An ageing population is a typical feature of many developed countries across the world. Analyzed from a biomedical and philosophical point of view, this phenomenon is also a potential risk factor for social sustainability of communities. The association between ageing and cancer seems to be more than apparent. Therefore, the further increase of epidemic-like incidence of malignant tumors in a population can be expected in the near future. Elderly people usually suffer from age-dependent diseases, and such polymorbidity can seriously affect the treatment of malignant tumors. Such an impending situation may be associated with multiple medical, social and economic issues. This article summarizes data about the possible molecular mechanism influencing rapid spreading of tumors in the elderly population. Reduction of the activity of DNA repair machinery is a likely genetic cause. Besides this, even epigenetic mechanisms can influence this process. In this context, the role of cancer stroma in controlling multiple biological properties of tumors is a prospective target for translational research with potential therapeutic outcomes.

Excessive connective tissue accumulation, a hallmark of hypertrophic scaring, results in progressive deterioration of the structure and function of organs. It can also be seen during tumor growth and other fibroproliferative disorders. These processes result from a wide spectrum of cross-talks between mesenchymal, epithelial and inflammatory/immune cells that have not yet been fully understood. In the present review, we aimed to describe the molecular features of fibroblasts and their interactions with immune and epithelial cells and extracellular matrix. We also compared different types of fibroblasts and their roles in skin repair and regeneration following burn injury. In summary, here we briefly review molecular changes underlying hypertrophic scarring following burns throughout all basic wound healing stages, i.e. during inflammation, proliferation and maturation.

Tumor stroma is an active part influencing the biological properties of malignanciesviamolecular cross‐talk. Cancer‐associated fibroblasts play a significant role in this interaction. These cells frequently express smooth muscle actin and can be classified as myofibroblasts. The adhesion/growth‐regulatory lectin galectin‐1 is an effector for their generation. In our study, we set the presence of smooth muscle actin‐positive cancer‐associated fibroblasts in relation to this endogenous lectin and anin vivocompetitor (galectin‐3). In squamous cell carcinomas of head and neck, upregulation of galectin‐1 presence was highly significantly correlated to presence of smooth muscle actin‐positive cancer‐associated fibroblasts in the tumor (p= 4 × 10⁻⁸). To pinpoint further correlations on the molecular level, we applied microarray analyses to the transcription profiles of the corresponding tumors. Significant correlations of several transcripts were detected with the protein level of galectin‐1 in the cancer‐associated fibroblasts. These activated genes (MAP3K2,TRIM23,PTPLAD1,FUSIP1,SLC25A40andSPIN1) are related to known squamous‐cell‐carcinoma poor‐prognosis factors, NF‐κB upregulation and splicing downregulation. These results provide new insights into the significance of presence of myofibroblasts in squamous cell carcinoma.

Members of the galectin family of endogenous lectins are potent adhesion/growth-regulatory effectors. Their multifunctionality opens possibilities for their use in bioapplications. We studied whether human galectins induce the conversion of human dermal fibroblasts into myofibroblasts (MFBs) and the production of a bioactive extracellular matrix scaffold is suitable for cell culture. Testing a panel of galectins of all three subgroups, including natural and engineered variants, we detected activity for the proto-type galectin-1 and galectin-7, the chimera-type galectin-3 and the tandem-repeat-type galectin-4. The activity of galectin-1 required the integrity of the carbohydrate recognition domain. It was independent of the presence of TGF-β1, but it yielded an additive effect. The resulting MFBs, relevant, for example, for tumor progression, generated a matrix scaffold rich in fibronectin and galectin-1 that supported keratinocyte culture without feeder cells. Of note, keratinocytes cultured on this substratum presented a stem-like cell phenotype with small size and keratin-19 expression. In vivo in rats, galectin-1 had a positive effect on skin wound closure 21 days after surgery. In conclusion, we describe the differential potential of certain human galectins to induce the conversion of dermal fibroblasts into MFBs and the generation of a bioactive cell culture substratum.

Interleukin-6 (IL-6) is a cytokine with multifaceted effects playing a remarkable role in the initiation of the immune response. The increased level of this cytokine in the elderly seems to be associated with the chronic inflammatory setting of the microenvironment in aged individuals. IL-6 also represents one of the main signals in communication between cancer cells and their non-malignant neighbours within the tumour niche. IL-6 also participates in the development of a premetastatic niche and in the adjustment of the metabolism in terminal-stage patients suffering from a malignant disease. IL-6 is a fundamental factor of the cytokine storm in patients with severe COVID-19, where it is responsible for the fatal outcome of the disease. A better understanding of the role of IL-6 under physiological as well as pathological conditions and the preparation of new strategies for the therapeutic control of the IL-6 axis may help to manage the problems associated with the elderly, cancer, and serious viral infections.