Lipid metabolism plays a central role in maintaining long-term energy supply and is regulated by a complex signaling network that has not yet been fully elucidated. In recent years, ERBB receptors have gained attention in obesity research. In particular, the expression of the epidermal growth factor receptor (EGFR) and ERBB4 has been linked to adipocyte differentiation and homeostasis. The transmembrane protein leucine-rich repeats and immunoglobulin-like domains 2 (LRIG2) acts as a key regulator of these ERBB receptors. While the role of LRIG2 has been primarily investigated in the context of cancer, its function in lipid metabolism remains unknown.

Cutaneous squamous cell carcinoma (cSCC) is the second most common type of skin cancer worldwide. While cSCC exhibits a heterogeneous mutational landscape, oncogenic HRAS mutations appear to occur predominantly in locally advanced or metastatic tumors, suggesting a role for aberrant RAS signaling in disease progression. The DIRAS protein family consists of three RAS-related small GTPases (DIRAS1-3) which have been proposed to antagonize RAS signaling. DIRAS1 has been reported to act as tumor suppressor in various types of cancer, including glioblastoma, colorectal cancer, and cervical carcinoma. To investigate its role in context of NMSC we analyzed publicly available transcriptomics data and found DIRAS1 expression upregulated in cSCC patient samples.

 Colitis is a severe inflammatory disease of the large intestine characterized by impaired epithelial integrity and a high unmet need for regenerative therapies. ERBB receptor signaling, particularly via EGFR and ERBB4, is increasingly recognized as a critical regulator of intestinal epithelial repair. To define the roles of these receptors during mucosal regeneration, we analyzed genetically engineered mouse models lacking EGFR or ERBB4 alongside transgenic mice ubiquitously overexpressing the EGFR/ERBB4 ligand betacellulin (BTC). In experimental colitis, BTC-overexpressing mice showed markedly reduced disease severity and enhanced epithelial regeneration compared with wild-type controls, highlighting betacellulin-mediated ERBB signaling as a promising therapeutic strategy for intestinal inflammation.

Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic cancer and remains one of the deadliest malignancies. Preclinical PDAC research and drug development rely heavily on in vivo mouse models. However, suitable in vitro alternatives are limited, as primary pancreatic acinar cells rapidly lose their phenotype and are difficult to maintain under conventional two-dimensional (2D) culture conditions. Our research aims to establish a physiologically relevant alternative to animal models by developing a three-dimensional (3D) bioprinted model of the exocrine pancreas. Bioprinting combines living cells with biomaterials (bioinks) to fabricate complex 3D tissue constructs that more closely recapitulate the native cellular microenvironment than conventional cell culture systems.