Comparison of characteristic computed tomographic findings of gastrointestinal and non-gastrointestinal stromal tumors in the small intestine

Sections from 35 formalin-fixed, paraffin-embedded, canine gastrointestinal stromal tumors consisting of 14 leiomyomas (five stomach, three small intestine, two colon, four rectum), 18 leiomyosarcomas (one stomach, five small intestine, nine cecum, three rectum), two undifferentiated sarcomas (two stomach), and one neurofibrosarcoma (small intestine) were examined for the expression of vimentin, S-100 protein, α-smooth muscle actin, and desmin via immunoperoxidase methodology using an avidin-biotin complex technique. The leiomyomas were 4/14 (29%) vimentin-positive, 3/14 (21%) S-100 protein-positive, 10/14 (71%) α-smooth muscle actin-positive and 13/14 (93%) desmin-positive. Leiomyosarcomas were 18/18 (100%) vimentin-positive, 11/18 (61%) S-100 protein-positive, 9/18 (50%) α-smooth muscle actin-positive, and 15/18 (83%) desmin-positive. The undifferentiated sarcomas were 2/2 (100%) vimentin-positive, 2/2 (100%) S-100 protein-positive, 1/2 (50%) α-smooth muscle actin-positive, and 0/2 (0%) desmin-positive. The neurofibrosarcoma was vimentin and S-100 protein-positive and α-smooth muscle actin- and desmin-negative. Thirty-one of thirty-five (89%) of all neoplasms demonstrated reactivity for either desmin and/or α-smooth muscle actin. S-100 protein reactivity occurred in 17/35 (49%) of all specimens. Lack of desmin and α-smooth muscle actin reactivity occurred in 4/35 (11%) of all specimens, all of which were vimentin-positive. The immunohistochemical results indicate that the majority of canine gastrointestinal stromal tumors (GIST) with light microscopic features of smooth muscle cells have immunohistochemical staining patterns supporting smooth muscle differentiation. Vimentin reactivity correlated with a light microscopic diagnosis of malignancy. The lack of smooth muscle cell markers in some tumors and the high percentage of cases positive for S-100 protein may suggest a more complex histogenesis or differentiation for subgroups of these tumors.

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Study of gastrointestinal stromal tumors with c-kit immunostaining

Journal of Pathology of Nepal ◽

10.3126/jpn.v1i1.4450 ◽

1970 ◽

Vol 1 (1) ◽

pp. 41-44

Author(s):

B Sigdel ◽

S Vaidya ◽

Sabira KC

Keyword(s):

Small Intestine ◽

Gastrointestinal Tract ◽

High Power ◽

Gastrointestinal Stromal Tumors ◽

Cystic Degeneration ◽

Age Group ◽

Mesenchymal Tumors ◽

Stromal Tumors ◽

Study Results ◽

Microscopic Features

Background: Mutation of the C-KIT oncogene is the central event in gastrointestinal stromal tumors which are the most common mesenchymal tumors arising from the tubular gastrointestinal tract. Materials and Methods: A study was conducted in Patan hospital from April 2003 to May 2010. Mesenchymal tumors arising from the tubular gastrointestinal tract with the microscopic features suggesting gastrointestinal stromal tumor were included in the study. Results: A total of 22 cases were studied. The incidence was highest amongst the older age group (86.36%), than in younger people (13.63%). The tumor most commonly involved the small intestine (54.54%), followed by the stomach (36.36%). Most (59.09%) of the tumors were of huge size measuring >100 mm, and showed necrosis, hemorrhage and cystic degeneration. Mitotic activity was high (>5/50 high power fields) in 55% of the cases. Conclusion: C-KIT immunostaining showed positivity in 19 (86.36%) of the tumors in this study. Mutation of the C-KIT oncogene is seen in most of the gastrointestinal stromal tumors. Keywords: Gastrointestinal; Stromal tumors; C-KIT oncogene DOI: 10.3126/jpn.v1i1.4450 Journal of Pathology of Nepal (2011) Vol.1, 41-44

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A Clinical Analysis of Gastrointestinal Stromal Tumors in Small Intestine: Comparison of Bleeding and Non-bleeding Group

Intestinal Research ◽

10.5217/ir.2013.11.2.113 ◽

2013 ◽

Vol 11 (2) ◽

pp. 113 ◽

Cited By ~ 1

Author(s):

Sang Jin Lee ◽

Jong Kyu Park ◽

Hyun Il Seo ◽

Koon Hee Han ◽

Young Don Kim ◽

...

Keyword(s):

Small Intestine ◽

Gastrointestinal Stromal Tumors ◽

Clinical Analysis ◽

Stromal Tumors

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Efficacy of Long-Term Adjuvant Therapy With Imatinib Mesylate After Extensive Surgical Treatment for Ruptured Gastrointestinal Stromal Tumors of the Small Intestine With Peritoneal Metastases: A Case Report

Journal of Investigative Medicine High Impact Case Reports ◽

10.1177/2324709620970736 ◽

2020 ◽

Vol 8 ◽

pp. 232470962097073 ◽

Cited By ~ 1

Author(s):

Toshihisa Kimura ◽

Tamotsu Togawa ◽

Kenji Onishi ◽

Atsushi Iida ◽

Yasunori Sato ◽

...

