scholarly journals Clinical, pathological, radiological characteristics, risk stratification and immunohistochemistry profile of gastrointestinal stromal tumors treated in a tertiary cancer centre located in Sub-Himalayan region: institutional experience of 20 patients and review of literature

2021 ◽  
Vol 8 (8) ◽  
pp. 2414
Author(s):  
Jyoti Sharma ◽  
Anup Negi ◽  
Manish Gupta ◽  
Vikas Fotedar ◽  
Siddharth Vats ◽  
...  
Keyword(s):  
Side Effects ◽  
Risk Stratification ◽  
Gastrointestinal Stromal Tumors ◽  
Common Finding ◽  
Risk Category ◽  
Adjuvant Imatinib ◽  
Curative Surgery ◽  
Mesenchymal Tumors ◽  
Stromal Tumors ◽  
Pain Abdomen

GIST (gastrointestinal stromal tumors) are the rare mesenchymal tumors. Treatment includes curative surgery along with targeted agents like TKI in neoadjuvant/adjuvant settings. A total of 20 patients of histology proven GIST who were registered between 2014 to 2020 were reviewed for clinico-pathological data, endoscopic and radiological investigations, sites, primary treatment received, histology, immunohistochemistry, stage, risk stratification and imatinib therapy. GIST was more common in males than females. Age group varied between 25 years to 76 years. Majority of patients consumed non vegetarian diet, half of them being smokers and consumed alcohol. Pain abdomen, abdominal lump, dysphagia, haematemesis, melena and blood in stools were presenting complaints. CECT revealed heterogeneously enhancing mass with necrosis as most common finding. Upper GI endoscopy/colonoscopy revealed extrinsic bulge, polypoidal growth or ulcers as main findings. Stomach was the most common site followed by jejunum. Few patients presented with metastatic disease to liver and lungs. HPE revealed spindle cell GIST as main histology (with one patient with mixed spindle and epithelioid cells) with all patients having immunoreactivity to CD117. Majority of patients belonged to stage III and high-risk category by NIH stratification criteria. In majority of patients treatment received was surgery followed by adjuvant imatinib. Few patients had unresectable disease at presentation and received imatinib as upfront therapy. Imatinib was well tolerated in majority of patients. Few experienced manageable side effects like headache, irritability, leukopenia, pain abdomen, vomiting. Duration of treatment was one to three years. GIST is a rare tumor with varied presentations. Surgery is the mainstay of treatment offering chances of cure and revolutionary adjuvant imatinib is well tolerated with mild and manageable side effects in our centre. Being a resource limited centre, affordability for special investigations like IHC (immunohistochemistry) for CD117 (which helps in further confirmation of the diagnosis), remains a challenge for the patient and so does the 2nd line agent like sunitinib in case of recurrence.

Risk stratification of gastrointestinal stromal tumors by CtBP2 and CD44 analysis.

2018 ◽  
Vol 36 (4_suppl) ◽  
pp. 48-48
Author(s):  
Priya Gopie ◽  
Oana C. Rosca ◽  
Ayesha Chawla ◽  
Lin Mei ◽  
Jorge Almenara ◽  
...  
Keyword(s):  
Risk Stratification ◽  
Gastrointestinal Stromal Tumors ◽  
Medical Center ◽  
Armed Forces ◽  
Response To Therapy ◽  
Risk Category ◽  
Self Renewal ◽  
Stromal Tumors ◽  
Virginia Commonwealth University ◽  
Expression Score

48 Background: C-terminal binding protein 2 (CtBP2) is an oncogenic transcription factor that promotes cancer stem cell (CSC) growth and self-renewal, and controls pathways for tumor initiation, progression, and response to therapy. Expression of CtBP2 is linked to aggressive behavior in ovarian cancer, while genetic or pharmacologic targeting of CtBP2 disrupts CSC growth and self-renewal. CD44 is a cell surface marker that has been linked to CSC populations in many solid tumors, though data is conflicting on its role as tumor suppressor or oncogene. Gastrointestinal stromal tumors (GIST) is an increasingly common malignancy where risk stratification is essential for guiding post-surgical adjuvant therapy. We hypothesized that CtBP2 and CD44 staining would enhance risk stratification of GIST which currently relies on purely non-molecular clinicopathologic criteria. Methods: We identified 149 GIST cases from 1990 to 2016 in the Virginia Commonwealth University Medical Center pathology archive. Clinical data for 121 patients was available. The Armed Forces Institute of Pathology (AFIP) criteria (Miettinen's criteria) was used to risk stratify GISTs using the size, site, and mitotic index of the primary tumor. Immunohistochemistry for CtBP2 and CD44 was then performed on GIST samples with adequate tumor (86, CD44; 87, CtBP2). Stains were scored 0 (negative) to 3 (maximum) by two independent pathologists. Statistical analysis (χ2) correlating AFIP risk category with CD44 and CtBP2 staining was performed using PRISM6. Results: Moderate and high risk GISTs, based on AFIP criteria, significantly correlated with high CtBP2 expression (score = 3, p = 0.046) and low CD44 expression (score = 0-2, p = 0.034). Conclusions: CD44 and CtBP2 staining can be used to risk stratify GIST, and may enhance and complement current clinical risk stratification systems. Our data also suggests a potential tumor suppressive role of CD44 in GIST. Additionally, based on our findings, investigation of therapeutics that target CtBP2 in GISTs should be pursued.

