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Although, many of the key gene-silencing events occur very early during the premalignant stages of tumor progression, the process of epigenetic gene silencing continues through the entire progression of human cancer, where DNMT1 plays the predominant role as the maintenance methyltransferase.
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Getting back to swimming was a natural progression in the process of recovery.
We studied treatment after brain trauma, but our EvolutionPred is applicable to any impairment, where progression or the process of recovery is of interest.
LncRNA could contribute to the cancer progression by controlling the process of proliferation and migration [ 16, 17].
An elevated level of MUC1 protein plays a role in tumor progression, especially in the process of metastasis (Hollingsworth and Swanson 2004; Kufe 2009).
The level of progression for the processes of epigenetic genome-wide alterations that are mediated by DNA methyltransferases (DNMTs 1o and 3a/3b) and histone deacetylases (HDACs) can be modulated (i.e., reversed) via exogenous inhibitors of these enzymes throughout in vitro culture of nuclear donor cells and/or cloned embryos [ 19, 36– 36].
Based on these discovered genetic, epigenetic, and expression alternations, models of tumor progression have been constructed, and the process of tumor progression and metastasis has been studied.
The type III transforming growth factor-β cell surface receptor (TβRIII) functions as a suppressor of breast cancer progression and also regulates the process of epithelial-to-mesenchymal transition (EMT), a consequence of which is the loss of cell polarity.
This could indicate that EPHB4, ITGB8 and TGFB1 are intrinsically regulated in prostate cancer cells, therefore contributing to cancer progression and metastasis through the process of EMT.
However, EpCAM protein expression levels can be significantly down regulated during cancer progression as a consequence of the process of epithelial to mesenchymal transition.
Unfortunately, the process of progression to disease is poorly understood.
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