Cancer is a complex disease that develops through the acquisition of a number of genetic lesions and epigenetic changes, some of which may lead cells a step closer to malignancy. Tumour cells can accumulate hundreds of mutations, and aggressive cancers may be composed of a number of genetically heterogeneous clones, making their molecular traits difficult to decipher. It is thus important to establish the contribution of different genes and pathways that cooperate in providing the tumour cells with specific phenotypical traits.

Both basic and translational cancer research have greatly benefited from the use of suitable cellular and animal models, which have helped characterise the molecular basis of many cancer hallmarks. In recent years, elaborate cellular models have been conceived that enable the in vitro study of intricate relationships occurring between cancer cells, blood vessels, and other stromal components. Additionally, sophisticated in vivo models have provided substantial insights into how tumour cells evolve and interact with the surrounding tissue during cancer initiation and progression, including mechanisms mediating systemic effects of cancer.

As cellular and molecular mechanisms governing cancer growth have shown to be highly conserved between humans, mice, fish, worms, and flies, we anticipate that other innovative experimental models will be developed and used in the future to address particular aspects of malignant transformation.

We invite investigators to contribute original research articles, as well as review articles that address the functional cooperation between different genes and pathways in epithelial cancers, using basic and translational experimental models.

Potential topics include but are not limited to the following:

• Intraepithelial tumour suppression
• Tumour-stroma interactions
• EMT, migration, and metastasis
• Cancer-related cell death
• Organotypic models of epithelial cancer
• Cell polarity and cell division in epithelial cancer
• Cancer stem cells
• Drug discovery