作者: Tsuyoshi Saito
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摘要: Synovial sarcoma (SS) tumor cells, which have the chromosomal translocation t(X;18)(p11.2;q11.2), an inherently greater propensity for epithelial differentiation than other mesenchymal tumors, especially spindle cell sarcomas. This is caused by de-repression of transcription E-cadherin SYT-SSX1 and SYT-SSX2, dissociate Snail or Slug, respectively, from promoter. However, a subset SS with loses expression despite adequate because mutations in E-cadherin, resulting monophasic histology. The ratio levels also associated expression: lower SYT-SSX1/Snail ratio, level expression, vice versa, thus affecting In addition, Wnt signal activation mutation β-catenin, APC, Axin 1 2 Remodeling extracellular matrix important. Only cells that survive all these steps can finally exhibit biphasic On hand, SYT-SSX2 fusion has weaker effect on promoter does SYT-SSX1, so it difficult SYT-SSX2-expressing tumors to achieve sufficient capacity form glandular structures. review provides interesting model this shows possible mechanism aberrant transition suggests might better be considered transition.