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Adding single-stranded RNA, conversely, stimulated the transformation of normal PrP to prion PrP.
This finding suggests MELK overexpression may be involved in the malignant transformation of normal stem cells.
Transformation of normal epithelium into cancer cells involves epigenetic and genetic changes and modifications in nuclear structure and tissue architecture.
ROS-induced damage on DNA can lead to enhanced mutation rates, driving the transformation of normal cells into a tumorigenic phenotype.
Tumorigenesis in humans is a multistep process involving genetic alterations that drive the progressive transformation of normal cells into malignant types.
It was previously demonstrated that oncogenic transformation of normal human cells can be induced by expressing hTERT, p53DD, cyclin D1, CDK4R24C, C-MYCT58A and H-RASG12V.
These results indicate that Wnt pathway activation alone is not sufficient to induce full malignant transformation of normal lung cells.
Checkpoint loss results in genomic instability and has been implicated in the transformation of normal cells into cancer cells [42].
Taken together, these data documented the smoke-induced transformation of normal bronchial epithelial cells to tumorigenic cells in our system.
The transformation of normal breast epithelial cells to metastatic cancer is the result of multiple epigenetic and genetic changes, leading to deregulated interactions with the microenvironment [2].
Given its critical role in proliferation, it is not surprising that aberrant or deregulated MYC expression participates in the malignant transformation of normal cells into cancer cells.
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