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ORIGINAL ARTICLE Table of Contents   
Year : 2010  |  Volume : 53  |  Issue : 4  |  Page : 628-633
Gastrointestinal stromal tumors: A 7-year experience from a tertiary care hospital


1 Department of Pathology, Christian Medical College and Hospital, Ida Scudder Road, Vellore - 632 004, Tamil Nadu, India
2 Department of Medical Oncology, Christian Medical College and Hospital, Ida Scudder Road, Vellore - 632 004, Tamil Nadu, India

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Date of Web Publication27-Oct-2010
 

   Abstract 

Background: Gastrointestinal stromal tumor (GIST), now the most common mesenchymal tumor of the gastrointestinal tract (GIT), has been frequently studied, especially with regard to its successful targeted therapy using imatinib mesylate. Aim: Our aim was to describe the clinicopathological features of a large number of cases from a tertiary care hospital in India and report on the follow-up after treatment of some of the cases, comparing them with series described in the west. Design: This is a retrospective study of cases encountered over a 7-year period (1999-2005). Results: Ninety-two cases of GIST were studied, which made up the largest group (52.8%) of mesenchymal tumors of the GIT, with smooth muscle tumors comprising 38.1%, the next large group. GISTs were almost equally prevalent in the stomach and the small intestine, unlike in most studies where stomach is the most common site. GIST may be considered as a cause of bleeding when upper and lower GI endoscopy is normal. Ninety-five percent of the GISTs were positive for CD117 (KIT), as is known. A majority of them (70.4%) were of the high-risk malignant category, unlike most studies where high-risk tumors make up 30-45%. Histologically, the majority had a pure spindle cell morphology and skenoid fibers were rare. Follow-up of 11 cases, the majority with high-risk tumor, treated with adjuvant imatinib for 6 months after surgical resection showed stable disease for periods from 2 to 5 years. However, 11 cases treated with imatinib for longer than 6 months had a poorer outcome due to recurrent, metastatic, or inoperable disease. Conclusion: In our study of a large number of GISTs, which were equally prevalent in the stomach and small intestine, the majority were of the high-risk malignant category and of pure spindle cell morphology. Limited numbers had follow-up after imatinib therapy, which showed in one group treated for 6 months, after resection of high-risk GIST, stable disease for periods ranging from 2 to 5 years. Molecular studies and larger numbers are required for meaningful conclusions to be drawn.

Keywords: GIT, imatinib, stromal tumor

How to cite this article:
Lakshmi VA, Chacko RT, Kurian S. Gastrointestinal stromal tumors: A 7-year experience from a tertiary care hospital. Indian J Pathol Microbiol 2010;53:628-33

How to cite this URL:
Lakshmi VA, Chacko RT, Kurian S. Gastrointestinal stromal tumors: A 7-year experience from a tertiary care hospital. Indian J Pathol Microbiol [serial online] 2010 [cited 2019 Dec 14];53:628-33. Available from: http://www.ijpmonline.org/text.asp?2010/53/4/628/72005



   Introduction Top


Gastrointestinal stromal tumor (GIST), now considered the most common mesenchymal tumor of the gastrointestinal tract (GIT), has been frequently studied and several large series have been published in the western literature. [1],[2],[3],[4],[5],[6] Its dramatic response to antityrosine kinase receptor agents like imatinib mesylate and molecular aspects of this response have been the subject of published articles. [7],[8],[9],[10],[11]

This series of 92 cases of GIST, which presented over a 7-year period at a tertiary care hospital, forms a large series from India. It details aspects of demographics, clinical presentation, pathology and follow-up of some of the cases following surgery and imatinib therapy, with comparisons made with series described in the west.


   Materials and Methods Top


Over a 7-year period (January, 1999-December, 2005) a total of 219 consecutive cases of mesenchymal tumors of the GIT were diagnosed at the pathology department of a tertiary care hospital. Eight cases with no paraffin blocks, 13 cases with no information about site of tumor and 22 cases with biopsies when surgical specimens were also available were excluded, leaving 176 cases.

