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Gastrointestinal Stromal Tumor in a Liver Transplant Recipient

Saidi, Reza F.; Sepehr, Alireza; Cosimi, A Benedict; Hertl, Martin

doi: 10.1097/TP.0b013e31816c7e2f
Letters to the Editor
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Department of Surgery, Transplantation Unit, Massachusetts General Hospital, Boston, MA (Saidi, Cosimi, Hertl)

Department of Pathology, Massachusetts General Hospital, Boston, MA (Sepehr)

Address correspondence to: Martin Hertl, MD, Department of Surgery, Massachusetts General Hospital, Boston, MA 02114.

E-mail: mhertl@partners.org

Received 11 January 2008.

Accepted 4 February 2008.

The development of de novo neoplastic lesions after liver transplantation has been well-described previously. Incidence rates of 3% to 15% have been reported, which is at least twice as high as that observed in general population (1). This higher incidence is due to complex interaction among multiple factors such as the underlying disease requiring transplantation, chronic immunosuppression, viral and opportunistic infections, and genetic predispostion (1, 2). The most common cancer after liver transplantation are skin cancer and lymphoproliferative disease (1, 2). Gastrointestinal stromal tumor (GIST) has not been reported previously in liver allograft recipients.

Here, we report a 54-year-old man who underwent successful of deceased donor liver transplantation for hepatitis C and a 4 cm hepatocellular carcinoma. Posttransplant immunosuppression consisted of tacrolimus and azathioprine. Eleven months after transplantation, he underwent routine colonoscopy, which revealed a 2.5 cm sessile polyp at the hepatic flexure that was biopsied. The biopsy showed a spindle cell lesion consistent with GIST. The patient underwent right hemicolectomy. His postoperative course was uneventful. Final pathology revealed well-circumscribed GIST. The lesion ulcerated colonic mucosa, invading the muscularis propria, focally traversed the muscle layer, and conjoined a large subserosal hemorrhagic focus. There was 1 mitotic figure in 50 high-power fields. The neoplastic cells stained strongly positive for C-kit, focally positive for S-100, faintly positive for smooth muscle actin, and negative for CD34 in immunohistochemical analysis. The resection margin was free of tumor. Based on the tumor size (>2 cm and <5 cm) and the low mitotic activity, this spindle-cell neoplasm of the colon was classified as GIST with low malignant potential. Therefore, Imatinib mesylate was not recommended. The patient is currently well 18 months after the surgery with no evidence of recurrent hepatocellular carcinoma or GIST.

Gastrointestinal stromal tumor is the most common of the primary mesenchymal GI neoplasm’s (3). GISTs have been reported through the entire length of the digestive tract; stomach (60%), small intestine (30%), duodenum (5%), colorectum (<5%), and esophagus (<1%) (2, 3). The tumor originates from the interstitial cells of Cajal and are characterized by the overexpression of the tyrosin kinase receptor C-KIT (3, 4). No risk factors or predisposing conditions have been identified for GIST. Epstein Barr-virus and Kaposi sarcoma-associated Herpes virus (HHV8) have not been detected in GISTs (4). Gastrointestinal bleeding (50%) is the most common presentation, followed by abdominal pain (20%–50%) and obstruction (20%). Approximately a third is detected incidentally (5). Surgery is the preferred management for GISTs where feasible. Lymph node metastases are rare and localized resection with a clear margin of 1 to 2 cm seems to be adequate treatment (5). Imatinib mesylate, a tyrosine kinase inhibitor, is an effective treatment for locally advance, unresectable, and metastatic GIST (5).

Reza F. Saidi

Department of Surgery, Transplantation Unit

Massachusetts General Hospital, Boston, MA

Alireza Sepehr

Department of Pathology

Massachusetts General Hospital, Boston, MA

A. Benedict Cosimi

Martin Hertl

Department of Surgery, Transplantation Unit

Massachusetts General Hospital, Boston, MA

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REFERENCES

1. Penn I. Posttransplantation de novo tumors in liver allograft recipients. Liver Transpl Surg 1996; 2: 52.
2. Sanchez EQ, Marubashi S, Ghapjoong J, et al. De novo tumors after liver transplantation: A single-institution experience. Liver Transpl 2002; 8: 285.
3. Miettinen M, Lasota J. Gastrointestinal stromal tumors. Review on morphology, molecular pathology, prognosis, and differential diagnosis. Arch Pathol Lab Med 2006; 130: 1466.
4. Su CC, Li CF, Liao YL, et al. Immunohistochemical and molecular assessment of human herpesvirus type 8 in gastrointestinal tumours. J Clin Pathol 2005; 58: 856.
5. DeMatteo RP, Lewis JJ, Leung D, et al. Two hundred gastrointestinal stromal tumour: Recurrence patterns and prognostic factors for survival. Ann Surg 2000; 231: 51.
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