WITHDRAWN

Jane Doe

doi:10.32388/tfo21v

Abstract

The document associated with this DOI has been withdrawn.

Highlights

Gastrointestinal stromal tumors (GISTs) are a subgroup of mesenchymal tumors originating from the interstitial cells of Cajal, which can arise from any part of the gastrointestinal tract, most frequently from the stomach and small intestine, characterized by the expression of the cellsurface transmembrane receptor KIT with tyrosine kinase activity in approximately 95% of tumors.[1,2] Tumor mutational status is biologically and clinically important in gastrointestinal stromal tumor (GIST) and make this tumor a paradigmatic model of oncogene addiction
Our research aimed to investigate the effect of the exact type and codon location of KIT exon 11 critical mutations on clinical outcome, and the potential association between pathogenic variant (PV) and metastatic sites in relapsed patients
Clinicopathological characteristics of KIT exon 11-mutated patients according to critical mutations We chose to investigate KIT exon 11-mutated patients because they represent the largest molecular subgroup of GISTs, and are characterized by wide variability in PV types and clinical behavior

Summary

Introduction

Gastrointestinal stromal tumors (GISTs) are a subgroup of mesenchymal tumors originating from the interstitial cells of Cajal, which can arise from any part of the gastrointestinal tract, most frequently from the stomach and small intestine, characterized by the expression of the cellsurface transmembrane receptor KIT with tyrosine kinase activity in approximately 95% of tumors.[1,2] Tumor mutational status is biologically and clinically important in GISTs and make this tumor a paradigmatic model of oncogene addiction. The gastrointestinal stromal tumor (GIST) genotype is not currently included in risk-stratification systems, a growing body of evidence shows that the pathogenic variant (PV) type and codon location hold a strong prognostic influence on recurrence-free survival (RFS). This information has relevance in the adjuvant setting, where an accurate prognostication could help to better identify highrisk tumors and guide clinical decision-making. Patients with GISTs stratified as intermediate risk, but carrying the 557/558 deletion, showed a similar outcome to the high- risk patients with tumors harboring deletions in other codons, or duplication/ insertion/SNV. Conclusion: Our data support the inclusion of the PV type and codon location in routine risk prediction models, and suggest that intermediate-risk patients whose GISTs harbor 557/558 deletions may need to be treated with adjuvant imatinib like the high-risk patients

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Discussion

Conclusion