Cases Of Gastrointestinal Stromal Tumors Research Articles

Expressions and clinical significance of CD133 and CD44 in gastrointestinal stromal tumors tissues

Objective To investigate the expressions of CD133 and CD44 and their prognostic significance in gastrointestinal stromal tumors (GIST). Methods Streptavidin perosidase (SP) method of immunohistochemistry was used to detect expressions of CD133 and CD44 proteins in 42 cases of GIST, and the relationship between their expressions and tumor size, mitotic count were analyzed by univariate and multivariate factor analyses. Results The expressions of CD133 and CD44 proteins in GIST were 21.4%(9/42)and 78.6% (33/42), respectively. The expressions of CD133 and CD44 proteins were significantly correlated with tumor size and mitotic count (P<0.05). Univariate factor analysis showed that the overall survival of GIST patients with positive CD133 protein (23.2 months) was shorter than that of patients with negative CD133 protein(63.1 months) (P<0.05). The overall survival of GIST patients with negative CD44 protein (23.2 months) was shorter than that of patients with positive CD44 protein(63.3 months)(P<0.05). Multivariate factor analysis showed that tumor size, mitotic count and CD44 protein were independent prognostic indicators for survival time after operation. Conclusions The positive expressions of CD133 and CD44 proteins might be the prognostic factors of GIST patients. Key words: Gastrointestinal stromal tumors/ME; Antigens, CD44/ME; Antigens, CD/ME; Prognosis

Somatic loss of function mutations in neurofibromin 1 and MYC associated factor X genes identified by exome-wide sequencing in a wild-type GIST case.

BackgroundApproximately 10–15 % of gastrointestinal stromal tumors (GISTs) lack gain of function mutations in the KIT and platelet-derived growth factor receptor alpha (PDGFRA) genes. An alternate mechanism of oncogenesis through loss of function of the succinate-dehydrogenase (SDH) enzyme complex has been identified for a subset of these “wild type” GISTs.MethodsPaired tumor and normal DNA from an SDH-intact wild-type GIST case was subjected to whole exome sequencing to identify the pathogenic mechanism(s) in this tumor. Selected findings were further investigated in panels of GIST tumors through Sanger DNA sequencing, quantitative real-time PCR, and immunohistochemical approaches.ResultsA hemizygous frameshift mutation (p.His2261Leufs*4), in the neurofibromin 1 (NF1) gene was identified in the patient’s GIST; however, no germline NF1 mutation was found. A somatic frameshift mutation (p.Lys54Argfs*31) in the MYC associated factor X (MAX) gene was also identified. Immunohistochemical analysis for MAX on a large panel of GISTs identified loss of MAX expression in the MAX-mutated GIST and in a subset of mainly KIT-mutated tumors.ConclusionThis study suggests that inactivating NF1 mutations outside the context of neurofibromatosis may be the oncogenic mechanism for a subset of sporadic GIST. In addition, loss of function mutation of the MAX gene was identified for the first time in GIST, and a broader role for MAX in GIST progression was suggested.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1872-y) contains supplementary material, which is available to authorized users.

Succinate dehydrogenase deficient gastrointestinal stromal tumor: a clinicopathologic analysis of eight cases