Presently, the defining feature of GIST is the expression of CD117, a marker of KIT activation, which is sensitive although not entirely specific. Five percent of GISTs are known to be negative for CD117 (KIT protein), [12],[13] although they resemble KIT-positive GISTs by cytomorphology.

Of the 176 cases of mesenchymal tumors of the GIT tract analyzed at entry to the study, 50% were smooth muscle tumors and 40.9% were GISTs. However, after immunostaining for CD117, 20 cases that were initially called smooth muscle tumors were reclassified as GIST, which then made up the largest group (52.8%) of mesenchymal tumors, with smooth muscle tumors comprising 38.1%.

Ninety-two cases of GIST were analyzed for the following features:

Demographics and clinical presentation.

Pathologic features including categorization into risk groups according to Fletcher [14] and CD117 immunostaining patterns, whether membranous, golgi, or cytoplasmic. Intensity of CD117 staining, whether 1+, readily visible only at high power or 2+, readily visible at low power.

Treatment and follow-up. Two groups of 11 patients each were followed-up for periods of 2-5 years. The first group was patients treated with imatinib mesylate for 6 months after surgical resection. The second group was patients with recurrent, metastatic, and inoperable disease who received imatinib therapy for periods longer than 6 months.

Immunochemistry was performed manually by the biotin-streptavidin peroxidase technique using antibodies shown in [Table 1].
Table 1 :List of antibodies used


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As the supply of the monoclonal CD 117 antibody by Zymed was discontinued, the polyclonal CD117 from DAKO was used for the last 10 cases. Cross-reaction with fibromatosis has been described with DAKO CD117 antibody when used in low dilutions of 1/50. [15]


   Results Top


Demographics and Clinical Presentation

GISTs were infrequent before the 3 rd decade (6.5%). The peak incidence was in the 4 th and 5 th decades (49.5%). The oldest patient was 82 years old. GISTs affected men more frequently, with a M:F ratio of 3:1.

In 23 cases, information on clinical presentation was not available. Of the remaining 69 cases, 50% presented with gastrointestinal bleed and 24% with a mass lesion or fullness of the abdomen. Fewer cases (5) had vague abdominal discomfort and 10 had a combination of the above symptoms. One patient each presented with dyspepsia, anemia, and acute abdomen due to tumor perforation. One patient was asymptomatic and in three cases, GIST was an incidental finding during investigation for hypertension, synchronous gastric carcinoid, and neurofibromatosis type I (NF1).

Pathologic Features


GISTs were almost equally prevalent in the small intestine (43%) and the stomach (39%). The colorectum had only 8.6% of the tumors and, much less frequently, GISTs were present in the esophagus (two cases) and in the anal canal (three cases).

GISTs ranged in size from 1.5 to 30 cm. The smallest was found in the gastric fundus synchronously with a carcinoid tumor.

Majority of the GISTs (40%) ranged in size from 5 to 10 cm and slightly fewer (34%) were >10 cm, which categorized the latter as definitely malignant and in the high-risk group.

Majority of the GISTs (53%) grossly presented as mass lesions and the next most frequent presentation (25%) was polypoid lesions [Figure 1]. The cut-surfaces were mainly firm to soft to fleshy and dark variegated, with 60% showing hemorrhage, 25% showing additional necrosis and 23% showing cystic change. In tumors <5 cm in size, these secondary changes were uncommon.
Figure 1 :Gross appearance of a polypoid GIST from the jejunum with a pale fleshy cut surface

