Cancer is a complex set of diseases involving genetic or epigenetic changes within cells, as well as interactions between the developing tumour cells and their microenvironment, which leads to uncontrolled tumour growth, altered differentiation, local invasion and metastasis to distant sites [1, 2] . Molecular changes in oncogenes or tumour suppressor genes promote various cancer hallmarks, including the continued proliferation, inhibition of differentiation, inhibition of apoptosis, changes to

more »

... metabolism, evasion of the immune system and the promotion of invasion/metastasis [3, 4] . Although many oncogenes and tumour suppressor gene mutations promote more than one hallmark of cancer, several mutations are required to generate malignant cancers, a process referred to as cooperative oncogenesis/tumourigenesis [5, 6] . Through decades of research, we have gained much knowledge on key molecular events and processes involved in the formation of cancer, and much of this knowledge has stemmed from investigations using model organisms, such as the mouse and the vinegar fly, Drosophila melanogaster, in addition to in vitro cell line studies. In this Special Issue, we present a collection of original research papers on various aspects of cancer research utilising human cell lines [7, 8] , or in vivo using Drosophila as a model system [9,10], as well as reviews highlighting the Drosophila model organism in cancer research [11] [12] [13] [14] [15] . Drosophila is a particularly useful model organism for the study of cancer mechanisms, because it has a rapid life cycle and is genetically manipulatable and since cancer genes and signalling pathways are highly conserved between humans and Drosophila, and interactions between tumour cells and surrounding normal cells can be readily examined in Drosophila tissues [6, [16] [17] [18] [19] [20] . In a research paper pertaining to in vitro models of cancer, Di Giorgio et al. [8] analyse the transcriptional response to the expression of three key oncogenes (RAS, MYC, and HDAC4) in human fibroblasts, revealing common signalling pathways that are deregulated by these genes, and suggesting potential therapeutic avenues for the treatment of cancers driven by these oncogenes. In the second research paper on this topic, Mayer et al. [7] focus on human pancreatic cancer, where they observe in tissue sections the infiltration of Th17-like T cells expressing IL21 and IL26, and the expression of receptors for IL21 and IL26 in the pancreatic epithelial cells. They show in human pancreatic cell lines that IL21 and IL26 signal through ERK1/2 and STAT, which leads to increased tumour cell growth in colony forming assays. In a research paper utilising the Drosophila model, Parniewska and Stocker [9] identify the novel splicing factor, SF2, which is essential for the survival and hyperproliferation of tissues that upregulate the target of rapamycin complex 1 (TORC1), a protein kinase involved in cellular growth that is upregulated in many cancers [21, 22] . The identification of SF2 as a key conserved target of TORC1, Int.