To study the clinicopathologic features, diagnosis and differential diagnosis of succinate dehydrogenase (SDH) deficient gastrointestinal stromal tumors (GISTs) as a unique tumor subtype. SDHB and SDHA immunohistochemistry was performed in 120 gastric GISTs, in addition to CD117, DOG-1, CD34, smooth muscle actin (SMA), desmin, S-100 protein, cytokeratin (CK) and Ki-67. Subset of the cases was further evaluated for the presence of mutations in CKIT exons 9, 11, 13 and 17 mutations and platelet derived growth factor receptor alpha(PDGFRA) exons 12 and 18. Eight of 120 (6.6%) GIST cases were found SDH-deficient including 3 male and 5 female patients (median age of 36.2 years; ranging 16 to 65 years of age). The tumors involved antrum (6 cases), lesser curvature (1 case) and fundus (1 case). Macroscopically, the dominant tumor masses varied from 3 to 10 cm in diameter with a multinodular or plexiform pattern involving the gastric wall. Microscopically,tumor cells had predominantly epithelioid morphology, with occasional mixed spindle cell nodules. Lymphovascular invasion was identified in 5 cases. Immunohistochemistry for SDHB was negative in all 8 cases, and SDHA was negative in 5 cases. All 8 SDHB negative cases also expressed CD117, DOG-1 and CD34, but were negative for SMA, desmin, S-100 and CK. All 8 cases were found to have wild-type CKIT and PDGFRA genes. Available clinical follow-up were obtained in 7 cases, ranging from 2 to 60 months (median follow-up 23.3 months), and all patient were alive. Three cases were found to have liver metastases at their first diagnosis, and one developed omental and mesenteric metastases in 17 months. SDH-deficient GIST is a distinct subtype of GIST, with a predilection to occur in young and female patients. Characteristic pathological findings include multinodular gastric wall involvement, epithelioid cell morphology, frequently lymphovascular invasion with occasional lymph node and liver metastases, but an overall indolent clinical behavior. Immunohistochemistry for SDHB is required for the diagnosis.

Extragastrointestinal Stromal Tumor of the Greater Omentum: A Case Report

Gastrointestinal stromal tumors (GISTs) are uncommon intra-abdominal tumors but they are the most common mesenchymal tumors of the gastrointestinal tract. We report a case of an extra-intestinal GIST (EGIST) located in the greater omentum of a 52 year-old male. Diagnosis is through immunohistochemical staining for CD 117 (c-KIT proto-oncogene product), CD 34, SMA, and DOG1. A small proportion of EGISTs originate in the omentum. There is limited data on the behavior of these EGISTs. A 52 year old African American male with a past medical history of type II diabetes mellitus, hypertension, rheumatoid arthritis, osteoarthritis, and fibromyalgia presented to the emergency department with a complaint of acute onset epigastric pain with radiation to RUQ of three days duration. A CT abdomen and pelvis showed a 3.7cm mass near the greater curvature of the stomach. An EGD was performed and the biopsies showed chronic active gastritis with positive immune-stain for H. pylori, but no mass was visualized. Outpatient endoscopic ultrasound (EUS) was later performed with fine needle aspiration positive for c-KIT, CD 34, and SMA making a diagnosis of EGIST. Subsequently, a sleeve gastrectomy was performed and histology confirmed the diagnosis of EGIST. Mutation analysis showed presence of c-KIT exon-11 and the patient was referred to oncology for imatinib therapy. GISTs are intra-abdominal tumors that are believed to originate in the gastrointestinal system's autonomic pacemaker cells, the interstitial cells of Cajal (ICC). Rarely, approximately 5-10 % of GISTs originate outside the gastrointestinal tract and are molecularly indistinguishable from GISTs; these tumors are known as EGISTs. A small proportion of EGISTs originate in the omentum expressing the KIT protein making them sensitive to tyrosine kinase inhibitor therapy. There is limited data on the behavior of these omental EGISTs. With EGISTs making up less than 10% of the GIST group, it has been challenging to obtain clear evidence on their behavior and even their incidence rates. Our search yielded a total of 79 cases of EGIST from 1997 to 2014. Out of the 79 cases found, 17 were located in the omentum, accounting for roughly 21.5% of the EGISTs reviewed. EGISTs are uncommon intra-abdominal tumors which account for less than 10% of GISTs. Of these, tumors originating in the greater omentum are rare. Grading systems have been suggested in order to estimate the aggressiveness of these tumors and to predict recurrence and prognosis. Surgical removal of these tumors is the treatment of choice for all resectable EGISTs, but the role of targeted therapeutic medical treatment is still unclear and requires further investigation.Figure 1Figure 2Figure 3

