Revisiting Ehrlich carcinoma in the era of precision oncology: bridging classical models with modern systems biology.

Abstract

Ehrlich carcinoma (EC) and its ascitic form, Ehrlich ascites carcinoma (EAC), are among the oldest and most widely used experimental tumor models in cancer research. Although they have traditionally been used for anticancer drug screening, their potential to address broader aspects of aggressive tumor biology has received comparatively less attention. EC/EAC exhibits several characteristics associated with advanced malignancy, including rapid tumor growth, angiogenesis, immune dysregulation, metabolic changes, therapeutic resistance, and complex interactions between the tumor and host. These features make EC/EAC a useful complementary model for studying different aspects of tumor progression. However, research using these models has largely focused on transcriptional changes and individual signalling pathways, while post-transcriptional regulatory mechanisms remain less explored. In particular, the role of the RNA-induced silencing complex (RISC), a major component of microRNA-mediated gene regulation, is still poorly understood in EC/EAC. In this review, we discuss the major limitations of current EC/EAC research, including the limited use of multi-omics approaches, single-cell and spatial analyses, functional genomics, immune checkpoint profiling, and integrated systems-level studies. We further discuss how incorporating RISC-centered regulatory networks with emerging approaches such as CRISPR-based studies, spatial transcriptomics, and metabolic profiling could provide deeper mechanistic insights and improve the translational value of these models. Bringing together the strengths of this established tumor model with contemporary approaches in cancer biology could help reposition EC/EAC as a relevant and versatile platform for studying tumor progression and therapeutic responses.