scholarly journals Gastrointestinal stromal tumors - definition, clinical, histological, immunohistochemical, and molecular genetic features and differential diagnosis

2001 ◽  
Vol 438 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Markku Miettinen ◽  
Jerzy Lasota
Keyword(s):  
Differential Diagnosis ◽  
Gastrointestinal Stromal Tumors ◽  
Molecular Genetic ◽  
Stromal Tumors ◽  
Genetic Features

scholarly journals Gastrointestinal stromal tumors (gists): Definition, clinical, histological, immunohistochemical and molecular genetic features and predictors of malignant potential and differential diagnosis

2002 ◽  
Vol 10 (4) ◽  
pp. 267-271 ◽  
Author(s):  
Vesna Zivkovic ◽  
Vuka Katic ◽  
Aleksandar Nagorni ◽  
Ljubinka Velickovic ◽  
Maja Milentijevic ◽  
...  
Keyword(s):  
Gastrointestinal Stromal Tumors ◽  
Molecular Genetic ◽  
Malignant Potential ◽  
Gi Tract ◽  
Mesenchymal Tumors ◽  
Stromal Tumors ◽  
Cellular Origin ◽  
Genetic Features ◽  
Exon 11 ◽  
Malignant Gists

Gastrointestinal stromal tumors (GISTs) represent a distinct and the most important subset of mesenchymal tumors of the gastrointestinal (GI) tract GISTs occur throughout the GI tract but are usually located in the stomach and small intestine. The cellular origin, differentiation, nomenclature and prognosis of GISTs are controversial. Because GISTs, like the interstitial cells of Cajal, the GI pacemaker cells, express CD117 (c-kit protein), the origin of GISTs from the Cajal cells has recently been suggested. GISTs are also known for their wide variability in clinical behavior and for the difficulty to determine their malignant condition The most reproducible predictors of malignancy are mitotic count >1-5 per10 high-powered fields (HPF), size >5 cm, tumor necrosis, infiltration and metastasis to other sites. However, some tumors with mitotic activity <1/10 HPF may metastasize indicating some uncertainty in malignant potential of GISTs, especially those larger than 5 cm. Recently, mutations in c-kit gene (exon 11) preferentially occur in malignant GISTs and may be a clinically useful adjunct marker in evaluation of GISTs. In conclusion, the strong CD117 expression mostly defines primary GI mesenchymal tumors as GIST. Specific identification of GIST may become clinically important if therapies targeting the c-kit tyrosine kinase activation become available.

scholarly journals Gastric schwannoma: a benign tumor often misdiagnosed as gastrointestinal stromal tumor

2015 ◽  
Vol 5 (3) ◽  
Author(s):  
Apurva S. Shah ◽  
Pravin M. Rathi ◽  
Vaibhav S. Somani ◽  
Astha M. Mulani
Keyword(s):  
Differential Diagnosis ◽  
Gastrointestinal Stromal Tumor ◽  
Gastrointestinal Stromal Tumors ◽  
Rare Case ◽  
Benign Tumor ◽  
Stromal Tumor ◽  
Mesenchymal Tumors ◽  
Stromal Tumors ◽  
Gastric Schwannoma ◽  
Gastric Mass

Gastric schwannomas are rare mesenchymal tumors that arise from the nerve plexus of gut wall. They present with nonspecific symptoms and are often detected incidentally. Preoperative investigation is not pathognomic and many are therefore misdiagnosed as gastrointestinal stromal tumors. We report a rare case of a 37-year old woman who underwent laparotomy for complex bilateral ovarian cyst with resection of gastric-gastrointestinal stromal tumor preoperatively, but confirmed to have a gastric schwannomas postoperatively. This case underscores the differential diagnosis of submucosal, exophytic gastric mass as schwannoma.

scholarly journals Immunohistochemical features of gastrointestinal stromal tumors and their role for differential diagnosis and prognosis

2021 ◽  
pp. 10-16
Author(s):  
Yana Miroshnichenko
Keyword(s):  
Differential Diagnosis ◽  
Tumor Cells ◽  
Gastrointestinal Stromal Tumors ◽  
Spindle Cell ◽  
Prognostic Markers ◽  
Mitotic Rate ◽  
Mesenchymal Tumors ◽  
Ki 67 ◽  
Stromal Tumors ◽  
Strong Expression