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GISTs demonstrate variable histology, including sheet-like arrangement, short fascicles, whorls, storiform, and organoid patterns. Short fascicular arrangement was the most common pattern in both benign and malignant tumors (51%) [Figure 2]a. Most tumors (66%) had a pure spindle cell morphology and only four cases had a pure epitheloid cell morphology [Figure 2]b. Mixed spindle and epitheloid cell morphology was found in 24% of the cases. Nuclear palisading was found in 27% of the cases reminiscent of nerve sheath tumors. Skenoid fibers [Figure 2]c were seen in only three cases, all of which were malignant. One case showed focal calcification.
Figure 2 :(a) Low power microscopic view of GIST showing characteristic short fascicles of spindle shaped cells with nuclear palisading. (H and E, ×200)
Figure 2b: High power view of gastric GIST with epitheliod cells showing abundant eosinophilic cytoplasm and round pale nuclei. (H and E, × 400)
Figure 2c: High power view of GIST with ropy eosinophilic skenoid fibers. (H and E, x400)


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Mitotic activity was assessed in order to assign tumors into risk groups as described by Fletcher et al.[14] The overall categorization of risk groups based on size and mitotic activity showed that the majority of the GISTs (70.4%) were of the high-risk group, with 20.6% in the intermediate-risk group and 8% and 1% in the low- and very-low-risk groups, respectively. Four of the 92 cases could not be classified as information on size was not available.

Immunochemistry for CD117 was positive in 87 of the 92 cases (94.5 %) and negative in five cases. Smooth Muscle Actin (SMA) was positive in 50%, CD34 was positive in 77%, Desmin was positive in 17%, and S100 was positive in 25% of the respective numbers of cases of GIST where these antibodies were used.

The intensity and staining patterns of CD117 in the various risk groups are shown in [Table 2]. The majority (73%) showed 2+ intensity of staining and 70% belonged to the high-risk group. However, this was not statistically significant. The staining pattern in the majority (45%) was pure membranous [Figure 3]a, and 80% of these were of the high-risk group, but again showed no statistical significance. In about 38% of the cases, combinations of staining patterns were present [Figure 3]b.
Table 2 :Intensity and Pattern of CD117 Staining in the GIST Risk Groups[14]


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Figure 3 :(a) High power view of membranous pattern of CD117 immnostaining of 2+ intensity. (IHC, ×400)
Figure 3b: High power view of mixed membranous and Golgi patterns of CD117 immunostaining. (IHC, ×400)


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Metastasis was demonstrated by imaging in 14 patients, eight of which were in the liver and two each in the pancreas, spleen, and urinary bladder. Histological demonstration of metastasis was made in only two cases, both of which were gastric GISTs with metastasis in the regional lymph nodes.

Imatinib Therapy

In all, 22 patients in this study received imatinib therapy and follow-up was possible for periods of 3-5 years.

One group had 11 patients who had received imatinib therapy for a period of 6 months following surgical resection, eight of whom were of the high-risk category, two of the intermediate-risk category, and one of the low-risk category. In two of these 11 patients, imatinib was started only after metastasis was encountered. In one patient, follow up was not possible. However, in the rest of the 10 patients, the disease was s table for periods of 2-5 years.

The second group had 11 patients who received imatinib therapy for periods longer than 6 months, eight of whom were of the high-risk category and one was of the intermediate-risk category. In two, the risk group was not known. Eight in the group had metastasis, following which imatinib therapy was started. Three patients in the group that had inoperable disease received imatinib after diagnosis. The period of s table disease after imatinib therapy was mostly 1 year or less in seven patients and 2 and 4 years in two other patients. In one patient, the disease progressed despite therapy and one patient had no follow-up.


   Discussion Top


This large study of 92 cases of GIST from an Indian tertiary care hospital has shown, as in the western literature, that it is the most frequent mesenchymal tumor of the GIT. [3],[6]

CD117 (KIT) expression (a protooncogene protein) has emerged as a sensitive, although not entirely, specific marker, being positive in 95% of our cases. Twenty cases at entry to the study were classified as smooth muscle tumors until CD117-positive immunostaining proved them to be GISTs, emphasizing that CD117 immunochemistry is mandatory to confirm the diagnosis of GIST, even on small biopsy specimens. Five percent of the tumors with histomorphological features of GIST were negative for CD117 (KIT), [12],[13] which is probably attributed to the presence of activating mutation of platelet-derived growth factor receptor-alpha (PDGFRA.)

