scholarly journals Review of Management of Gastrointestinal Stromal Tumor in Low-Resource Centers

2021 ◽  
Vol 2 (6) ◽  
pp. 5-9
Author(s):  
Seke Manase Ephraim Kazuma ◽  
Bright Chirengendure ◽  
Patrick Musonda ◽  
Joseph Musowoya ◽  
Royd Ngoma ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Tyrosine Kinase ◽  
Interstitial Cells Of Cajal ◽  
Kinase Inhibitors ◽  
Standard Treatment ◽  
Abdominal Mass ◽  
Tyrosine Kinase Receptor ◽  
Mesenchymal Tumors ◽  
Tumor Reduction ◽  
Cells Of Cajal

Gastrointestinal stromal tumors (GIST) account for 1% to 3% of gastrointestinal tract tumors and are the most common of the mesenchymal tumors. Carcinogenesis of GIST arises in the interstitial cells of Cajal (ICC) and in the myenteric plexus of the gastrointestinal tract due to a mutation of the kinase receptor (KIT, also known as CD117) and the platelet-derived growth factor A (PDGFA) gene leading to activation of the tyrosine kinase receptor. The exact incidence and prevalence of GIST is not known. Symptoms of GIST are non-specific; they present with GI bleeding due to ulceration (50%), abdominal pain (20% to 50%), dysphagia (esophageal GIST) and GI obstruction (10% to 30%) (7,10). Signs include abdominal mass and fullness. A computerized tomographic (CT) scan is the preferred imaging to evaluate GIST. Diagnosis is confirmed by immunohistochemical (IHC) staining a of biopsy sample for medical treatment tyrosine kinase inhibitors (TKI). Surgical resection with negative microscopic margins is the gold standard treatment of GIST. TKI are required for tumor reduction to increase chances of respectability (neoadjuvant therapy) or to prevent recurrence and reduce the progression of advanced, resectable GIST.

Impaired development of interstitial cells and intestinal electrical rhythmicity in steel mutants

1995 ◽  
Vol 269 (6) ◽  
pp. C1577-C1585 ◽  
Author(s):  
S. M. Ward ◽  
A. J. Burns ◽  
S. Torihashi ◽  
S. C. Harney ◽  
K. M. Sanders
Keyword(s):  
Small Intestine ◽  
Gastrointestinal Tract ◽  
Tyrosine Kinase ◽  
Myenteric Plexus ◽  
Interstitial Cells Of Cajal ◽  
Interstitial Cells ◽  
Slow Waves ◽  
Tyrosine Kinase Receptor ◽  
Steel Factor ◽  
Cells Of Cajal

Electrical rhythmicity in the gastrointestinal tract may originate in interstitial cells of Cajal (IC). Development of IC in the small intestine is linked to signaling via the tyrosine kinase receptor, c-kit. IC express c-kit protein, and disruption of c-kit signaling causes breakdown in IC networks and loss of slow waves. We tested whether mutations in steel factor, the ligand for c-kit, affect the development of IC networks. IC were found in the region of the myenteric plexus (IC-MY) in mice with steel mutations (i.e., Sl/Sld) at 5-10 days postpartum, but these cells formed an abnormal network. IC-MY were not observed in adult Sl/Sld animals. IC in the deep muscular plexus (IC-DMP) appeared normal in Sl/Sld animals. Electrical slow waves, normally present in the small intestine, were absent in Sl/Sld animals (10-30 days postpartum). Neural inputs were intact in Sl/Sld animals. Steel factor appears important for the development of certain classes of IC, and IC-MY appear to be involved in the generation of electrical rhythmicity in the small intestine.

Large Omental Metastases of a Gastrointestinal Stromal Tumor

Medicina ◽  
2011 ◽  
Vol 47 (11) ◽  
pp. 86
Author(s):  
Povilas Ignatavičius ◽  
Tomas Petraitis ◽  
Žilvinas Saladžinskas ◽  
Lilija Butkevičienė ◽  
Kristina Žvinienė
Keyword(s):  
Case Report ◽  
Gastrointestinal Tract ◽  
Gastrointestinal Stromal Tumor ◽  
Gastrointestinal Stromal Tumors ◽  
Interstitial Cells Of Cajal ◽  
Metastatic Tumor ◽  
Stromal Tumor ◽  
Mesenchymal Tumors ◽  
Stromal Tumors ◽  
Cells Of Cajal

Gastrointestinal stromal tumors are rare tumors, originating from the interstitial cells of Cajal. They are the most common mesenchymal tumors of the gastrointestinal tract. Metastatic tumor is treated with imatinib mesylate. A case of large metastases of a gastrointestinal stromal tumor to the omentum, diagnosis and treatment principles are presented in this case report.