A Case of Rapidly Recurring GIST

Introduction: GIST (Gastrointestinal stromal tumor), a mesenchymal tumor originated from interstitial cells of cajal, a complex network of muscle layer of GI tract is largely treated with surgical resection and medically in current era of medicine. Recurrence is also reported in such tumors. We present a case of small intestinal GIST, treated with surgical resection followed by chemotherapy, found to have recurrence after 10 years even after stringent follow up. Case: A 79-year-old female presented with complaints of dyspnea and rectal bleeding. She had multiple episodes of watery diarrhea 2 days before admission, which subsided at the time of admission. She had history of small intestinal GIST, which was resected 10 years ago and was closely followed with yearly CT scan of abdomen for 8 years. Latest abdominal imaging (CT scan), 2 years ago was negative for recurrence. Since there was no recurrence for 8 years, plan was to do follow up imaging every 2 years. Two years after last CT, patient was admitted with rectal bleeding. CT abdomen revealed an18 cm heterogeneous abdominal mass involving the mesentery, parenchyma and surrounding tissue. At surgery, found to have 16cm intraabdominal tumor with necrosis involving the last 3 feet of an ileum, extensive adhesions and a tumor implant in transverse colon. The patient underwent exploratory laparotomy with resection of tumor, 3 feet of terminal ileum, transverse colon tumor resection and adhesiolysis. Tumor was confirmed as recurrent GIST with C-kit mutation and CD34 positive of spindle cell type. Tumor was graded as T4 N0 M0. Discussion: About 25 to 30% of GISTs originate from Jejunum and Ileum. Contrast enhanced CT abdomen & pelvis, every 3-6 months is imaging of choice post-treatment surveillance. It is unclear, for how long follow up imaging should be continued in chronic stable surgically treated patients. In this patient, increasing follow-up imaging interval resulted in a large recurrent GIST, even after 10 years of close follow up. Recurrence of GIST is not clear in sporadic or familial cases and further research is needed for long term follow up of treated GIST patients. Prognostic determinants include tumor size, location and mitotic rate. Tumor rupture (during surgery or spontaneously), though not included in TNM stating, is an independent risk factor that negatively impacts disease-free survival.Figure 1

Gastrointestinal stromal tumor revealing multiple endocrine neoplasia type 1

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumor of the gastrointestinal tract. The most common primary sites for GISTs are the stomach (60%) and the small intestine (30%). We reported one case of GIST revealing multiple endocrine neoplasia type 1 (MEN1). Case report A 59-year-old female admitted for prolonged fever with cutaneous lesions. The physical exam revealed epigastric pain. The abdominal ultrasonography showed two masses located in the left hypochondrium (intersplenorenal) and epigastric. The abdominal CT scan showed the masses in the splenic hilum and the small gastric curvature. The fine-needle aspiration biopsy concluded to a double location of a stromal tumor. Their immunohistochemical profile was KIT positive. The cuatneous lesions biopsy was inconclusive. The cervico-thoracic CT scan revealed two metastatic pulmonary nodules. Medical treatment using Imatinib (Glivec = 400 mg/d) was indicated. However, one year later the Glivec treatment does not result in complete response. Moreover, during the hospitalization, blood investigations revealed a severe hypercalcemia of 2,96 mmol/l. The diagnosis of primary hyperparathyroidism was confirmed with high level of parathyroid hormone (PTH = 217 pg/mL). The neck ultrasonography showed a parathyroid adenoma. A multiple endocrine neoplasia type 1 was suspected. The MRI concluded to a microadenoma (3 mm). The assessment of MEN1 gene mutation was not documented. Conclusion Our patient represents an undescribed combination of the GIST with MEN 1. Occurrence of GIST could be consistent with the possibility that this neoplasm arose by a mechanism related to the MEN1 gene.

Multimodality therapy of rectal gastrointestinal stromal tumors in the era of imatinib-an Indian series.