Immunostaining for PDGFRA can help in these CD117-negative tumors. [8] However, that was not performed in this study. GISTs are characterized by activating mutations affecting KIT or the PDGFRA gene. These are mutually exclusive. However, they can be coexpressed with various modulations of immunostaining, depending on which gene is mutated.

The peak incidence of GIST was found in the 4 th and 5 th decades (49.5%), with a male preponderance in a ratio of 3:1, as is generally known. [3],[6]

The most common clinical presentation was GI bleeding (50%) probably due to mucosal ulceration followed by abdominal fullness due to a mass lesion (24%) also reported by others. [3],[16],[17] GISTs may also be asymptomatic, [3] as seen in three cases of the study where GIST was an incidental finding. One patient in the study presented as acute abdomen due to tumor rupture, which prompted surgical intervention. Tumor rupture confers clearly increased risk of recurrence. [18]

The western literature documents GIST as being most prevalent in the stomach (50-60%), with much fewer being present in the small bowel (22-30%). [14] Our cases were almost equally located in the small bowel (44%) and in the stomach (38.7%), which is probably due to differences in population studies. More studies from India need to be evaluated for this to be supported. Nongastric GISTs have a higher rate of recurrence when matched for size and mitotic rate than gastric GISTs. [18]

Because GISTs are frequently present in the small intestine, it should be considered as a possible cause of GI bleeding when upper and lower GI endoscopy have been found to be normal.

Most tumors in the study (71.9%) had a pure spindle cell morphology, and pure epitheloid cell morphology was seen in only four cases. 23.6% of the tumors only had combined spindle and epitheloid cell cytomorphology, unlike the literature, which documents that combined morphology is present in most GISTs. [3],[16],[17]

Skenoid fibers or whorled extracellular collagen were seen in only three cases; two in the small intestine and one in the stomach, all three being malignant, contrary to the series by Miettinen et al., [3] where skenoid fibers were described in nearly half of the small intestinal GISTs, most of which were benign. Majority of the tumors (70.4%) were of the high-risk/malignant category, with much fewer (20%) being of the intermediate-risk group. Studies from the west show much lower prevalence of high-risk GIST, 44% in a study from Finland [18] and 30% in a study from the UK. [19]

As with most sarcomas, GISTs rarely metastasize to lymph nodes, demonstrated in only two cases of the study. Visceral metastasis is also uncommon, [16] and was seen mainly in tumors of the high- and intermediate-risk groups and most commonly found in the liver.

The finding that most GISTs have KIT expression has led to the hypothesis that targeting KIT protein and selectively inhibiting KIT receptor tyrosine kinase might be useful in medical therapy in addition to it being a diagnostic marker for GIST. [14],[20]

GISTs are resistant to conventional chemotherapy and radiation. Surgical resection is still the best modality of treatment.

The survival of patients with metastatic and inoperable GIST has improved dramatically since the introduction of imatinib mesylate into treatment protocols. [10] Adjuvant imatinib treatment after surgical resection is beneficial in high-risk tumors and is being characterized in several ongoing clinical trials. A pilot study carried out on cases with high-risk GIST showed that no recurrences occurred within 2 years when patients received adjuvant imatinib for 1 year after complete curative resection when compared with historical controls without imatinib therapy who had 67% recurrence. [9]

The limited number of 11 patients in this study, majority with high-risk/malignant tumors, who received adjuvant imatinib therapy for 6 months after curative resections showed s table disease for periods ranging from 2 to 5 years, which supports evidence that adjuvant imatinib after curative resections in the high-risk category decreases incidence of recurrence. [9] However, KIT mutation studies have not been carried out in this study as it has been shown that KIT mutation status is an independent prognostic factor in GIST. [11] KIT exon 11 mutants respond well to imatinib.

