Gastrointestinal stromal tumors (GISTs): Focus on histopathological diagnosis and biomolecular features

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Abstract

Gastrointestinal stromal tumors (GISTs) are mesenchymal tumors of the gastrointestinal tract that are believed to originate from a neoplastic transformation of the intestinal pacemaker cells (interstitial cells of Cajal) normally found in the bowel wall or their precursors. Although the microscopic features have been known for a long time, the defining characteristic of GIST is the presence of the cell-surface antigen CD117 (KIT), which is demonstrated by immunohistochemistry. KIT, which is a growth factor transmembrane receptor, is the product of the proto-oncogene c-kit (chromosome 4). Surgical removal remains the only curative treatment for patients with GISTs. Tumor size, mitotic index, anatomic location, tumor rupture and disease-free interval are the classic characteristics used to predict the clinical course of patients who undergo complete gross resection. Most GISTs express constitutively activated mutant isoforms of KIT or kinase platelet-derived growth factor receptor alpha (PDGFRA) that are potential therapeutic targets for imatinib mesylate. Imatinib mesylate is a rationally designed, molecularly specific oral anticancer agent that selectively inhibits several protein tyrosine kinases central to the pathogenesis of human cancer and which has demonstrated remarkable clinical efficacy in patients with chronic myeloid leukemia and malignant GISTs. More recently Sunitinib, a new KIT/PDGFRA kinase inhibitor, has been tested in patients with GIST resistant to imatinib, with promising results. © 2007 European Society for Medical Oncology.
Lingua originaleEnglish
pagine (da-a)vi136-vi140
Numero di pagine5
RivistaAnnals of Oncology
Volume18
Stato di pubblicazionePublished - 2007

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Gastrointestinal Stromal Tumors
Platelet-Derived Growth Factor alpha Receptor
Neoplasms
Phosphotransferases
Interstitial Cells of Cajal
Chromosomes, Human, Pair 4
Mitotic Index
Growth Factor Receptors
Proto-Oncogenes
Surface Antigens
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Antineoplastic Agents
Protein-Tyrosine Kinases
Gastrointestinal Tract
Rupture
Protein Isoforms
Immunohistochemistry
Therapeutics
Imatinib Mesylate

All Science Journal Classification (ASJC) codes

  • Hematology
  • Oncology

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title = "Gastrointestinal stromal tumors (GISTs): Focus on histopathological diagnosis and biomolecular features",
abstract = "Gastrointestinal stromal tumors (GISTs) are mesenchymal tumors of the gastrointestinal tract that are believed to originate from a neoplastic transformation of the intestinal pacemaker cells (interstitial cells of Cajal) normally found in the bowel wall or their precursors. Although the microscopic features have been known for a long time, the defining characteristic of GIST is the presence of the cell-surface antigen CD117 (KIT), which is demonstrated by immunohistochemistry. KIT, which is a growth factor transmembrane receptor, is the product of the proto-oncogene c-kit (chromosome 4). Surgical removal remains the only curative treatment for patients with GISTs. Tumor size, mitotic index, anatomic location, tumor rupture and disease-free interval are the classic characteristics used to predict the clinical course of patients who undergo complete gross resection. Most GISTs express constitutively activated mutant isoforms of KIT or kinase platelet-derived growth factor receptor alpha (PDGFRA) that are potential therapeutic targets for imatinib mesylate. Imatinib mesylate is a rationally designed, molecularly specific oral anticancer agent that selectively inhibits several protein tyrosine kinases central to the pathogenesis of human cancer and which has demonstrated remarkable clinical efficacy in patients with chronic myeloid leukemia and malignant GISTs. More recently Sunitinib, a new KIT/PDGFRA kinase inhibitor, has been tested in patients with GIST resistant to imatinib, with promising results. {\circledC} 2007 European Society for Medical Oncology.",
author = "Nicolo' Gebbia and Antonio Russo and Gianni Pantuso and Luigi Sandonato and Vito Rodolico and Giuseppe Cicero and Giuseppe Badalamenti and Fabio Fulfaro and Chiara Intrivici and Lorena Incorvaia",
year = "2007",
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journal = "Annals of Oncology",
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TY - JOUR

T1 - Gastrointestinal stromal tumors (GISTs): Focus on histopathological diagnosis and biomolecular features

AU - Gebbia, Nicolo'

AU - Russo, Antonio

AU - Pantuso, Gianni

AU - Sandonato, Luigi

AU - Rodolico, Vito

AU - Cicero, Giuseppe

AU - Badalamenti, Giuseppe

AU - Fulfaro, Fabio

AU - Intrivici, Chiara

AU - Incorvaia, Lorena

PY - 2007

Y1 - 2007

N2 - Gastrointestinal stromal tumors (GISTs) are mesenchymal tumors of the gastrointestinal tract that are believed to originate from a neoplastic transformation of the intestinal pacemaker cells (interstitial cells of Cajal) normally found in the bowel wall or their precursors. Although the microscopic features have been known for a long time, the defining characteristic of GIST is the presence of the cell-surface antigen CD117 (KIT), which is demonstrated by immunohistochemistry. KIT, which is a growth factor transmembrane receptor, is the product of the proto-oncogene c-kit (chromosome 4). Surgical removal remains the only curative treatment for patients with GISTs. Tumor size, mitotic index, anatomic location, tumor rupture and disease-free interval are the classic characteristics used to predict the clinical course of patients who undergo complete gross resection. Most GISTs express constitutively activated mutant isoforms of KIT or kinase platelet-derived growth factor receptor alpha (PDGFRA) that are potential therapeutic targets for imatinib mesylate. Imatinib mesylate is a rationally designed, molecularly specific oral anticancer agent that selectively inhibits several protein tyrosine kinases central to the pathogenesis of human cancer and which has demonstrated remarkable clinical efficacy in patients with chronic myeloid leukemia and malignant GISTs. More recently Sunitinib, a new KIT/PDGFRA kinase inhibitor, has been tested in patients with GIST resistant to imatinib, with promising results. © 2007 European Society for Medical Oncology.

AB - Gastrointestinal stromal tumors (GISTs) are mesenchymal tumors of the gastrointestinal tract that are believed to originate from a neoplastic transformation of the intestinal pacemaker cells (interstitial cells of Cajal) normally found in the bowel wall or their precursors. Although the microscopic features have been known for a long time, the defining characteristic of GIST is the presence of the cell-surface antigen CD117 (KIT), which is demonstrated by immunohistochemistry. KIT, which is a growth factor transmembrane receptor, is the product of the proto-oncogene c-kit (chromosome 4). Surgical removal remains the only curative treatment for patients with GISTs. Tumor size, mitotic index, anatomic location, tumor rupture and disease-free interval are the classic characteristics used to predict the clinical course of patients who undergo complete gross resection. Most GISTs express constitutively activated mutant isoforms of KIT or kinase platelet-derived growth factor receptor alpha (PDGFRA) that are potential therapeutic targets for imatinib mesylate. Imatinib mesylate is a rationally designed, molecularly specific oral anticancer agent that selectively inhibits several protein tyrosine kinases central to the pathogenesis of human cancer and which has demonstrated remarkable clinical efficacy in patients with chronic myeloid leukemia and malignant GISTs. More recently Sunitinib, a new KIT/PDGFRA kinase inhibitor, has been tested in patients with GIST resistant to imatinib, with promising results. © 2007 European Society for Medical Oncology.

UR - http://hdl.handle.net/10447/216525

M3 - Article

VL - 18

SP - vi136-vi140

JO - Annals of Oncology

JF - Annals of Oncology

SN - 0923-7534

ER -