MASH1

AcronymDefinition
MASH1Mammalian Achaete-Scute Homolog 1
References in periodicals archive ?
To date, there have been no comprehensive immunohistochemistry studies with mASH1 on nonneuroendocrine neoplasms, especially NSCLC, such as adenocarcinoma and squamous cell carcinoma.
The titer for mASH1 (for in vitro diagnostic use; 24B72D11.1, Biocare Medical, Concord, California) was optimized at 1:200, followed by a 2-step immunohistochemistry horseradish peroxidase micropolymer detection system and visualized with 3,30-diaminobenzidine chromogen.
In NSCLC, mASH1 stained 1.1% (1 of 93) of adenocarcinomas, 0.9% (1 of 111) of squamous cell carcinomas, and 0% (0 of 30) of large cell carcinomas, and LCNEC stained 66.7% (6 of 9) (Figure 1, A; Table 2).
In this study, various normal and nonneuroendocrine neoplastic tissues were tested for sensitivity and specificity with mASH1. In normal tissues, m/hASH1 was observed only in cerebellum, normal thyroid C cells, and epithelial cells in thymus (Table 1).
Both studies used classic neuroendocrine markers, but did not use mASH1. Therefore, in tumors of unknown origin, breast cancer must be considered, especially when using chromogranin and synaptophysin as diagnostic markers.
Although NSCLC atypical carcinoids were positive (42.9%; cases had >10% positive cells) for mASH1, they stained less frequently than LCNEC (66.7%, P < .001) (Table 3) and SCLC, consistent with previous reports.
mASH1 stained only 1.1% (1 of 93) and 0.9% (1 of 114) of lung adenocarcinoma and lung squamous cell carcinoma cases, respectively (Table 3).
However, although not organ specific, mASH1 was highly specific for HGNECs versus carcinoids and other non-neuroendocrine neoplasms including NSCLC in the lung.
The expression of NeuroD and mASH1 in the gastroenteropancreatic neuroendocrinetumors.
The overexpression of Hes5 inhibited the Wnt signaling pathway, downregulated Mash1, and induced neuronal differentiation (the purple arrows).
Kageyama, "Mash1 promotes neuronal differentiation in the retina," Genes to Cells: Devoted to Molecular & Cellular Mechanisms, vol.