Keyword(s):

Small Intestine ◽

Adjuvant Therapy ◽

Imatinib Mesylate ◽

Surgical Resection ◽

Gastrointestinal Stromal Tumors ◽

Peritoneal Metastases ◽

Metastatic Recurrence ◽

Stromal Tumors ◽

Dose Change

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract. Although most patients with advanced GISTs benefit from imatinib mesylate (IM) as standard targeted therapy, the optimal duration of adjuvant IM for GIST patients with high risk of recurrence who underwent surgical resection remains unknown. In this article, we present a case of a ruptured GIST of the small intestine accompanied by peritoneal metastases, which was effectively treated by surgical procedure followed by long-term adjuvant therapy with IM. Surgical resection was performed for the ruptured small intestinal GIST, and multitude of peritoneal metastases were cauterized. The patient received adjuvant therapy with IM (400 mg/day) for 12 years without an interruption or a dose change. Peritoneal metastatic recurrence was observed by the follow-up computed tomography scan obtained 12 years after surgery, and surgical resection of the recurrent GIST was performed. The molecular examination indicated a KIT exon 11 deletion mutation in both the primary GIST and recurrent GIST. An additional point mutation was observed in the recurrent GIST in exon 17 that caused resistance to IM. The present case might indicate that extensive removal of the tumor cells through surgery and long-term administration of IM without an interruption or a dose change were important for achieving improved recurrence-free survival in patients with ruptured GISTs of the small intestine with peritoneal metastases.

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Primary, resectable gastrointestinal stromal tumors (GISTs) originating from stomach and small intestine as different prognostically subtypes of disease

Journal of Clinical Oncology ◽

10.1200/jco.2008.26.15_suppl.10559 ◽

2008 ◽

Vol 26 (15_suppl) ◽

pp. 10559-10559

Author(s):

P. Rutkowski ◽

Z. I. Nowecki ◽

W. Michej ◽

J. A. Siedlecki ◽

W. Ruka

Keyword(s):

Small Intestine ◽

Gastrointestinal Stromal Tumors ◽

Stromal Tumors

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Prognostic significance of p53 protein overexpression in localized gastrointestinal stromal tumors of the small intestine.

Journal of Clinical Oncology ◽

10.1200/jco.2013.31.4_suppl.212 ◽

2013 ◽

Vol 31 (4_suppl) ◽

pp. 212-212

Author(s):

Young Soo Park ◽

Young Wha Kon ◽

Min-Hee Ryu ◽

Baek-Yeol Ryoo ◽

Hye Jin Park ◽

...

Keyword(s):

Small Intestine ◽

Prognostic Factor ◽

Gastrointestinal Stromal Tumors ◽

Prognostic Significance ◽

Risk Groups ◽

Risk Category ◽

Intermediate Risk ◽

P53 Overexpression ◽

Kit Mutation ◽

Stromal Tumors

212 Background: Mutation of c-kit is a relatively early event in the tumorigenesis of gastrointestinal stromal tumors (GISTs). p53 alteration has been suggested as an additional genetic change that affects patient outcome in some studies. However there has been few studies in GISTs of the small intestine. The aim of this study was to determine the prognostic significance of p53 alterations in localized GISTs of the small intestine. Methods: We retrospectively reviewed 113 patients with completely resected localized GISTs in the small intestine who were not treated with adjuvant imatinib between 1994 and 2008. Immunohistochemical staining of CD117, CD34, S-100, SMA and p53 were performed in all patients and mutational analyses of c-kit exons 9, 11, 13 and 17 were conducted in 81 (56.6%) patients. Results: The median follow-up after diagnosis was 84 months (range, 40-146 months). Overexpression of p53 were observed in 38 patients (33.6%). p53 overexpression was strongly correlated with high mitotic index (p = 0.01) and higher risk groups based on the National Institutes of Health’s (NIH) risk category (p = 0.019). On univariate analysis, patients with p53 overexpression showed worse recurrence-free survival (RFS, p = 0.003). c-kit mutation status was not a prognostic factor (p = 0.411). Multivariate analysis indicated that p53 overexpression remained as independent poor prognostic factors for RFS (hazard ratio = 2.66, p = 0.026) as well as tumor size and mitosis. The p53 overexpression was marginally associated with poor RFS in the low or intermediate risk groups according to NIH's risk category (p = 0.081). Conclusions: Our results suggest that the p53 overexpression is an independent prognostic factor for RFS in localized GISTs of the small intestine. Additionally, p53 overexpression could be a helpful marker for selecting patients for further treatment in low or intermediate risk group patients.

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