Expression of SMARCA2 and SMARCA4 in gastric adenocarcinoma and construction of a nomogram prognostic model

Zhang, Zhenkun; Li, Qiujing; Sun, Shanshan; Li, Zhe; Cui, ZhengGuo; Liu, Qian; Zhang, Yujie; Xiong, Sili; Zhang, Shukun

doi:10.1007/s10147-023-02403-0

Cited by 2 publications

(1 citation statement)

References 38 publications

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“…However, the evidence specific to GEA is sparse and inconsistent. Schallenberg et al reported that SMARCA4 loss of function was not correlated with shortened overall survival in esophageal adenocarcinoma [29], while Zhang et al observed that the SMARCA4-lost group correlates with worse prognosis compared to the corresponding SMARCA4-present groups [30], implying a divergence in research regarding survival implications of the mutations in GEA. In addition, these studies primarily assessed SMARCA4 through immunohistochemistry (IHC), differing from our NGS panel approach.…”

Section: Discussionmentioning

confidence: 99%

SMARCA4 Mutations in Gastroesophageal Adenocarcinoma: An Observational Study via a Next-Generation Sequencing Panel

Yamashita,

Sewastjanow-Silva,

Yoshimura

et al. 2024

Cancers

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Background: The clinical impact of SMARCA4 mutations (SMARCA4ms) in gastroesophageal adenocarcinoma (GEA) remains underexplored. This study aimed to examine the association of SMARCA4ms with clinical outcomes and co-occurrence with other gene mutations identified through a next-generation sequencing (NGS) panel in GEA patients. Methods: A total of 256 patients with metastatic or recurrent GEA who underwent NGS panel profiling at the MD Anderson Cancer Center between 2016 and 2022 were included. Comparative analyses were performed to assess clinical outcomes related to SMARCA4ms. The frequency and types of SMARCA4ms and their co-occurrence with other gene mutations were also examined. Results: SMARCA4ms were identified in 19 patients (7.4%). These SMARCA4ms were significantly associated with non-signet ring cell subtype (p = 0.044) and PD-L1 positive expression (p = 0.046). No difference in survival between the SMARCA4m and SMARCA4-normal group was observed (p = 0.84). There were significant associations between SMARCA4ms and FANCA, IGF1R, KRAS, FANCL, and PTEN alterations. Notably, 15 of the 19 SMARCA4m cases involved SNV missense mutations, with frequent co-occurrences noted with TP53, KRAS, ARID1A, and ERBB2 mutations. Conclusions: These results serve as the first comprehensive examination of the relationship between SMARCA4ms and clinical outcomes in GEA.

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Section: Discussionmentioning

confidence: 99%