Primary objective was to determine if sphincter preservation is possible with the use of neoadjuvant imatinib in cases of rectal gastrointestinal stromal tumor (GIST). Secondary objectives were to determine clinicopathological characteristics and intermediate term oncological outcomes of the cases of rectal GIST. This is a retrospective review of 13 cases of GIST of the rectum diagnosed between January 1, 2010 and June 30, 2015 at Tata Memorial Centre, Mumbai, India. Clinical parameters that were assessed were duration of the neoadjuvant imatinib therapy, type of surgery performed as well as perioperative morbidity. Pathological parameters that were assessed included the size of the tumor, completeness of resection, mitotic count and mutational analysis. Of the 13 patients included, 11 were nonmetastatic at the time of presentation. All the patients received neoadjuvant imatinib in view of locally advanced nature of the tumors. Median distance from anal verge was 2 cm. Median duration of imatinib was 9 months. Of the 9 patients who underwent surgery, three had sphincter preserving surgery (33%) whereas the rest had abdomino-perineal resection. Two patients had perineal wound infections. All the operated patients received adjuvant imatinib therapy for 3 years. Median follow up period was 34 months. One patient developed distant metastasis; otherwise rest had no local or distant recurrence. In cases of rectal GIST, sphincter preservation may not be possible in spite of neoadjuvant therapy with imatinib.

ETV1 mRNA is specifically expressed in gastrointestinal stromal tumors.

Gastrointestinal stromal tumors (GISTs) develop from interstitial cells of Cajal (ICCs) mainly by activating mutations in the KIT or PDGFRA genes. Immunohistochemical analysis for KIT, DOG1, and PKC-θ is used for the diagnosis of GIST. Recently, ETV1 has been shown to be a lineage survival factor for ICCs and required for tumorigenesis of GIST. We investigated the diagnostic value of ETV1expression in GIST. On fresh-frozen tissue samples, RT-PCR analysis showed that ETV1 as well as KIT, DOG1, and PKC-θ are highly expressed in GISTs. On tissue microarrays containing 407 GISTs and 120 non-GIST mesenchymal tumors of GI tract, we performed RNA in situ hybridization (ISH) for ETV1 together with immunohistochemical analysis for KIT, DOG1, PKC-θ, CD133, and CD44. Overall, 387 (95 %) of GISTs were positive for ETV1, while KIT and DOG1 were positive in 381 (94 %) and 392 (96 %) cases, respectively, showing nearly identical overall sensitivity of ETV1, KIT, and DOG1 for GISTs. In addition, ETV1 expression was positively correlated with that of KIT. Notably, ETV1 was positive in 15 of 26 (58 %) KIT-negative GISTs and even positive in 2 cases of GIST negative for KIT and DOG1, whereas only 6 (5 %) non-GIST mesenchymal GI tumors expressed ETV1. We conclude that ETV1 is specifically expressed in the majority of GISTs, even in some KIT-negative cases, suggesting that ETV1 may be useful as ancillary marker in diagnostically difficult select cases of GIST.

Gastrointestinal Stromal Tumors: A Clinicopathologic and Risk Stratification Study of 255 Cases from Pakistan and Review of Literature.

To describe the clinicopathological features of gastrointestinal stromal tumors (GIST) diagnosed in our section and to perform risk stratification of our cases by assigning them to specific risk categories and groups for disease progression based on proposals by Fletcher et al and Miettinen and Lasota. We retrieved 255 cases of GIST diagnosed between 2003 and 2014. Over 59% were male. The age range was 16 to 83 years with a mean of 51 years. Over 70% occurred between 40 and 70 years of age. Average diameter of tumors was 10 cms. The stomach was the most common site accounting for about 40%. EGISTs constituted about 16%. On histologic examination, spindle cell morphology was seen in almost of 85% cases. CD117 was the most useful immunohistochemical antibody, positive in 98%. Risk stratification was possible for 220 cases. Based on Fletcher's consensus proposal, 62.3 gastric, 81.8% duodenal, 68% small intestinal, 72% colorectal and 89% EGISTs were assigned to the high risk category; while based on Miettinen and Lasota's algorithm, about 48% gastric, 100% duodenal, 76% small intestinal, 100% colorectal and 100% EGISTs in our study were associated with high risk for disease progression, tumor metastasis and tumor related death. Follow up was available in 95 patients; 26 were dead and 69 alive at follow up. Most of the patients who died had high risk disease and on average death occurred just a few months to a maximum of one to two years after initial surgical resection. Epidemiological and morphologic findings in our study were similar to international published data. The majority of cases in our study belonged to the high risk category.

