“The incidence of hepatocellular carcinoma (HCC) is increasing worldwide, and HCC is one of the leading causes of cancer deaths worldwide”

Oncotarget released “Characterization of the inflammatory microenvironment and hepatic macrophage subsets in experimental hepatocellular carcinoma models“, Who reported that HCC typically develops against a background of chronic inflammation and fibrosis, with tumor-associated macrophages playing an important role in chronic inflammation-induced HCC and its progression.

However, the liver is home to unique macrophages, resident liver Kupffer cells, and monocyte-derived macrophages, and their contribution to HCC and the population of TAMs is incompletely known.

Here the authors characterized the tumor microenvironment and the proportion and transcription profile of hepatic macrophages in two frequently used HCC mouse models.

Gradually increased expression of inflammatory, immunoregulatory, fibrotic and cell proliferation pathways and markers was observed during diethylnitrosamine – and non-alcoholic steatohepatitis-induced HCC development.

These findings are useful to further elucidate sequential pathogenic events during hepatocarcinogenesis and to guide the future development of new treatment strategies for HCC.

Dr. Lindsey Devisscher from Ghent University said: “The incidence of hepatocellular carcinoma (HCC) is increasing worldwide, and HCC is a leading cause of cancer death worldwide.

The incidence of hepatocellular carcinoma (HCC) is increasing worldwide, and HCC is a leading cause of cancer death worldwide.

HCC is considered a classic inflammatory cancer in which inflammation drives carcinogenesis by inducing continuous cycles of tissue damage, necrosis with regeneration and subsequent fibrosis, cell dysplasia and ultimately HCC lesions.

The observations that there were at least 4 nodules with an average tumor growth rate of 150% by the age of 16-20 weeks, no visible metastases, and preserved liver function suggested that the HCC induced in this model corresponds to the more advanced stages B to C of the Barcelona Clinic’s liver cancer staging system for patients.

The microenvironment of the liver tumor consists of cancer cells surrounded by extracellular matrix elements and various stromal cells such as fibroblasts, endothelial cells and inflammatory cells that secrete a variety of growth factors, cytokines or matrix remodeling enzymes.

In fact, they previously reported that Mo massively infiltrates liver KCs in models of DEN- and NASH-induced HCC, while KCs are partially depleted during chronic liver damage, including end-stage HCC.

This study evaluated the time-dependent properties of the inflammatory microenvironment in the two HCC mouse models mentioned above, with an emphasis on the differential transcription profile of Liver-M / Users / anxiolydiot / Desktop / press-formatting-html.html subsets and the sequential changes in the Phenotype during the progression of HCC.

The Devisscher Research Team concluded in its Oncotarget Research Output: “HCC is an inflammation-related tumor in which hepatic macrophage populations play a central role. KCs, Mo, and Mo-M / Users / anxiolydiot / Desktop / press-formatting-html.html have distinct phenotypes that change as the disease progresses, and these cell populations contribute to the population of TAMs in HCC. The knowledge that KCs also express typical TAM markers further contributes to the understanding of hepatocarcinogenesis in two different frequently used experimental mouse HCC models.

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DOI – https: //doi.Organization/10.18632 /onkoziel.27906

Full text – https: //www.onkoziel.com /Items/27906 /Text/

Correspondence – Lindsey Devisscher – [email protected]

keywords
Hepatocellular carcinoma,
Macrophage subgroups,
Tumor microenvironment,
tumor-associated macrophages,
inflammation

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