Publications by authors named "M Barcena-Varela"
Hepatocellular carcinoma (HCC) represents a global health challenge, and ranks among one of the most prevalent and deadliest cancers worldwide. Therapeutic advances have expanded the treatment armamentarium for patients with advanced HCC, but obstacles remain. Precision oncology, which aims to match specific therapies to patients who have tumours with particular features, holds great promise.
View Article and Find Full Text PDFHepatocellular carcinoma presents strong sexual dimorphism, being 2-3 times more frequent in males than in females; however, the role of sex in response to immunotherapies in HCC remains unknown. We demonstrate that NOTCH1, an understudied oncogene in HCC, elicits sexually dimorphic anti-tumor immunity and response to FDA-approved immunotherapies. Surprisingly, males harboring NOTCH1-driven tumors displayed enhanced anti-tumor immune responses, which, in mice, were mediated by dendritic and T cells.
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- TGF-β is implicated in promoting cancer development, and the study investigates a specific protein's role in hepatocellular carcinoma (HCC), finding its overexpression linked to aggressive cancer features.
- The research involved analyzing tumor data from a large number of HCC patients and using mouse models to explore molecular effects, revealing a connection between the protein’s levels and immune system suppression.
- The findings suggest that overexpressing this protein contributes to tumor growth and poor patient outcomes, highlighting its potential as a target for cancer treatment.
Liver cancer, the third leading cause of cancer-related mortality worldwide, has two main subtypes: hepatocellular carcinoma (HCC), accounting most of the cases, and cholangiocarcinoma (CAA). NOTCH pathway regulates the intrahepatic development of bile ducts, which are lined with cholangiocytes, but it can also be upregulated in 1/3 of HCCs. To better understand the role of NOTCH in HCC, we developed a novel mouse model driven by activated NOTCH1 intracellular domain (NICD1) and MYC overexpression in hepatocytes.
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