Analysis of mutation of the c-Kit gene and PDGFRA in gastrointestinal stromal tumors.

The aim of the present study was to investigate mutation status of the c-Kit gene (KIT) and PDGFRA in patients with a gastrointestinal stromal tumor (GIST). In total, 93 patients with a GIST were included in the study, in which polymerase chain reaction amplification and gene sequencing were used to detect the sequences of exons 9, 11, 13 and 17 in KIT and exons 12 and 18 in PDGFRA. KIT mutations were detected in 64 cases (68.82%), of which exon 11 mutations were detected in 56 cases (60.22%), exon 13 mutations were detected in three cases (3.23%) and one case (1.08%) was shown to have a mutation in exon 17. The most common mutation in exon 11 was a deletion, which accounted for 55.36% (31/56) of the cases, followed by a point mutation observed in 26.79% (15/56) of the cases, while an insertion (tandem repeats) was identified in 14.29% (8/56) of the cases, and 3.57% (2/56) of the exon 11 mutations were deletions associated with a point mutation. The majority of the mutations were heterozygous, with only a few homozygous mutations. Mutational analysis revealed the mutations to be more concentrated in the classic hot zone at the 5'-end, followed by the tandem repeat frame at the 3'-end. In four cases, a mutation was detected in exon 18 of PDGFRA, of which one was associated with a mutation in KIT. The remaining three cases (10.34%, 3/29) were not associated with mutations in KIT and accounted for 37.5% (3/8) of the CD117-negative GIST cases. Therefore, the majority of the GIST cases were characterized by mutations in KIT or PDGFRA, which were directly associated with the disease. Pairs of different mutations in the same exon of KIT, or KIT mutations coupled with pairs of mutations in PDGFRA, were detected in a small number of patients. Imatinib is a small molecule tyrosine kinase inhibitor and is the first line targeted treatment for GIST, resulting in markedly improved survival rates. Thus, gene mutation genotyping may provide inspiration and guidance for imatinib-based targeted cancer therapy.

Prognostic angiogenic markers (endoglin, VEGF, CD31) and tumor cell proliferation (Ki67) for gastrointestinal stromal tumors.

To evaluate the correlation between the immunoexpression of angiogenic markers [CD31, CD105 and vascular endothelial growth factor (VEGF)], proliferative index (Ki67), and prognosis of patients with gastrointestinal stromal tumors (GIST). This is a retrospective study of 54 GIST cases. Medical records were searched to obtain the GIST patients' demographic and clinical data, and paraffin-embedded blocks of tumor samples were retrieved from the hospital archives to conduct a new immunohistochemical evaluation. The tumor samples of GIST patients were subject to immunohistochemical evaluation for endoglin (CD105), CD31, VEGF, and Ki67 expression. The CD105 and CD31 intratumoral microvascular density (IMVD) was measured using automated analysis. We determined the correlation between the immunoexpression of CD105, CD31, VEGF, Ki67 and prognosis. In addition, we conducted a cutoff analysis using the receiver-operating characteristic curve. VEGF positivity was classified as either null/weak or strong. Ki67 was evaluated using a cutoff of 5% positive cells. The prognosis was classified as good (patient alive without recurrence) or poor (patient with recurrence/death). The distribution of tumor sites among the 54 analyzed samples was as follows: 27 (50%) in the stomach, 20 (37.1%) in the small intestine, 6 (11.1%) in the colon, and 1 (1.8%) in the esophagus. The size of the tumors ranged from 2 to 33 cm (median: 8 cm); in 12 cases (22.2%), the tumor was below 5 cm at the largest diameter, but in 42 cases (77.7%), the tumor was larger than 5 cm. The means of CD105 and CD31 were significantly higher in the group with poor prognosis (P < 0.001). The cut-off values of CD105 (> 1.2%) and CD31 (> 2.5%) in the receiver-operating characteristic curve were related to a poorer prognosis. Cases with a better prognosis showed significantly null/weak staining for VEGF (P < 0.001). Ki-67 expression of ≥ 5% was strongly correlated with a worse prognosis (P < 0.001). In the multivariate analysis, CD105 was the variable that most strongly correlated with prognosis. The IMVD cutoff values for the angiogenic markers CD105 and CD31, may be prognostic factors for GIST, in addition to VEGF and Ki67.

