Hormonal Influence on Hepatic Lesions and Tumors

Hormonal signals play a pivotal role in the initiation, progression and malignant transformation of hepatic lesions and tumours. Androgens, oestrogens and prolactin influence hepatocellular proliferation, apoptosis and the hepatic microenvironment, altering susceptibility to both benign and malignant growths. Elevated androgen levels, whether endogenous or exogenous, have been linked to the development of hepatocellular adenomas and progression towards hepatocellular carcinoma, particularly in the context of activating β-catenin mutations. Conversely, oestrogen signalling can exert protective effects through modulation of hepatic stellate cell activity and attenuation of fibrosis, yet may also promote lesion growth under certain receptor-expressing conditions. Prolactin receptor activation in cholestatic injury models has been shown to drive early neoplastic changes. Understanding the balance and interplay of these hormonal pathways is essential for refining diagnostic markers, tailoring pharmacological interventions and mitigating risks associated with hormonal therapies.

Research from Nature Portfolio

Recent studies have elucidated the role of androgen receptor activation in β-catenin-driven hepatic adenomas, demonstrating that ligand-dependent receptor signalling enhances cell cycle progression and histological complexity. Another investigation characterised oestrogen receptor β within hepatic stellate cells, revealing its ability to suppress fibrogenic gene programmes and limit the fibrotic niche that facilitates tumour emergence. A further analysis of prolactin receptor dynamics in cholestatic injury models highlighted how chronic receptor stimulation can initiate preneoplastic hepatic foci via STAT-mediated transcriptional networks, suggesting potential targets for early intervention.

Hormonal Influence on Hepatic Lesions and Tumors publication trend

The graph below shows the total number of articles in hormonal influence on hepatic lesions and tumors across all publications each year (not limited to Nature Index journals).

Technical terms

Androgen receptor (AR): A nuclear hormone receptor that, upon binding testosterone or dihydrotestosterone, regulates gene expression promoting cell proliferation and survival.

Oestrogen receptor β (ERβ): One isoform of the oestrogen receptor family; modulates diverse processes in non-reproductive tissues, including anti-fibrotic signalling in the liver.

Hepatocellular adenoma (HCA): A benign monoclonal liver neoplasm often associated with hormonal exposures, which can undergo malignant transformation.

Hepatic peliosis: A rare vascular condition characterised by blood-filled cavities within the liver parenchyma, linked to anabolic steroid use.

Hepatic stellate cell (HSC): A perisinusoidal cell that, when activated, produces extracellular matrix components driving liver fibrosis and influencing tumour microenvironment.

References

1. Hepatic Peliosis and Hemorrhage after Anabolic Steroid Abuse. Journal of Gastrointestinal and Abdominal Radiology (2024).