miRNA Landscape in Primary Tumors and Matched Metastases in Gastrointestinal Stromal Tumors

Ravegnini, Gloria; Serrano, César; Ricci, Riccardo; Zhang, Qianqian; Terrenato, Irene; Graziosi, Agnese; Valori, Giorgia; Landolfi, Stefania; Hrelia, Patrizia; Angelini, Sabrina

doi:10.2217/epi-2020-0303

Cited by 2 publications

(1 citation statement)

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“…LncRNAs can fine-tune the expression of neighbor genes in a distinct context-dependent way via multifaceted mechanisms [ 120 ]. The largest study on miRNAs on primary tumors and metastases highlighted perpetuation of miRNAs features in metastatic lesions and that the primary origin appears to be the main determinant of the metastases miRNA profile [ 121 ].…”

Section: Kit Mutations and Expression In Gistmentioning

confidence: 99%

KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST

Zhou,

Abdihamid,

Tan

et al. 2024

Cell Commun Signal

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Gastrointestinal stromal tumor (GIST) is the most common sarcoma located in gastrointestinal tract and derived from the interstitial cell of Cajal (ICC) lineage. Both ICC and GIST cells highly rely on KIT signal pathway. Clinically, about 80-90% of treatment-naive GIST patients harbor primary KIT mutations, and special KIT-targeted TKI, imatinib (IM) showing dramatic efficacy but resistance invariably occur, 90% of them was due to the second resistance mutations emerging within the KIT gene. Although there are multiple variants of KIT mutant which did not show complete uniform biologic characteristics, most of them have high KIT expression level. Notably, the high expression level of KIT gene is not correlated to its gene amplification. Recently, accumulating evidences strongly indicated that the gene coding, epigenetic regulation, and pre- or post- protein translation of KIT mutants in GIST were quite different from that of wild type (WT) KIT. In this review, we elucidate the biologic mechanism of KIT variants and update the underlying mechanism of the expression of KIT gene, which are exclusively regulated in GIST, providing a promising yet evidence-based therapeutic landscape and possible target for the conquer of IM resistance.

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Section: Kit Mutations and Expression In Gistmentioning

confidence: 99%