Gastrointestinal stromal tumors during pregnancy: a systematic review of an uncommon but treatable malignancy.

Although modern social structure and medical advances have led to the increasing number of women childbearing in older age, cancer remains a rare diagnosis during pregnancy. There is little given information throughout the literature concerning gestation associated with the coexistence of gastrointestinal stromal tumor (GIST). In this review, we present 12 reported cases of GIST during pregnancy and we discuss the maternal and fetal outcome, as well as the therapeutic plan that was followed in each situation. From the collected data, 8 out of 12 cases had an uneventful outcome of their fetus. In 11 out of 12 cases surgical excision of the tumor was the treatment of choice, while seven women were treated with imatinib. Two of them were already on imatinib therapy during conception due to preexisting GIST diagnosis. Surgery remains the gold standard for the treatment of local or resectable GIST, while published data concerning the use of imatinib during pregnancy indicate that teratogenicity or fetal loss might be induced, especially if given during the first trimester of pregnancy. GIST during gestational period is a rare tumor in which a multidisciplinary approach should be designed, taking always into consideration that it has a favorable outcome on targeted treatment.

Successful treatment of gastrointestinal stromal tumor with multiple liver metastases with radiofrequency ablation and imatinib: A case report.

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumor of the gastrointestinal tract, and typically metastasize to the liver. In patients with recurrent metastatic GISTs, no single treatment is effective. The current study reports a case of GIST with 27 metastases in the liver, which was successfully treated using radiofrequency ablation (RFA) combined with surgical resection and imatinib therapy. The patient remains tumor-free 36 months after the first RFA treatment. This case suggests that comprehensive therapy including surgical resection, RFA and imatinib, may be an effective strategy for the treatment of GIST with multiple liver metastases.

Underreporting of Gastrointestinal Stromal Tumors: Is the True Incidence Being Captured?

BackgroundHospital cancer registries are only required to report gastrointestinal stromal tumors (GISTs) if labeled malignant or metastatic, leading to potential loss of cases in national cancer registries. Our objective was to determine whether GISTs are underreported in the US. MethodsRetrospective review of pathology reports between 2010 and 2013 with diagnosis of GIST was performed at two academic medical centers. Recurrent GISTs were excluded. Pathology reports were cross-referenced to cases reported by each cancer registry. Risk for metastasis/death was determined according to National Comprehensive Cancer Network (NCCN) guidelines. ResultsForty-nine cases of non-recurrent GIST were identified. Only 19/49 (38.8 %) cases were reported. None of the 30 non-reported cases were labeled malignant/metastatic on final pathology. To illustrate malignant potential, these tumors were risk stratified. Most (60 %) of the non-reported cases were low risk, but there were 4 (13.3 %) cases each in the intermediate, high, and unknown risk groups. Additionally, 7/30 (23.0 %) cases were treated with tyrosine kinase inhibitors, highlighting clinical concern of malignant GIST. ConclusionsOur results show that nearly two thirds of GIST cases have been underreported, suggesting that current reporting practices underestimate its true incidence. Revision of reporting guidelines may result in a more accurate estimation of the US disease burden of GIST.

