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Editorial
. 2017 Dec;6(6):404-407.
doi: 10.21037/hbsn.2017.10.02.

Landscape of genomic alterations in hepatocellular carcinoma: current knowledge and perspectives for targeted therapies

Kévin Bévant  1 , Cédric Coulouarn  1
Affiliations
Editorial

Landscape of genomic alterations in hepatocellular carcinoma: current knowledge and perspectives for targeted therapies

Kévin Bévant et al. Hepatobiliary Surg Nutr. 2017 Dec.
No abstract available

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Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Integrative genomics to decrypt HCC tumor heterogeneity and to identify new therapeutic strategies. HCC is a heterogeneous disease characterized by a unique combination of genetic, epigenetic and transcriptomic alterations. The TCGA study illustrates the potential of large-scale analysis using multiple genomic platforms (e.g., exome sequencing, DNA copy number and methylation analysis, gene expression and protein profiling) to characterize the molecular landscape of genomic alterations in HCC. Data integration is used to define the core hallmarks altered in most HCC, as well as to stratify HCC into clinically relevant subtypes. Such integrative approach not only provides mechanistic insights into the molecular mechanisms involved in HCC carcinogenesis but also identifies key oncogenic pathways to be targeted for combined personalized therapies.
Figure 2
Figure 2
Targeted therapy using specific immune checkpoint inhibitors. T-cell activation involves co-stimulatory signals initiated by the interaction of B7 with CD28 while T-cell inactivation involves interaction of B7 with CTLA-4. T-cells are also negatively regulated by the interaction of PD-1 with its ligand PD-L1 commonly over-expressed in tumor cells. Targeted therapies using immune checkpoint inhibitors represent a promising approach to boost the activation of immune cell effectors and to avoid their inactivation. The identification of a specific HCC subtype expressing immune checkpoint genes (e.g., CTLA4, PD1, PDL1) at high levels opens promising therapeutic opportunities using immune checkpoint inhibitors.
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References

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