The aim. To clarify all most important immunohistochemical features of gastrointestinal stromal tumors with different histological patterns and analyze the role of expression of Ki-67, MMP-9, VEGF and p16ink4A as a predictive markers of tumor progression. Materials and methods. The study is based on analysis of 100 primary GISTs for description of their morphological features and 36 GISTs taken from this 100 for study of prognostic markers. Results. All spindle cell GISTs have shown diffuse expression of CD117 in tumor cells. The levels of CD117 expression varied from strong expression (3+) until mild expression (1+). Strong expression were seen in 75,8 % of spindle cell GISTs. Epithelioid GISTs demonstrated heterognous moderate or mild expression of CD117. All primary epithelioid GISTs from patients that had relapse of tumor in period from 1 till 3 years demonstrated focal mild expression of CD 117 in tumor cells. Expression of DOG-1 were seen in all 100 cases of GISTs, that were included in our study. The strong expression of DOG-1 (3+) were seen in all 45 GISTs that had low mitotic rate (≤5 mitoses per 50HPF) and not associated with their histological pattern. GISTs with high mitotic rate demonstrated heterogeneous expression of DOG-1 in tumors: moderate expression (2+) with patchy areas of strong expression (3+). Expression of CD56 was not found in spindle cell GISTs, but single tumor cells of epithelioid GISTs that had high mitotic rate demonstrated expression of this marker. The average expression of p16ink4A were higher in tumors that gave relapses compared with tumors without relapses (50,3 % versus 5,7 % respectively, U-test=16.5; p≤0,01).The average expression of MMP-9 also were significantly higher in GISTs that gave relapses: 63,2 % compared with 13,4 % in GISTs without relapse (U-test=16; p≤0 ,01).The strong VEGF expression was found in 66,7 % of GISTs that had relapses and only in 8,3 % of GISTs without relapses. 50 % of GISTs without relapses was negative for VEGF. Finally, the average expression of Ki-67 were 13,4 % in GISTs with relapses and 8,7 % in GISTs without them (U-test=16; p≤0,01). Conclusion. We highly recommend using DOG-1 for epithelioid GISTs. Additionally in epithelioid GISTs can be used CD56 that can give focal positive reaction in some tumour cells. The following minimal panel of markers for differential diagnosis of spindled GISTs from other mesenchymal tumors of gastrointestinal tract is proposed: CD117, DOG-1 and SMA, where the first too markers will demonstrated the moderate or strong diffuse expression and SMA can be occasionally positive in some tumor cells. p16ink4A, ki-67, VEGF and MMP-9 can be used as additional prognostic markers in GISTs.

MOLECULAR AND GENETIC FEATURES OF GASTROINTESTINAL STROMAL TUMORS

2019 ◽  
Vol 65 (1) ◽  
pp. 69-76
Author(s):  
Foat Akhmetzyanov ◽  
Sergey Petrov ◽  
Dinar Khalikov
Keyword(s):  
Tyrosine Kinases ◽  
Gastrointestinal Stromal Tumors ◽  
Mutational Analysis ◽  
Scientific Information ◽  
Prognostic Significance ◽  
Driver Mutations ◽  
Stromal Tumors ◽  
Activating Mutations ◽  
Genetic Features ◽  
Cells Of Cajal

In this review presented the most relevant scientific information on the molecular and genetic features of gastrointestinal stromal tumors (GISTs). GISTs is a heterogeneous group of mesenchymal neoplasms of the gastrointestinal tract, which according to modern ideas originate from the interstitial cells of Cajal. It was found that this disease is largely somatic mutations: in the overwhelming majority of cases, activating mutations in kit or PDGFRA genes that encode effector tyrosine kinases are found in tumor cells. Constitutive activation of these enzymes triggers a complex cascade of intracellular reactions, the result of which is the enhancement of cell proliferation and tumor growth. In the absence of the above-mentioned driver mutations, the GISTs is referred to as a “wild type”. The profile of mutations affects the aggressiveness of the GISTs flow and the sensitivity to target antitumor drugs. Thus, carrying out a mutational analysis in the case of a GISTs is of great prognostic significance.

CURRENT UNDERSTANDING OF THE MOLECULAR MECHANISMS IN ONCOGENESIS OF GASTROINTESTINAL STROMAL TUMORS

2020 ◽  
Vol 66 (1) ◽  
pp. 13-22
Author(s):  
Dmitriy Gvaldin ◽  
Yekaterina Omelchuk ◽  
Natalya Timoshkina ◽  
Vladimir Trifanov ◽  
Yuriy Sidorenko
Keyword(s):  
Gastrointestinal Stromal Tumors ◽  
Molecular Mechanisms ◽  
Molecular Genetic ◽  
Current Understanding ◽  
Dna Hypomethylation ◽  
Stromal Tumors ◽  
Activating Mutations ◽  
New Therapeutic Approaches ◽  
Risk Of Progression ◽  
Cpg Hypermethylation

The association of genetic driver changes in gastrointestinal stromal tumors (GIST) with clinical implications is the most studied aspect in all solid tumors. Genotyping of particular exons c-KIT and PDGFRA included in the standard practice of diagnosis and treatment of GIST. The review analyzes the current understanding of the molecular-genetic mechanisms and markers that underlie the GIST profiling. Of particular interest are wild-type tumors of c-KIT and PDGFRA, in which activating mutations of the RAS, BRAF and EGFR oncogenes are found, associated with the early stages of disease progression. The data of studies of genetic and epigenetic changes in GIST, which revealed the prognostic value of inactivation of CDKN2A and p53, deletions of 22q, 1p and 15q, CpG hypermethylation are presented. New factors that determine a high risk of progression of GISTs are described: inactivation of dystrophin, DNA hypomethylation, increased expression of miRNAs and HOTAIR. The progress achieved in understanding the molecular mechanisms of GISTs give the opportunity of developing and effectively applying new therapeutic approaches, expanding the range of molecular genetic markers that determine patient surveillance.

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