Expression of L1 protein correlates with cluster of differentiation 24 and integrin β1 expression in gastrointestinal stromal tumors

The present study examined 66 cases of gastrointestinal stromal tumors (GISTs), 20 cases of smooth muscle tumors, 20 cases of schwannomas and 20 cases of normal gastric tissues in order to analyze the expression of L1, cluster of differentiation (CD)24 and integrin β1 by immunohistochemical staining. Patients were subjected to follow-up, and survival data were evaluated. L1 expression was detected in 57.6% of GIST cases; this was a significantly higher percentage compared with that found in the smooth muscle tumor cases or the normal control group. CD24 and integrin β1 were also expressed at significantly higher levels in the GIST cases than in the normal control group, although no significant difference was found in the expression levels of these proteins in smooth muscle tumor or schwannoma cases. These higher levels of L1 and integrin β1 expression were associated with an increased risk of invasive GIST, and were significantly positively correlated with Ki-67 expression. CD24 expression was not associated with the risk of GIST invasion or Ki-67 expression. There were positive correlations between L1, CD24 and integrin β1 expression; however, these had no significant association with patient survival. Therefore, L1 alone or in conjunction with CD24 (L1 + CD24), or integrin β1 (L1 + integrin β1) can be considered a valuable indicator for the differential diagnosis of GIST. Furthermore, L1 and integrin β1 can be used alone or in combination to evaluate the biological behavior of GISTs. Future studies are required to evaluate the prognostic value of these markers.

Suture granuloma: a rare differential diagnosis of residual/recurrent gastrointestinal stromal tumor of stomach

In the present era of modern surgical practice, the incidence of intra-abdominal suture granuloma is extremely rare with reduced use of non-absorbable silk sutures and even rarer following laparoscopic procedures. We report herein a case of silk granuloma presenting as large submucosal polypoidal lesion in a recently operated case of gastrointestinal stromal tumor (GIST) of stomach. Though endoscopic biopsy showed chronic non-specific gastritis with no evidence of malignancy, our patient underwent excision of lesion due to high likelihood of neoplastic lesion suggested by radiological evaluation and recent history of surgery for GIST but histopathology surprisingly showed Giant cell silk granuloma. In summary, the possibility of suture granulomas should always be considered while evaluating postoperative CT scan/PET scan for a mass lesion at operated site, particularly in patients who have undergone surgery with non-absorbable silk sutures.

Gastrointestinal stromal tumors

A case of gastrointestinal stromal tumors (GIST) in the Third Affiliated Hospital of Inner Mongolia Medical University was collected and analyzed on the basis of diagnosis, physical examination and treatment. Misdiagnosis of GIST is very common since it is a rare disease. So this paper aims to enhance the doctors’ awareness of GIST during clinical practice.

Bone metastasis of a gastrointestinal stromal tumor: A report of two cases.

Gastrointestinal stromal tumors (GISTs) are the most frequently diagnosed mesenchymal tumors of the GI tract. GISTs usually arise from the stomach, followed by the small intestine, rectum and other locations in the GI tract. The most common metastatic sites are the liver and peritoneum, whereas GISTs rarely metastasize to the bone. Although a small number of previous studies have described bone metastases originating from GISTs, the true prevalence is yet to be elucidated. The present study describes two cases of bone metastasis in patients with GISTs and reviews the relevant literature. Case one was of a 78-year-old male who presented with bone metastasis to the femoral neck five years after the resection of a GIST. The metastasis was completely resected and the patient remains alive nine years after the initial diagnosis of the GIST. Case 2 was of a 41-year-old male who presented with bone metastases to the ribs following resection of GISTs seven and 17 years earlier. The metastases were completely resected and the patient remains alive 17 years after the initial diagnosis. In total, only 10 cases of GISTs with metastases to the bone have been reported in the English literature. The possibility of bone metastases originating from a GIST should be considered during clinical follow-up, particularly in the presence of liver metastases. If feasible, bone metastases should be completely surgically excised.

Histopathological study using computer database of 10 000 consecutive gastric specimens: (2) malignant lesions.