Less-common KIT exon 9 mutations occur predominantly in intestinal GISTs and are less sensitive to imatinib. The most common PDGFRA mutation is in exon 18 and GISTs with this are resistant to imatinib. [20]

The second group of 11 patients that was treated for longer than 6 months with imatinib had poorer outcome due to metastatic, recurrent, or inoperable disease being present in all patients except one.

Larger numbers of patients with high-risk GIST need to be followed-up after adjuvant imatinib therapy for meaningful conclusions to be drawn from our patients. Molecular studies of KIT and PDGFRA gene mutations also need to be correlated with these treatment protocols and outcomes as it has been recently shown that changing patterns of KIT expression and morphological differentiation can occur in GISTs treated with imatinib that develop resistance to therapy. [21],[22]

In conclusion, this is a large series of GISTs reported from a tertiary referral hospital where a majority was of the high-risk category. GISTs were almost equally prevalent in the stomach and in the small intestine, and most had a pure spindle cell morphology, with skenoid fibers being rare. Small intestinal GIST should be considered as a possible cause of GI bleeding when upper and lower GI endoscopy is found to be normal. Adjuvant imatinib therapy after resection of high-risk GIST in limited numbers of cases has resulted in stable disease for periods ranging from 2 to 5 years. Larger numbers however need to be followed-up along with molecular studies in order for meaningful conclusions to be drawn.

 
   References Top

1.Miettinen M, Sarlomo-Rikala M, Sobin LH, Lasota J. Esophageal stromal tumors - A clinicopathological, immunohistochemical and molecular genetic study of 17 cases and comparison with esophageal leiomyomas and leiomyosarcomas. Am J Surg Pathol 2000;24:211-22.  Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.Miettinen M, Sobin LH, Lasota J. Gastrointestinal stromal tumors of the stomach - A clinicopathological, immunohistochemical and molecular genetic study of 1765 cases with long term follow up. Am J Surg Pathol 2005;29:52-98.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.Miettinen M, Hala M, Sobin LH, Lasota J. Gastrointestinal stromal tumors of the jejunum and ileum. A clinicopathological, immunohistochemical and molecular genetics study of 906 cases before imatinib with long term follow up. Am J Surg Pathol 2006;30:477-89.  Back to cited text no. 3
    
4.Miettinen M, Sarlomo-Rikala M, Sobin LH, Lasota J. Gastrointestinal stromal tumours and leiomyosarcomas in the colon. A clinicopathological, immunohisto- chemical and molecular genetic study of 44 cases. Am J Surg Pathol 2000;24:1339-92.  Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.Miettinen M, Furlong M, Sarlomo-Rikala M, Burke A, Sobin LH, Lasota J. Gastrointestinal stromal tumors, intramural leiomyomas and leiomyosarcomas in the rectum and anus - A clinicopathological, immunohistochemical and molecular genetic study of 144 cases. Am J Surg Pathol 2001;25:1121-33.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Miettinen M, Lasota J, Sobin LH. Gastrointestinal stromal tumors of the stomach in children and growing adults. A clinicopathological, immunohistochemical and molecular genetics study of 44 cases with long term follow up and review of literature. Am J Surg Pathol 2005;29:1373-81.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.Miettinen M, Kopczynski J, Makhlouf HR, Sarlomo-Rikala M, Gyorffy H, Burke A, et al. Gastrointestinal stromal tumours, intramural leiomyomas and leiomyosarcomas in duodenum. A clinicopathologic, immunohistochemical and molecular genetics study of 167 cases. Am J Surg Pathol 2003;27:625-41.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.Miselli F, Millefanti C, Conca E, Negri T, Piacenza C, Pierotti MA, et al. PDGFRA immunostaining can help in the diagnosis of gastrointestinal stromal tumors. Am J Surg Pathol 2008;32:738-43.  Back to cited text no. 8
[PUBMED]  [FULLTEXT]  
9.Nilsson B, Sjolund K, Kindblom LG, Meis-Kindblom JM, Bumming P, Nilsson D, et al. Adjuvant imatinib treatment improves recurrence free survival in patients with high-risk gastrointestinal stromal tumours (GIST). Br J Cancer 2007;96:1656-8.  Back to cited text no. 9
    
