Diagnosis of gastrointestinal stromal tumors: A consensus approach.

By C. Fletcher, J. Berman, Christopher Corless, F. Gorstein, J. Lasota, B. Longley, M. Miettinen, T. O'Leary, H. Remotti, B. Rubin and 3 more. Human Pathology, 2002

3,676 citations recorded by the source corpus.

Subfields: Gastroenterology, Pulmonary and Respiratory Medicine, Surgery

View Paper: https://www.semanticscholar.org/paper/e267bd736cc9946943af24429ffb8d4b967411ac

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Gastroenterology

1. Christopher Corless
2. M. Heinrich
3. Heikki Joensuu
4. J. Fletcher
5. C. Fletcher

In Pulmonary and Respiratory Medicine

1. Heikki Joensuu
2. Christopher Corless
3. M. Heinrich
4. Brian J. Druker

In Surgery

1. Heikki Joensuu
2. Christopher Corless
3. Brian J. Druker
4. A. Odén
5. M. Heinrich
6. J. Kanis

Citations in the corpus

• Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors. (2002, background): “…gastrointestinal stromal tumor was confirmed by central review in 135 of 137 cases (98.5 percent); 2 patients were judged to be ineligible because of the absence of CD117 expression in the proper histopathological context, 19 and in 10 cases, pathologic material was unavailable for central review.”
• One vs three years of adjuvant imatinib for operable gastrointestinal stromal tumor: a randomized trial. (2012, background): “Primary tumor diameter, median (range), cm 9 (2-35) 10 (2-40)”
• Risk stratification of patients diagnosed with gastrointestinal stromal tumor. (2008, methodology): “It does not attempt to distinguish between benign and malignant tumors, given that even very small tumors and those with low mitotic counts Table 1 NIH consensus classification criteria for defining risk of aggressive clinical course of primary GISTs Risk category Tumor size in largest dimension Mit”
• Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. (2003, background): “wall and are typically characterized by the expression of the receptor tyrosine kinase KIT (CD117).(1,2) Recent studies have”
• Gastrointestinal stromal tumors (2006, methodology): “Tumor location, clinical symptoms at presentation, tumor size, and mitotic rate were recorded and tumors were classified according to a recently described consensus approach [20] (Table 1, Fig.”
• The novel marker, DOG1, is expressed ubiquitously in gastrointestinal stromal tumors irrespective of KIT or PDGFRA mutation status. (2004, background): “Current recommendations in the literature emphasize a diffuse, strong KIT immunoreactivity for the diagnosis of GIST.”
• Incidence patterns of soft tissue sarcomas, regardless of primary site, in the surveillance, epidemiology and end results program, 1978–2001: An analysis of 26,758 cases (2006, background): “Currently, smooth muscle tumors of the GI tract, omentum and mesentery are recognized as GI stromal tumors (GIST).(50) GIST do not show true smooth muscle differentiation and are driven by activating mutations in c-kit and PDGF receptor a.”
• Consensus meeting for the management of gastrointestinal stromal tumors. Report of the GIST Consensus Conference of 20-21 March 2004, under the auspices of ESMO. (2005, methodology): “tumors >5 cm or with a mitotic index >5/50 high power fields [7], a reasonable follow-up would be a CT scan every 3–4 months for 3 years, then every 6 months until 5 years, and yearly thereafter.”
• Gastrointestinal stromal tumors: The incidence, prevalence, clinical course, and prognostication in the preimatinib mesylate era (2005, methodology): “…presented with multiple gastrointestinal stromal tumors: The data for the largest tumor were recorded. b Risk groups were determined according to the groups reported by Fletcher et al., 2002,1 as follows: VL, very low risk; L, low risk; Int, intermediate risk; H, high risk; OM, overtly malignant.”