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Only when assuming both higher GIST incidence and longer third-line treatment-eligible GIST survival we obtained a 37.9% probability of remaining below the threshold of interest.
Given the importance of the choice of two of the base-case values on model results, three alternative scenarios were defined based on higher GIST incidence, higher survival assumptions for third-line treatment-eligible GIST and higher for both incidence and third-line treatment-eligible GIST survival.
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Indeed, they are associated with some familial cases (Nishida et al, 1998), and similarly KIT-mutated knock-in mice display high GIST incidence (Sommer et al, 2003).
Therefore, protein expression of cyclin H may allow subclassification of "very-high risk" (cyclin H-positive high risk GIST) from high risk GIST.
Although the classification distinguishes the tumours using a four-point scale (very low, low, intermediate and high risk of malignancy), this scale is only useful to differentiate between high-risk and non-high-risk GIST.
The Tmean and TSD were significantly higher in GIST than in leiomyoma and schwannoma (p < 0.001).
Indeed, KIT and ETV1 mRNA expression were significantly higher in GIST compared with GI-LMS (Supplementary Figure 5).
After post-standardized image analysis, both the Tmean and TSD were significantly higher in GIST than in leiomyoma and schwannoma.
The Tmean, which is indicative of echogenicity, was significantly higher in GIST than in leiomyoma and schwannoma (82.8 ± 22.5, 39.8 ± 18.9, and 47.0 ± 12.0, respectively; p < 0.001) (Table 1).
In addition, the TSD, which is indicative of heterogeneity, was also significantly higher in GIST than in leiomyoma and schwannoma (83.5 ± 14.4, 54.3 ± 21.7, and 58.3 ± 17.5, respectively; p < 0.001).
Accordingly, cyclin H expression differentiated high risk and "very-high risk" GIST with regard to disease-specific mortality and might be a valuable tool for further treatment decisions.
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