GIST

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Gastrointestinal Stromal Tumour. A relatively uncommon mesenchymal tumour of the gastrointestinal tract; two-thirds arise in the stomach, nearly one-third in the small intestine and less than 10% elsewhere. They are often incidental findings at endoscopy—especially in Japan due to mass screening for gastric cancer—or at surgery for other causes
Epidemiology More common in the middle-aged to elderly
DiffDx Leiomyoma, schwannoma, sarcoma, adenocarcionoma, ectopic pancreas
Management Most GISTs respond well to the tyrosine-kinase inhibitor imatinib mesylate (Gleevec/STI-571)

GIST

Gastrointestinal stromal tumor, see there.

GIST

gastrointestinal stromal tumor.
References in periodicals archive ?
Microscopically, most GISTs demonstrate 3 main histologic subtypes: spindle cell type (most common), epithelioid type, and mixed spindle and epithelioid type.
This insight into the way GISTs develop has already helped to identify new treatments for this sarcoma.
Activating mutations of Kit or PDGF receptors are critical to the pathogenesis of more than 90 percent of GIST.
One approach classified all mesenchymal tumors of the GI tract as GISTs, regardless of the immunohistochemical profile.
5) Because of immunophenotypic and ultrastructural similarities, investigators (2,5-8) have postulated that GISTs are derived from the interstitial cells of Cajal.
Besides, the tumor cells showed mostly positive reactions in CD117; the c-kit proto-oncogene protein, which includes a tyrosine kinase component, is expressed in and is a useful marker of GISTs.
Use of Gleevec after surgery shows significant benefit for gastrointestinal stromal tumor (GIST) patients, dramatically reducing risk of relapse -- GIST, a life-threatening cancer, recurs in as many as one of two patients; recurrent tumors are often more aggressive than primary tumors -- For GIST patients who were assigned to Gleevec, more than nine out of
The purpose of the present investigation is to test the hypothesis that GISTs originate from CD34-positive stem cells and differentiate toward an ICC phenotype by immunohistochemical studies using selected lineage-directed monoclonal antibodies for ICCs (c-kit), smooth muscle (desmin), Schwann cells (S100 protein), stem cells (CD34), myofibroblasts ([Alpha]-actin), and proliferative cells (MIB-1).
The logical first step would be testing for the specific c-Kit mutations present in GISTs, before the start of treatment.
This study entailed analysis of the spectrum of mutations identified in a series of GISTs from more than 1,000 patients, coupled with assessment of the impact of various mutations on sensitivity/resistance to imatinib.
However, many GISTs cannot be surgically removed, because they are too large or have already spread to other parts of the body before diagnosis.
Each year approximately 900 people in the UK are diagnosed with GISTs, and today's positive recommendation means around 250 of these people whose tumours have spread to other parts of their bodies, or are unsuitable for surgery, can now receive Glivec - the only effective treatment for GISTs - on the NHS.