scholarly journals Gastrointestinal Stromal Tumors of Small Intestine

2019 ◽  
Vol 05 (03) ◽  
pp. e92-e95 ◽  
Author(s):  
Tanweerul Huda ◽  
Mahendra Pratap Singh
Keyword(s):  
Gastrointestinal Tract ◽  
Interstitial Cells Of Cajal ◽  
Surgical Excision ◽  
Biological Behavior ◽  
Pacemaker Cells ◽  
Mesenchymal Tumors ◽  
Stromal Tumors ◽  
Cells Of Cajal ◽  
Oncogene Protein

AbstractGastrointestinal stromal tumor (GIST) is defined as mesenchymal tumors of the gastrointestinal tract expressing proto-oncogene protein CD117. They are the most common sarcomatous tumors of the gastrointestinal tract. GISTs are presumed to arise from interstitial cells of Cajal or gastrointestinal pacemaker cells which control gut motility. They have unpredictable biological behavior. Prognosis is dependent on tumor size as well as mitotic count. Radical surgical excision is the treatment of choice. They rarely metastasize to lymph nodes. Imatinib therapy is used as an adjuvant therapy. The follow-up of patients postsurgery is not standardized.

scholarly journals Gastrointestinal Stromal Tumors Etiology, Clinical Presentation And Review Of The Literature In Greek Patients

2020 ◽  
Vol 3 (3) ◽  
pp. 01-03
Author(s):  
Panagiota Xaplanteri
Keyword(s):  
Tyrosine Kinase ◽  
Gastrointestinal Stromal Tumors ◽  
Kinase Inhibitors ◽  
Complete Removal ◽  
Patient Treatment ◽  
Tyrosine Kinase Receptor ◽  
Stromal Tumors ◽  
The One ◽  
Nih Classification ◽  
Cells Of Cajal

Gastrointestinal stromal tumors (GIST) represent rare malignancies of mesenchymal origin that can appear at any site of the gastrointestinal tract. Their classification, patient treatment and prognosis had been a source of controversy. The biology of these tumors revealed association to the type III tyrosine kinase receptor and the KIT CD117 protein expression. GIST mesenchymal lesions derive from the interstitial cells of Cajal. Classification methods include the one by Miettinen and Lasota and the ‘‘modified NIH classification’’. The treatment of choice is surgical intervention and complete removal of the neoplasm. In patients with tumors that cannot be excised, have given metastasis, or are of high risk for metastasis, treatment also involves Kit/PDGFRA tyrosine kinase inhibitors, such as imatinib. In Greece, several cases have been described.

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).

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.

CD34 immunoreactivity and interstitial cells of Cajal in the human and mouse gastrointestinal tract

2000 ◽  
Vol 302 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Jean-Marie Vanderwinden ◽  
Jüri J. Rumessen ◽  
Marc-Henri De Laet ◽  
Jean-Jacques Vanderhaeghen ◽  
Serge N. Schiffmann
Keyword(s):  
Gastrointestinal Tract ◽  
Interstitial Cells Of Cajal ◽  
Interstitial Cells ◽  
Cells Of Cajal ◽  
Human And Mouse

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.

scholarly journals Immunization against ROS1 by DNA Electroporation Impairs K-Ras-Driven Lung Adenocarcinomas

Vaccines ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 166
Author(s):  
Federica Riccardo ◽  
Giuseppina Barutello ◽  
Angela Petito ◽  
Lidia Tarone ◽  
Laura Conti ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Cell Line ◽  
Kinase Inhibitors ◽  
Immune Memory ◽  
Tyrosine Kinase Receptor ◽  
Preclinical Model ◽  
Primary Tumors ◽  
Improve Patient Survival ◽  
Transplantable Cell ◽  
Lung Adenocarcinomas

Non-small cell lung cancer (NSCLC) is still the leading cause of cancer death worldwide. Despite the introduction of tyrosine kinase inhibitors and immunotherapeutic approaches, there is still an urgent need for novel strategies to improve patient survival. ROS1, a tyrosine kinase receptor endowed with oncoantigen features, is activated by chromosomal rearrangement or overexpression in NSCLC and in several tumor histotypes. In this work, we have exploited transgenic mice harboring the activated K-Ras oncogene (K-RasG12D) that spontaneously develop metastatic NSCLC as a preclinical model to test the efficacy of ROS1 immune targeting. Indeed, qPCR and immunohistochemical analyses revealed ROS1 overexpression in the autochthonous primary tumors and extrathoracic metastases developed by K-RasG12D mice and in a derived transplantable cell line. As proof of concept, we have evaluated the effects of the intramuscular electroporation (electrovaccination) of plasmids coding for mouse- and human-ROS1 on the progression of these NSCLC models. A significant increase in survival was observed in ROS1-electrovaccinated mice challenged with the transplantable cell line. It is worth noting that tumors were completely rejected, and immune memory was achieved, albeit only in a few mice. Most importantly, ROS1 electrovaccination was also found to be effective in slowing the development of autochthonous NSCLC in K-RasG12D mice.

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