Alfonso García-Valverde

TL;DR: The present review aims at summarizing current and forthcoming treatment directions in advanced imatinib-resistant GIST supported by a strong biological rationale.

TL;DR: CTDNA evaluation with amplicon-based NGS detects KIT primary and secondary mutations in metastatic GIST patients, particularly after imatinib progression, finding that GIST had relatively low ctDNA shedding, and mutations were at low allele frequencies.

TL;DR: In this article, the authors systematically dissected the current wealth of data of ctDNA in Gastrointestinal Stromal Tumor (GIST) and provided a critical understanding of the promises and limitations of the current technologies.

TL;DR: It is shown that SH3BP2 is expressed in primary tumors and cell lines from GIST patients and that SH 3BP2 silencing leads to a downregulation of oncogenic KIT and PDGFRA expression and an increase in apoptosis in imatinib‐sensitive and imatinIB‐resistant GIST cells.

TL;DR: Ripretinib as mentioned in this paper was used in combination with MEK inhibitors to induce and enhance the apoptotic response and prevent growth of resistant colonies in both imatinib-sensitive and resistant GIST cell lines, even after long-term removal of drugs.