefit. Direct all efforts at avoiding tumor rupture during the operation. A tumor rupture is associated with a worse prognosis due to peritoneal seeding. Similarly, preoperative percutaneous biopsy of the tumor is not indicated in most cases, because there is a potential for needle track seeding. Preoperative percutaneous biopsy is pursued if the newly available information changes management, as it would in the case of a lymphoma.

The role for surgery in treating GIST metastasis is minimal. Metastasectomy may provide a survival benefit in select patients. These may include patients with well-differentiated GISTs, longstanding disease-free survival, and isolated liver metastases. In patients with good response to imatinib treatment, in whom gross disease can be removed, surgery may be considered on an individual case-by-case basis.

Consultations

No specific consultations are required.

Diet

Diet advancement decisions in people who have had surgery are based on the type of surgery and are individualized for each person. No specific diet restrictions are recommended for people with GISTs.

Activity

No specific activity restrictions exist.

Medication

The goals of pharmacotherapy are to induce remission, reduce morbidity, and prevent complications.

Tyrosine kinase inhibitors

These agents inhibit the activation of tyrosine kinases, which halt their downstream signal cascades.


Imatinib mesylate (Gleevec)

Competitive inhibitor of specific tyrosine kinases ABL, BCR-ABL, KIT, and platelet-derived growth factor. Competes with ATP by binding its kinase-binding site. This inhibits the kinase activity of the protein, thus halting autophosphorylation and phosphorylation of other kinases and transcription factors. In GISTs, KIT is constitutively active, but for this to occur it needs ATP binding. Imatinib inhibits this step, thus blocking the KIT signaling pathway, skewing the balance of cell cycle away from proliferation, toward apoptosis. The drug has little or no effect on other tyrosine kinases not mentioned above. Half-life of ~20 hours, and serum concentrations >1 µmol/L show therapeutic effect.

Adult

Typically, 400 mg/d PO with food, may be increased to 800 mg/d divided bid in the absence of adverse effects

Pediatric

Not established

Metabolized by the P450 system in the liver, CYP3A4; primary excretion via stool through bile salt excretion; other drug interactions to be aware include CYP3A4 inhibitors (ketoconazole increases distribution of imatinib), CYP3A4 substrates (simvastatin increases maximum concentration of imatinib by a 2- to 3.5-fold factor), CYP3A4 inducers (phenytoin decreases area under curve [AUC] by approximately one fifth of typical AUC); substrates of CYP2C9, CYP2D6, and CYP3A4/5 are likely to increase serum concentrations

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

More common side effects include periorbital and lower extremity edema, diarrhea, headache, myalgia, dermatitis, neutropenia, and anemia; about 5% of the patients can develop bleeding into the abdominal cavity or bowel; dose must be reduced for worsening side effects such as anemia, edema, transaminitis, grade 3-4 neutropenia, and thrombocytopenia

Multikinase inhibitors

These agents elicit actions via multiple tyrosine kinase inhibitors implicated in tumor growth, pathologic angiogenesis, and metastatic progression.


Sunitinib (Sutent)

Mulitkinase inhibitor that targets several tyrosine kinase inhibitors implicated in tumor growth, pathologic angiogenesis, and metastatic progression. Inhibits platelet-derived growth factor receptors (ie, PDGFR-alpha, PDGFR-beta), vascular endothelial growth factor receptors (ie, VEGFR1, VEGFR2, VEGFR3), stem cell factor receptor (KIT), Fms-like tyrosine kinase-3 (FLT3), colony-stimulating factor receptor type 1 (CSF-1R), and the glial cell-line–derived neurotrophic factor receptor (RET).
Indicated for persons with gastrointestinal stromal tumors (GISTs) whose disease has progressed or who are unable to tolerate treatment with imatinib (Gleevec). Delays median time to tumor progression.

Adult

Standard dose: 50 mg PO qd on a schedule of 4 wk on treatment followed by 2 wk off treatment, then repeat cycle
Dose modification: Increase or reduce dose in 12.5-mg increments based on individual safety and tolerability
Coadministration with potent CYP4503A4 inhibitors: Minimum dose of 37.5 mg PO qd during treatment phase of cycle
Coadministration with CYP4503A4 inducers: Maximum dose of 87.5 mg PO qd during treatment phase of cycle

Pediatric

Not established

Potent CYP4503A4 inhibitors (eg, ketoconazole, itraconazole, clarithromycin, atazanavir, indinavir, nefazodone, nelfinavir, ritonavir, saquinavir, telithromycin, voriconazole) may increase plasma concentrations; CYP4503A4 inducers (eg, dexamethasone, phenytoin, carbamazepine, rifampin, rifabutin, phenobarbital) may decrease plasma concentrations; St John's wort induces metabolism and decreases plasma concentrations unpredictably (do not take concurrently)

Documented hypersensitivity; concurrent administration with St John's wort

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Common adverse effects include diarrhea, skin discoloration, mouth irritation, weakness, and altered taste; may cause fatigue, hypertension, bleeding, swelling, and hypothyroidism; in clinical trials, decreased left ventricular ejection fraction to below lower limits of normal in 15% of patients (monitor for CHF and discontinue if clinical manifestations of CHF develop); may cause hemorrhagic events that may include epistaxis or rectal, gingival, GI, genital, or wound bleeding

More on Intestinal Stromal Tumors

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

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Keywords

GIST, IST, GISTs, gastrointestinal stromal tumors, gastrointestinal mesenchymal tumors, GI mesenchymal tumors, gastrointestinal tumors, GI tumors, leiomyosarcoma, intestinal stromal tumors, interstitial cells of Cajal, GI tract, gastrointestinal malignancies, GI malignancies, gastric stromal tumors, gastrointestinal cancer, GI cancer, stomach cancer, stomach malignancy, stomach tumor, Carney triad, gastric stromal sarcoma, extra-adrenal paraganglioma, pulmonary chondroma, neurofibromatosis I

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Contributor Information and Disclosures

Author

Prashanth Vallabhajosyula, MD, MS, Clinical Fellowship, Oxford Hospital, UK
Prashanth Vallabhajosyula, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

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.

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.

Managing Editor

Marcel E Conrad, MD, (Retired) Distinguished Professor of Medicine, University of South Alabama
Marcel E Conrad, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American Association of Blood Banks, American Chemical Society, American College of Physicians, American Physiological Society, American Society for Clinical Investigation, American Society of Hematology, Association of American Physicians, Association of Military Surgeons of the US, International Society of Hematology, Society for Experimental Biology and Medicine, and Southwest Oncology Group
Disclosure: No financial interests None None

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
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

 
 
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