Epidemiological studies have revealed that high consumption of soy products is associated with low incidences of hormone-dependent cancers, including breast and prostate cancer. Soybeans contain large amounts of isoflavones, such as the genistein and daidzain. Previously, it has been demonstrated that genistein, one of the predominant soy isoflavones, can inhibit several steps involved in carcinogenesis. It is suggested that genistein possesses pleiotropic molecular mechanisms of action including inhibition of tyrosine kinases, DNA topoisomerase II, 5α-reductase, galectin-induced G₂/M arrest, protein histidine kinase, and cyclin-dependent kinases, modulation of different signaling pathways associated with the growth of cancer cells (e.g., NF-κB, Akt, MAPK), etc. Moreover, genistein is also a potent inhibitor of angiogenesis. Uncontrolled angiogenesis is considered as a key step in cancer growth, invasion, and metastasis. Genistein was found to inhibit angiogenesis through regulation of multiple pathways, such as regulation of VEGF, MMPs, EGFR expressions and NF-κB, PI3-K/Akt, ERK1/2 signaling pathways, thereby causing strong antiangiogenic effects. This review focuses on the antiangiogenic properties of soy isoflavonoids and examines their possible underlying mechanisms.

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.

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Objective: The purpose of this study was to evaluate, from the histological point of view, the effect of diode laser irradiation on skin wound healing in Sprague-Dawley rats. Background Data: Various biological effects have been described in different studies after low-level laser therapy (LLLT). Methods: Two parallel fullthickness skin incisions were performed on the back of each rat ( n = 49) and immediately sutured. After surgery, one wound of each rat was exposed to laser irradiation (continuous mode, 670 nm, daily dose 30 J/cm 2 ), whereas the parallel wound was not irradiated and served as control. Both wounds were removed 24, 48, 72, 96, 120, 144, and 168 h after surgery and routinely fixed and embedded in paraffin sections, stained with hematoxylin and eosin, van Gieson, periodic acid Schiff + periodic acid Schiff diastase, Mallory's phosphotungstic hematoxylin, and azur and eosin, and histopathologically evaluated. Results: As compared to nonirradiated control wounds, laser stimulation shortened the inflammatory phase as well as accelerated the proliferative and maturation phase, and positively stimulated the regeneration of injured epidermis and the reparation of injured striated muscle. Conclusion: LLLT at 670 nm positively influences all phases of rat skin wound healing.

Wound healing represents a complex and evolutionarily conserved process across vertebrates, encompassing a series of life-rescuing events. The healing process runs in three main phases: inflammation, proliferation, and maturation/remodelling. While acute inflammation is indispensable for cleansing the wound, removing infection, and eliminating dead tissue characterised by the prevalence of neutrophils, the proliferation phase is characterised by transition into the inflammatory cell profile, shifting towards the prevalence of macrophages. The proliferation phase involves development of granulation tissue, comprising fibroblasts, activated myofibroblasts, and inflammatory and endothelial cells. Communication among these cellular components occurs through intercellular contacts, extracellular matrix secretion, as well as paracrine production of bioactive factors and proteolytic enzymes. The proliferation phase of healing is intricately regulated by inflammation, particularly interleukin-6. Prolonged inflammation results in dysregulations during the granulation tissue formation and may lead to the development of chronic wounds or hypertrophic/keloid scars. Notably, pathological processes such as autoimmune chronic inflammation, organ fibrosis, the tumour microenvironment, and impaired repair following viral infections notably share morphological and functional similarities with granulation tissue. Consequently, wound healing emerges as a prototype for understanding these diverse pathological processes. The prospect of gaining a comprehensive understanding of wound healing holds the potential to furnish fundamental insights into modulation of the intricate dialogue between cancer cells and non-cancer cells within the cancer ecosystem. This knowledge may pave the way for innovative approaches to cancer diagnostics, disease monitoring, and anticancer therapy.

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.