The world’s population is ageing at an accelerated pace. Ageing is a natural, physiological but highly complex and multifactorial process that all species in the Tree of Life experience over time. Physical and mental disabilities, and age‐related diseases, would increase along with the increasing life expectancy. Ginger (Zingiber officinale) is a plant that belongs to the Zingiberaceae family, native to Southeast Asia. For hundreds of years, ginger has been consumed in various ways by the natives of Asian countries, both as culinary and medicinal herb for the treatment of many diseases. Mounting evidence suggests that ginger can promote healthy ageing, reduce morbidity, and prolong healthy lifespan. Ginger, a well‐known natural product, has been demonstrated to possess antioxidant, anti‐inflammatory, anticancer, and antimicrobial properties, as well as an outstanding antiviral activity due to a high concentration of antiviral compounds. In this review, the current evidence on the potential role of ginger and its active compounds in the prevention of ageing is discussed.

Keratins (KRTs) are the intermediate filament-forming proteins of epithelial cells, classified, according to their physicochemical properties, into “soft” and “hard” keratins. They have a key role in several aspects of cancer pathophysiology, including cancer cell invasion and metastasis, and several members of the KRT family serve as diagnostic or prognostic markers. The human genome contains both, functional KRT genes and non-functional KRT pseudogenes, arranged in two uninterrupted clusters on chromosomes 12 and 17. This characteristic renders KRTs ideal for evolutionary studies. Herein, comprehensive phylogenetic analyses of KRT homologous proteins in the genomes of major taxonomic divisions were performed, so as to fill a gap in knowledge regarding the functional implications of keratins in cancer biology among tumor-bearing species. The differential expression profiles of KRTs in diverse types of cancers were investigated by analyzing high-throughput data, as well. Several KRT genes, including the phylogenetically conserved ones, were found to be deregulated across several cancer types and to participate in a common protein-protein interaction network. This indicates that, at least in cancer-bearing species, these genes might have been under similar evolutionary pressure, perhaps to support the same important function(s). In addition, semantic relations between KRTs and cancer were detected through extensive text mining. Therefore, by applying an integrative in silico pipeline, the evolutionary history of KRTs was reconstructed in the context of cancer, and the potential of using non-mammalian species as model organisms in functional studies on human cancer-associated KRT genes was uncovered.

Mechanisms governing tumor progression differ from those of initiation. One enigmatic prometastatic process is the recapitulation of pathways of neural plasticity in aggressive stages. Cancer and neuronal cells develop reciprocal interactions via mutual production and secretion of neuronal growth factors, neurothrophins and/or axon guidance molecules in the tumor microenvironment. Understanding cancer types where this process is active, as well as the drivers, markers and underlying mechanisms, has great significance for blocking tumor progression and improving patient survival. By applying computational and systemic approaches, in combination with experimental validations, we provide compelling evidence that genes involved in neuronal development, differentiation and function are reactivated in tumors and predict poor patient outcomes across various cancers. Across cancers, they co-opt genes essential for the development of distinct anatomical parts of the nervous system, with a frequent preference for cerebral cortex and neural crest-derived enteric nerves. Additionally, we show that p73, a transcription factor with a dual role in neuronal development and cancer, simultaneously induces neurodifferentiation and stemness markers during melanoma progression. Our data yield the basis for elucidating driving forces of the nerve–tumor cell crosstalk and highlight p73 as a promising regulator of cancer neurobiology.

Ionizing radiation (IR) is a genuine genotoxic agent and a major modality in cancer treatment. IR disrupts DNA sequences and exerts mutagenic and/or cytotoxic properties that not only alter critical cellular functions but also impact tissues proximal and distal to the irradiated site. Unveiling the molecular events governing the diverse effects of IR at the cellular and organismal levels is relevant for both radiotherapy and radiation protection. Herein, we address changes in the expression of mammalian genes induced after the exposure of a wide range of tissues to various radiation types with distinct biophysical characteristics. First, we constructed a publicly available database, termed RadBioBase, which will be updated at regular intervals. RadBioBase includes comprehensive transcriptomes of mammalian cells across healthy and diseased tissues that respond to a range of radiation types and doses. Pertinent information was derived from a hybrid analysis based on stringent literature mining and transcriptomic studies. An integrative bioinformatics methodology, including functional enrichment analysis and machine learning techniques, was employed to unveil the characteristic biological pathways related to specific radiation types and their association with various diseases. We found that the effects of high linear energy transfer (LET) radiation on cell transcriptomes significantly differ from those caused by low LET and are consistent with immunomodulation, inflammation, oxidative stress responses and cell death. The transcriptome changes also depend on the dose since low doses up to 0.5 Gy are related with cytokine cascades, while higher doses with ROS metabolism. We additionally identified distinct gene signatures for different types of radiation. Overall, our data suggest that different radiation types and doses can trigger distinct trajectories of cell-intrinsic and cell-extrinsic pathways that hold promise to be manipulated toward improving radiotherapy efficiency and reducing systemic radiotoxicities.

The dog, Canis lupus familiaris, is an important model for studying human diseases. Unlike many model organisms, the dog genome has a comparatively poor functional annotation, which hampers gene discovery for development, morphology, disease, and behavior. To fill this gap, we established a comprehensive tissue biobank for both the dog and wolf samples. The biobank consists of 5485 samples representing 132 tissues from 13 dogs, 12 dog embryos, and 24 wolves. In a subset of 100 tissues from nine dogs and 12 embryos, we characterized gene expression activity for each promoter, including alternative and novel, i.e., previously not annotated, promoter regions, using the 5’ targeting RNA sequencing technology STRT2-seq. We identified over 100,000 promoter region candidates in the recent canine genome assembly, CanFam4, including over 45,000 highly reproducible sites with gene expression and respective tissue enrichment levels. We provide a promoter and gene expression atlas with interactive, open data resources, including a data coordination center and genome browser track hubs. We demonstrated the applicability of Dog Genome Annotation (DoGA) data and resources using multiple examples spanning canine embryonic development, morphology and behavior, and diseases across species.

Natural products, like turmeric, are considered powerful antioxidants which exhibit tumor‐inhibiting activity and chemoradioprotective properties. Nowadays, there is a great demand for developing novel, affordable, efficacious, and effective anticancer drugs from natural resources. In the present study, we have employed a stringent in silico methodology to mine and finally propose a number of natural products, retrieved from the biomedical literature. Our main target was the systematic search of anticancer products as anticancer agents compatible to the human organism for future use. In this case and due to the great plethora of such products, we have followed stringent bioinformatics methodologies. Our results taken together suggest that natural products of a great diverse may exert cytotoxic effects in a maximum of the studied cancer cell lines. These natural compounds and active ingredients could possibly be combined to exert potential chemopreventive effects. Furthermore, in order to substantiate our findings and their application potency at a systems biology level, we have developed a representative, user‐friendly, publicly accessible biodatabase, NaturaProDB, containing the retrieved natural resources, their active ingredients/fractional mixtures, the types of cancers that they affect, and the corresponding experimentally verified target genes.