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Splicing alterations contributing to cancer hallmarks in the liver: central role of dedifferentiation and genome instability

  
@article{TGH4651,
	author = {Maddalen Jimenez and María Arechederra and Matías A. Ávila and Carmen Berasain},
	title = {Splicing alterations contributing to cancer hallmarks in the liver: central role of dedifferentiation and genome instability},
	journal = {Translational Gastroenterology and Hepatology},
	volume = {3},
	number = {0},
	year = {2018},
	keywords = {},
	abstract = {Hepatocellular carcinoma (HCC) is a major cause of cancer-related death worldwide. HCCs are molecularly heterogeneous tumors, and this complexity is to a great extent responsible for their poor response to conventional and targeted therapies. In this review we summarize recent evidence indicating that imbalanced expression of mRNA splicing factors can be a relevant source for this heterogeneity. We also discuss how these alterations may play a driver role in hepatocarcinogenesis by impinging on the general hallmarks of cancer. Considering the natural history of HCC, we focused on two pathogenic features that are characteristic of liver tumors: chromosomal instability and phenotypic de-differentiation. We highlight mechanisms connecting splicing derangement with these two processes and the enabling capacities acquired by liver cells along their neoplastic transformation. A thorough understanding of the alterations in the splicing machinery may also help to identify new HCC biomarkers and to design novel therapeutic strategies.},
	issn = {2415-1289},	url = {https://tgh.amegroups.org/article/view/4651}
}