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- W2765165592 endingPage "846" @default.
- W2765165592 startingPage "839" @default.
- W2765165592 abstract "Cellular transformation and the accumulation of genomic instability are the two key events required for tumorigenesis. K-Ras (Kirsten-rat sarcoma viral oncogene homolog) is a prominent oncogene that has been proven to drive tumorigenesis. K-Ras also modulates numerous genetic regulatory mechanisms and forms a large tumorigenesis network. In this review, we track the genetic aspects of K-Ras signaling networks and assemble the sequence of cellular events that constitute the tumorigenesis process, such as regulation of K-Ras expression (which is influenced by miRNA, small nucleolar RNA and lncRNA), activation of K-Ras (mutations), generation of reactive oxygen species (ROS), induction of DNA damage and apoptosis, induction of DNA damage repair pathways and ROS detoxification systems, cellular transformation after apoptosis by the blebbishield emergency program and the accumulation of genomic/chromosomal instability that leads to tumorigenesis." @default.
- W2765165592 created "2017-11-10" @default.
- W2765165592 creator A5006097717 @default.
- W2765165592 creator A5053062159 @default.
- W2765165592 creator A5065938903 @default.
- W2765165592 creator A5074107640 @default.
- W2765165592 creator A5084911456 @default.
- W2765165592 date "2017-10-23" @default.
- W2765165592 modified "2023-09-25" @default.
- W2765165592 title "Molecular genetics and cellular events of K-Ras-driven tumorigenesis" @default.
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