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• W2789966375 abstract "Comprehensive genomic profiles of HCC and iCCA have revealed the molecular events driving and supporting liver cancers and defined cancer subtypes with distinct prognoses. TERT promoter mutations are the most frequent alterations in HCC as well as in cirrhosis. TP53 is frequently mutated in HCC and iCCA, especially in hepatitis B virus-associated liver cancers. Genetic alterations in the WNT/β-catenin signaling pathway cooperate with other signaling pathways to facilitate liver cancer initiation and progression. TGF-β signaling has a context-dependent role in HCC initiation and progression. Defective TGF-β signaling impairs DNA damage repair, while overactive signaling facilitates immunosuppression. Obesity contributes to the burden of HCC and iCCA. Obesity-driven dysfunctional adipose tissue and gut dysbiosis promote liver cancer initiation and progression via immune cell infiltration, inflammatory signaling, and metabolic alterations. Hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA), the two most common primary liver cancers, represent the second most common cancer-related cause of death worldwide, with most cases being diagnosed at an advanced stage. Recent genome-wide studies have helped to elucidate the molecular pathogenesis and genetic heterogeneity of liver cancers. This review of the genetic landscape of HCC and iCCA discusses the most recent findings from genomic profiling and the current understanding of the pathways involved in the initiation and progression of liver cancer. We highlight recent insights gained from metabolic profiling of HCC and iCCA. This knowledge will be key to developing clinically useful diagnostic/prognostic profiles, building targeted molecular and immunologic therapies, and ultimately curing these complex and heterogeneous diseases. Hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA), the two most common primary liver cancers, represent the second most common cancer-related cause of death worldwide, with most cases being diagnosed at an advanced stage. Recent genome-wide studies have helped to elucidate the molecular pathogenesis and genetic heterogeneity of liver cancers. This review of the genetic landscape of HCC and iCCA discusses the most recent findings from genomic profiling and the current understanding of the pathways involved in the initiation and progression of liver cancer. We highlight recent insights gained from metabolic profiling of HCC and iCCA. This knowledge will be key to developing clinically useful diagnostic/prognostic profiles, building targeted molecular and immunologic therapies, and ultimately curing these complex and heterogeneous diseases. a fungal carcinogen present in mycotoxin-contaminated food supplies. AFB1-related HCC is highly associated with a specific hotspot mutation at R249S in the tumor suppressor gene TP53. a microbial imbalance or maladaptation on or inside the body, such as an impaired microbiota. a group of genes that mediate DNA damage response. Mutations in these genes lead to Fanconi anemia, a rare genetic disease. a rare liver cancer that accounts for <1% of primary liver cancers, affecting primarily young adults (10–35 years of age) with no underlying chronic liver disease. The most remarkable genomic characteristic of FLC is a somatic, DNAJB1–PRKACA fusion transcript on chromosome 19. a mutation that confers new or enhanced activity on a protein. the most common pediatric liver tumor, comprising 1% of total pediatric malignancies with an annual incidence of 1.5 cases per million. Hepatoblastomas are embryonal neoplasms that are most commonly diagnosed during the first 3 years of life. The Wnt signaling pathway gene CTNNB1 is the most frequently mutated gene in hepatoblastoma. a rare benign liver tumor, long associated with use of estrogen­based oral contraceptives. HCA develops in the absence of cirrhotic liver disease. Development of HCA into HCC likely entails a multistep processes, although the classic histologic precursor features seen in premalignant cirrhotic lesions have not yet been observed in HCA-derived HCC. a malignancy classification system based on expression of immune-related gene products. A recent study established immune classes within HCC, including exhausted and active immune subclasses [66Sia D. et al.Identification of an immune-specific class of hepatocellular carcinoma, based on molecular features.Gastroenterology. 2017; 153: 812-826Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar]. Approximately 25% of HCCs demonstrated a high degree of immune infiltration with high expression levels of PD-1/PD-L1, suggesting that these HCC cases may be well-suited for PD-1 modulating immunotherapy [66Sia D. et al.Identification of an immune-specific class of hepatocellular carcinoma, based on molecular features.Gastroenterology. 2017; 153: 812-826Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar]. the early and late TGF-β signatures were initially established using transgenic TGF-β receptor 2-knockout mouse models and subsequently validated in human HCC [68Coulouarn C. et al.Transforming growth factor-beta gene expression signature in mouse hepatocytes predicts clinical outcome in human cancer.Hepatology. 2008; 47: 2059-2067Crossref PubMed Scopus (158) Google Scholar]. Tumors from patients bearing a late TGF-β signature showed significantly shortened mean survival time compared to patients with an early TGF-β signature [68Coulouarn C. et al.Transforming growth factor-beta gene expression signature in mouse hepatocytes predicts clinical outcome in human cancer.Hepatology. 2008; 47: 2059-2067Crossref PubMed Scopus (158) Google Scholar]. a systematic study of chemical processes involving metabolite profiles. a change in the genetic structure that is not inherited from a parent, and also is not passed to offspring. There are several common types of nonsynonymous somatic mutations, including missense mutations (point mutations that result in the substitution of a different amino acid in the encoded protein) and nonsense mutations (substitution of an original amino acid codon for a stop codon, causing termination of the protein product). a multi-institutional effort to understand the molecular basis of cancer through genome analysis technologies, including large-scale genome sequencing technologies. a systematic study of transcriptomes, including mRNA, rRNA, tRNA, and other non-coding RNAs, as well as their structures and functions." @default.
• W2789966375 created "2018-03-29" @default.
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• W2789966375 date "2018-04-01" @default.
• W2789966375 modified "2023-10-01" @default.
• W2789966375 title "Genomic Profiling and Metabolic Homeostasis in Primary Liver Cancers" @default.
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