Publications by authors named "Agnese Collino"
Article Synopsis
- Chronic inflammation can lead to cancer development through creating a toxic environment that requires cells to adapt for survival.
- In a specific study on pediatric liver cancer related to a genetic defect in bile salt transport, researchers found that inflammation ultimately resulted in oncogenic transformation in mouse models (Mdr2-/- mice).
- The activation of a nuclear receptor called CAR was linked to this process, as it helped detoxify harmful bile acids and promote cancer cell survival, making CAR a potential target for therapeutic interventions to inhibit cancer progression.
Article Synopsis
- ST18 is implicated in both tumor suppression and oncogenesis, with evidence showing its critical role in liver cancer progression and maintenance in a mouse model.
- ST18 expression is induced by inflammatory signals, particularly from macrophages, and its knockdown significantly slows tumor growth and causes drastic tumor regression.
- The study highlights the interaction between ST18 and tumor-associated macrophages, suggesting that targeting this relationship could be a potential therapeutic strategy in liver cancer treatment.
An increasing number of noncoding RNAs (ncRNAs) have been implicated in various human diseases including cancer; however, the ncRNA transcriptome of hepatocellular carcinoma (HCC) is largely unexplored. We used CAGE to map transcription start sites across various types of human and mouse HCCs with emphasis on ncRNAs distant from protein-coding genes. Here, we report that retroviral LTR promoters, expressed in healthy tissues such as testis and placenta but not liver, are widely activated in liver tumors.
View Article and Find Full Text PDFHepatocellular carcinoma (HCC) is almost invariably associated with an underlying inflammatory state, whose direct contribution to the acquisition of critical genomic changes is unclear. Here we map acquired genomic alterations in human and mouse HCCs induced by defects in hepatocyte biliary transporters, which expose hepatocytes to bile salts and cause chronic inflammation that develops into cancer. In both human and mouse cancer genomes, we find few somatic point mutations with no impairment of cancer genes, but massive gene amplification and rearrangements.
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- LINE-1 (L1) retrotransposons make up about 17% of the human genome and their role in cancer, particularly hepatocellular carcinoma (HCC), is still being understood.
- Researchers analyzed 19 HCC genomes using a technique called retrotransposon capture sequencing, which revealed two main ways L1 insertions can contribute to tumor formation.
- One mechanism involved the germline retrotransposition of the tumor suppressor gene MCC, leading to increased oncogenic signaling, while the other showed an L1 insertion that activated the ST18 gene, a potential liver oncogene, by disrupting its regulatory feedback loop.
- These findings highlight the significant role that L1 retrotransposition may have in the development of
ΔNp73α, a dominant-negative inhibitor of p53 and p73, exhibits antiapoptotic and transforming activity in in vitro models and is often found to be upregulated in human cancers. The mechanisms involved in the regulation of ΔNp73α protein levels in normal and cancer cells are poorly characterized. Here, we show that that IκB kinase beta (IKKβ) increases ΔNp73α protein stability independently of its ability to activate NF-κB.
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