Gastrointestinal Stromal Tumor: Genotype Frequency and Prognostic Relevance

Kumari, Niraj; Priyaa, Valli; Shukla, Pooja; Kumar, Ashok; Aggarwal, Rakesh; Krishnani, Narendra

doi:10.1097/pai.0000000000000395

Cited by 6 publications

(1 citation statement)

References 34 publications

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“…Indeed, tumors harboring the PDGFRA exon 18 D842V pathogenetic alteration appeared to be enriched in immune cells, mainly CD8+ T cells, as compared to non-D842V ones [10]. Moreover, the expression of immune checkpoints, such as PD-L1, PD-1, and CTLA-4, and their relationship to the clinical phenotype in GIST are emerging as potential prognostic biomarkers and could lead to improved prognostication in GIST, traditionally based on mitotic indices, tumor location, and tumor size [5,[11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Exploring the Dynamic Crosstalk between the Immune System and Genetics in Gastrointestinal Stromal Tumors

Dimino

Brando

Algeri

et al. 2022

Cancers

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Gastrointestinal Stromal Tumors (GISTs) represent a paradigmatic model of oncogene addiction. Despite the well-known impact of the mutational status on clinical outcomes, we need to expand our knowledge to other factors that influence behavior heterogeneity in GIST patients. A growing body of studies has revealed that the tumor microenvironment (TME), mostly populated by tumor-associated macrophages (TAMs) and lymphocytes (TILs), and stromal differentiation (SD) have a significant impact on prognosis and response to treatment. Interestingly, even though the current knowledge of the role of immune response in this setting is still limited, recent pre-clinical and clinical data have highlighted the relevance of the TME in GISTs, with possible implications for clinical practice in the near future. Moreover, the expression of immune checkpoints, such as PD-L1, PD-1, and CTLA-4, and their relationship to the clinical phenotype in GIST are emerging as potential prognostic biomarkers. Looking forward, these variables related to the underlying tumoral microenvironment in GIST, though limited to still-ongoing trials, might lead to the potential use of immunotherapy, alone or in combination with targeted therapy, in advanced TKI-refractory GISTs. This review aims to deepen understanding of the potential link between mutational status and the immune microenvironment in GIST.

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