Corrigendum to ‘Molecular characterisation of hepatocellular carcinoma in patients with non-alcoholic steatohepatitis’ [J Hepatol 75 (2021) 865–878]

Establishment of a tumor immune microenvironment-based molecular classification system of breast cancer for immunotherapy

“…Compared with patients lacking stromal-activated signatures, patients with stromal-activated signatures showed higher TGF-β signatures, such as the Wnt/TGF-β, fibroblast TGF-β response (fibroblast-TBR), T cell TGF-β response (T cell-TBR), late TGF-β, and cancer-associated ECM (C-ECM) signatures ( Figure 2A ). Pinyol et al reported a Wnt/TGF-β proliferation subclass with immunosuppressive pro-carcinogenic microenvironment [ 21 ]. TGF-β suppresses CD4 + T helper 2 cell-mediated anti-cancer immunity, and blocks TGF-β signaling prevents breast cancer progression [ 22 ].…”

Multidimensional landscape of non‐alcoholic fatty liver disease‐related disease spectrum uncovered by big omics data: Profiling evidence and new perspectives

“…Reproduced with permission. 51 Copyright 2021, Elsevier. (C) Hallmark pathways significantly enriched for H3K27ac modifications in NASH and CHC compared with control patient samples.…”

“…60 Genetic risk factors and mutations associated with NAFLD were also identified using GWAS 61 and WES. 51 The spatial proteogenomics atlas showed that lipid-associated macrophages are recruited to steatotic regions in the livers of NAFLD patients. 53 Overall, these omics techniques and data analysis have provided valuable insights into NAFLD progression and potential therapeutic targets.…”

Unravelling the role of obesity and lipids during tumor progression

“…Gross histopathology examination of resected HCC tumors often shows irregular nodules that are more yellow and soft than the adjacent normal ( Schlageter et al, 2014 ), indicating steatosis and altered lipid metabolism. A recent characterization of the NASH-HCC transcriptome shows apparent upregulation of the pathways involved in FA metabolism ( Pinyol et al, 2021 ). The complex metabolic and inflammatory aberrations lead to increased proliferation of hepatobiliary progenitors ( Gadd et al, 2014 ), deranged genomic and epigenomic stability ( Nishida et al, 2016 ), and escape from immune surveillance ( Pfister et al, 2021 ), which ultimately drive tumorigenesis.…”