Multislice imaging of gastrointestinal stromal tumors

2018 ◽  
pp. 3-14
Keyword(s):  
Computed Tomography ◽  
Key Words ◽  
Gold Standard ◽  
Gastrointestinal Stromal Tumors ◽  
Mesenchymal Tumors ◽  
Stromal Tumors ◽  
Preferential Localization ◽  
Multislice Imaging ◽  
Computed Tomography Diagnosis

Gastrointestinal stromal tumors (GIST) are the most common mesenchymal tumors of the digestive tract (1%). These tumors express the CD 117 in 95% of cases. The stomach is the preferential localization (70%). Diagnosis is difficult and sometimes late. Progress of imaging has greatly improved the management and the prognosis. Computed tomography (CT) is the gold standard for diagnosis, staging, and treatment follow-up. The increasing recognition of GIST’s histopathology and the prolonged survival revealed some suggestive imaging aspects. Key words: gastro-intestinal stromal tumors; computed tomography; diagnosis

scholarly journals Relationship between FDG uptake and the pathological risk category in gastrointestinal stromal tumors

2010 ◽  
Vol 57 (3,4) ◽  
pp. 270-274 ◽  
Author(s):  
Yoichi Otomi ◽  
Hideki Otsuka ◽  
Naomi Morita ◽  
Kaori Terazawa ◽  
Kaori Furutani ◽  
...  
Keyword(s):  
Gastrointestinal Stromal Tumors ◽  
Risk Category ◽  
Stromal Tumors ◽  
Fdg Uptake

scholarly journals Gastrointestinal Stromal Tumors (GISTs): Novel Therapeutic Strategies with Immunotherapy and Small Molecules

2021 ◽  
Vol 22 (2) ◽  
pp. 493
Author(s):  
Christos Vallilas ◽  
Panagiotis Sarantis ◽  
Anastasios Kyriazoglou ◽  
Evangelos Koustas ◽  
Stamatios Theocharis ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Gastrointestinal Stromal Tumors ◽  
Kinase Inhibitors ◽  
Checkpoint Inhibitors ◽  
Survival Rates ◽  
Cancer Therapeutics ◽  
Gastrointestinal Neoplasms ◽  
Mesenchymal Tumors ◽  
Stromal Tumors

Gastrointestinal stromal tumors (GISTs) are the most common types of malignant mesenchymal tumors in the gastrointestinal tract, with an estimated incidence of 1.5/100.000 per year and 1–2% of gastrointestinal neoplasms. About 75–80% of patients have mutations in the KIT gene in exons 9, 11, 13, 14, 17, and 5–10% of patients have mutations in the platelet-derived growth factor receptor a (PDGFRA) gene in exons 12, 14, 18. Moreover, 10–15% of patients have no mutations and are classified as wild type GIST. The treatment for metastatic or unresectable GISTs includes imatinib, sunitinib, and regorafenib. So far, GIST therapies have raised great expectations and offered patients a better quality of life, but increased pharmacological resistance to tyrosine kinase inhibitors is often observed. New treatment options have emerged, with ripretinib, avapritinib, and cabozantinib getting approvals for these tumors. Nowadays, immune checkpoint inhibitors form a new landscape in cancer therapeutics and have already shown remarkable responses in various tumors. Studies in melanoma, non-small-cell lung cancer, and renal cell carcinoma are very encouraging as these inhibitors have increased survival rates. The purpose of this review is to present alternative approaches for the treatment of the GIST patients, such as combinations of immunotherapy and novel inhibitors with traditional therapies (tyrosine kinase inhibitors).

scholarly journals Skeletal Muscle Metastasis of a GIST: A Case Report and Review of the Literature

2016 ◽  
Vol 2016 ◽  
pp. 1-5
Author(s):  
Olga D. Savvidou ◽  
George D. Chloros ◽  
Georgios D. Agrogiannis ◽  
Penelope Korkolopoulou ◽  
Georgios N. Panagopoulos ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Case Report ◽  
Soft Tissue ◽  
Gastrointestinal Stromal Tumors ◽  
Review Of The Literature ◽  
Soft Tissue Metastasis ◽  
Mesenchymal Tumors ◽  
Stromal Tumors ◽  
Skeletal Muscle Metastasis ◽  
Muscle Metastasis

Gastrointestinal stromal tumors (GISTs) are the most common malignant mesenchymal tumors of the gastrointestinal tract. The most common sites of metastasis are the liver and the peritoneum, whereas metastasis to soft tissue is rare. The authors present the case of a 78-year-old male with a soft tissue metastasis of a GIST and the current literature is reviewed.