10.Verwii J, Casali PG, Zalcberg J, Le Cesne A, Reichardt P, Blay JY, et al. Progression free survival in gastrointestinal stromal tumours with high dose imatinib: randomised trial. Lancet 2004;364:1127-34.  Back to cited text no. 10
    
11.Andersson J, Bumming P, Meis-Kindblom JM, Sihto H, Nupponen N, et al. Gastrointestinal stromal tumours with KIT exon 11 deletions are associated with poor prognosis. Gastroenterology 2006;130:1573-81.  Back to cited text no. 11
    
12.Debeic-Rychter M, Wasag B, Stul M, Wever ID, Oosterom AV, Hagemeijer A, et al. Gastrointestinal stromal tumours (GISTs) negative for KIT (CD117 antigen) immuno reactivity. J Pathol 2004;202:430-8.  Back to cited text no. 12
    
13.Medeiros F, Corless CL, Duensing A, Hornick JL, Oliveira AM, Henrich MC, et al. KIT negative gastrointestinal stromal tumors: proof of concept and therapeutic implications. Am J Surg Pathol 2004;28:889-94.  Back to cited text no. 13
    
14.Fletcher CD, Berman JJ, Corless C, Gonstein F, Lasota J, Longley BJ, et al. Diagnosis of gastrointestinal tumours: a consensus approach. Hum Pathol 2002;33:459-65.  Back to cited text no. 14
    
15.Lucas DR, al-Abbadi M, Tabaczka P, Hamre MR, Weaver DW, Mott MJ. c-kit expression in desmoid fibromatosis. Comaritive immnohistochemical evaluation of two commercial antibodies. Am J Clin Pathol 2003;119:339-45.  Back to cited text no. 15
[PUBMED]  [FULLTEXT]  
16.Rubin BP. Gastrointestinal stromal tumors: an update. Histopathology 2006;48:83-96.  Back to cited text no. 16
[PUBMED]  [FULLTEXT]  
17.Suster S. Gastrointestinal stromal tumors. Semin Diagn Pathol 1996;13:297-313.   Back to cited text no. 17
[PUBMED]    
18.Joensuu H. Risk stratification of patients diagnosed with gastrointestinal stromal tumor. Hum Pathol 2008;39:1411-9.   Back to cited text no. 18
[PUBMED]  [FULLTEXT]  
19.Ahmed I, Welch NT, Parsons SL. Gastrointestinal stromal tumours (GIST)- 17 years experience from Mid Trent Region (United Kingdom). Eur J Surg Oncol 2008;34:445-9.  Back to cited text no. 19
[PUBMED]  [FULLTEXT]  
20.Lasota J, Miettinen M. Clinical significance of oncogenic KIT and PDGRFA mutations in gastrointestinal stromal tumours. Histopathology 2008;53:245-66.   Back to cited text no. 20
[PUBMED]  [FULLTEXT]  
21.Liegl B, Hornick JL, Antonescu CR, Corless CL, Fletcher CD. Rhabdomyosarcomatous differentiation in gastrointestinal stromal tumors after tyrosine kinase inhibitor therapy. Am J Surg Pathol 2009;33:218-26.  Back to cited text no. 21
[PUBMED]  [FULLTEXT]  
22.Pauwels P, Debiec-Rychter M, Stul M, De Wever I, Van Oosteroin AT, Sciot R. Changing phenotype of gastrointestinal stromal tumours under imatinib mesylate treatment: a potential diagnostic pitfall. Histopathology 2005;47:41-7.  Back to cited text no. 22
    

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Correspondence Address:
Susy Kurian
Department of Pathology, Christian Medical College, Ida Scudder Road, Vellore - 632 004, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.72005

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