Using a computer database, the author investigated the histopathology of 10 000 consecutive gastric specimens collected in the last 12 years 2002–2013 at his pathology laboratory in a relatively large hospital in Japan. Examination of histological sections was done when appropriate. The gastric specimens were made up of 8579 benign conditions and 1421 malignant lesions. The latter comprised gastric carcinoma in 1342 cases (94.4%), gastrointestinal stromal tumor (GIST) in 34 (2.4%), mucosal-associated lymphoid tissue (MALT) lymphoma in 25 (1.8%), non-Hodgkin's malignant lymphoma in 19 (1.3%), and metastatic carcinoma in 1 case (0.1%). Of the 1342 cases of gastric carcinoma, the histological type was as follows: tubular adenocarcinoma in 755 cases, papillary adenocarcinoma in 176, mucinous adenocarcinoma in 147, signet ring cell carcinoma in 145, poorly differentiated adenocarcinoma in 114, adenosquamous carcinoma in 4, and metastatic small cell carcinoma from the lung in 1. In surgically resected cases, the number of early gastric carcinomas was 258 and of advanced carcinoma, 521 cases. In GIST (n = 34), there were 2 cases of the epithelioid type and 32 of the spindle cell type. The size of GIST ranged from 1–15 cm, with a mean of 5.6 cm. KIT (CD117) was positive in 34/34 cases, CD34 in 31/34, desmin 2/34, and S100 4/34. A genetic analysis was performed in 6 cases of GIST, all of which showed point mutation of KIT and/or PDGFRA genes. In MALT lymphoma (n = 25), centrocyte-like cells and lymphoepithelial lesions were seen in every case. Helicobactor pylori infection was noted in 92%. In non-Hodgkin's lymphoma (n = 19), 17 cases were of diffuse large B-cell lymphoma, and 1 was peripheral T-cell lymphoma, while 1 was NK-cell lymphoma.

Survival trends in advanced gastrointestinal stromal tumor patients: A population-based study.

136 Background: In February 2002, imatinib was approved by US FDA for treatment of patients with advanced gastrointestinal stromal tumor (GIST). This study was performed to evaluate survival trends in patients with advanced GIST in pre- (1992-2001) and post- (2002-2008) imatinib era in the United States. Methods: We selected adult patients (≥18 years) with advanced GIST (regional and distant metastasis based on SEER’s LRD staging) from the Surveillance, Epidemiology, and End Results 18 database diagnosed during 1992-2008. We excluded patients diagnosed at autopsy or from death certificate only, or those without survival date. We analyzed 1- and 3- year relative survival (RS) rates of the patients by age (all ages,18-64yrs,64+yrs), race [White, Black and Others (American Indian/AK Native, Asian/Pacific Islander)], and gender in pre-imatinib (1992-2001) and post-imatinib (2002-2008) eras. We used Z-test in SEER*Stat to compare RS rates. Results: There were total of 1,734 cases of advanced GIST (regional and distant metastasis) during the study duration. Of the total population, 744 were females and 990 were males. The 1- and 3- year RS rates were significantly higher for patients diagnosed in post-imatinib era compared to those in pre-imatinib era (83.8±1.1% vs 72.5±2.3%; Z 4.47 at one year and 68.8±1.4% vs 51.0± 2.6%; Z 6.25). The survival rates in younger patients (18-64 years) improved significantly in post-imatinib era compared to pre-imatinib era (88.60±1.2% vs 74.20±2.9%; Z 5.19 at 1 year and 75±1.6% vs 56.1±3.4%; Z 5.81 at 3 years). Among older patients, there was improvement in 3- year survival rate (76.90±2% vs 70.40±3.5%; Z 1.22 at 1 year and 59.80±2.5% vs 44.9±4%; Z 2.82 at 3 years). Survival rates improved for both sexes and for Whites and Blacks (1 year RS: 83.80±1.3% vs 73.40±vs2.6%; Z 3.45 for Whites and 85±2.4% vs 68.80±6%; Z 2.53 for Blacks; 3 year RS: 68.60±1.7% vs 51.20±3.1%; Z 5.02 for Whites and 69.10±3.3% vs 42.6±6.6%; Z 3.76 for Blacks). There was no improvement in survival rates for Others. Conclusions: Overall, survival rates of advanced GIST patients have improved significantly in post-imatinib era compared to pre-imatinib era. There was no improvement in survival rates of Others.