Imatinib in the Management of Multiple Gastrointestinal Stromal Tumors Associated With a Germline KIT K642E Mutation

2007 ◽  
Vol 131 (9) ◽  
pp. 1393-1396
Author(s):  
Janet Graham ◽  
Maria Debiec-Rychter ◽  
Christopher L. Corless ◽  
Robin Reid ◽  
Rosemarie Davidson ◽  
...  
Keyword(s):  
Gastrointestinal Stromal Tumors ◽  
Interstitial Cells Of Cajal ◽  
Germline Mutations ◽  
Mesenchymal Tumors ◽  
Stromal Tumors ◽  
Pdgfra Gene ◽  
Oncogenic Mutations ◽  
Esophageal Tumors ◽  
Exon 11 ◽  
Cells Of Cajal

Abstract Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gut and are distinguished by expression of CD117 (c-Kit). Oncogenic mutations in the KIT or PDGFRA gene are detected in approximately 85% of sporadic GISTs. In recent years, examples of familial GIST have been reported in which germline mutations of KIT or PDGFRA result in multiple GISTs, skin disorders, and other abnormalities. The most common germline mutations are in KIT exon 11, mutations in exons 8 and 17 have also been described, and there are 2 families with germline PDGFRA mutations. We present a case in which a germline KIT exon 13 mutation (K642E) was discovered in a patient with multiple GISTs of rectum, small intestine, and esophagus, as well as diffuse hyperplasia of the interstitial cells of Cajal. To our knowledge, this is only the second germline example of this particular mutation. The patient's esophageal tumors were stabilized with imatinib.

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 Interobserver Variability of Mitotic Index and Utility of PHH3 for Risk Stratification in Gastrointestinal Stromal Tumors

2015 ◽  
Vol 143 (3) ◽  
pp. 385-392 ◽  
Author(s):  
Ahmad Alkhasawneh ◽  
John D. Reith ◽  
Tania Zuluaga Toro ◽  
Ayed O. Ayed ◽  
Xiaomin Lu ◽  
...  
Keyword(s):  
Risk Stratification ◽  
Mitotic Index ◽  
Gastrointestinal Stromal Tumors ◽  
Interobserver Variability ◽  
Stromal Tumors

scholarly journals The importance of molecular biology in development, prognosis, treatment and resistance to targeted therapy in gastrointestinal stromal tumors

2011 ◽  
pp. 69-79
Author(s):  
Alessandro Comandone ◽  
Elisa Berno ◽  
Simona Chiadò Cutin ◽  
Antonella Boglione
Keyword(s):  
Tyrosine Kinase ◽  
Gastrointestinal Stromal Tumors ◽  
Kinase Inhibitors ◽  
Growth Factor Receptor ◽  
Neoplastic Transformation ◽  
Response To Therapy ◽  
Mesenchymal Tumors ◽  
Kit Mutation ◽  
Stromal Tumors ◽  
Receive Treatment

Gastrointestinal stromal tumors (GISTs) are the commonest mesenchymal tumors of the gastroenteric tract, and are generally believed to originate from the neoplastic transformation of the interstitial cells of Cajal, the pacemaker structures of the stomach and intestine. Exon and genetic mutations (point/deletions) are fundamental for the development of GISTs: the constitutional characteristic of this neoplasm is the presence of the cell surface Kit receptor. Kit is the product of the proto-oncogene cKit, situated in chromosome 4. Ninety-eight percent of GISTs express mutated isoforms of Kit or of PDGFRA (Platelet growth factor receptor a). Kit mutation is the basic condition for autophosphorylation of tyrosine kinase residues in proteins. Autophosphorylation initiates pathogenetic processes in Cajal cells, toward a neoplastic transformation. Imatinib mesilate and, more recently, sunitinib are tyrosine kinase inhibitors, specific antagonists for Kit and PDGFRA, with good activity against GISTs. Most molecular and clinical data currently available concern imatinib. Exon mutations are strategic as prognostic and as predictive factors. In recent years, much evidence suggests that survival, response to therapy and resistance to imatinib are related to different mutations. In the near future, GIST patients will receive treatment differentiated by expressed Kit and PDGFRA mutations, thus truly individualized therapy.

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