Altered levels of reactive oxygen species (ROS) are recognized as one of the key factors in mediating tumor cell survival in the tissue microenvironment, where they play a role in the initiation, progression and recurrence/relapse of colorectal cancer (CRC). Tumor cells can adapt to oxidative stress (OS) using genetic or metabolic reprogramming in the long or short term. In addition, tumor cells defend themselves through positive regulation of antioxidant molecules, enhancing ROS-driven proliferation. Balanced oxidative eustress levels can influence chemotherapy resistance, allowing tumor cells to survive treatment. Secondary effects of chemotherapy include increased ROS production and redox stress, which can kill cancer cells and eliminate drug resistance. Anticancer treatments based on manipulating ROS levels could represent the gold standard in CRC therapy. Therefore, exploring the modulation of the response to OS in deregulated signaling pathways may lead to the development of new personalized CRC treatments to overcome therapy resistance. In this review, we explore the role of ROS in the initiation and progression of CRC and their diagnostic implications as biomarkers of disease. Furthermore, we focused on the involvement of ROS in different CRC therapeutic options, such as surgery, radiotherapy, theranostic imaging, chemotherapy and immunotherapy and other precision medicine approaches.

The accelerated spread of bacterial resistance has been demonstrated to reduce the effectiveness of antibiotic treatments for infections, resulting in higher morbidity and mortality rates, as well as increased costs for livestock producers. It is expected that the majority of future antimicrobial use will be in animal production. The management of antimicrobial resistance (AMR) in the livestock sector poses significant challenges due to the multifaceted nature of the problem. In order to identify appropriate solutions to the rise of antimicrobial resistance, it is imperative that we have a comprehensive understanding of the disease dynamics underpinning the ways in which antimicrobial resistance is transmitted between humans and animals. Furthermore, in consideration of the anticipated requirement to satisfy the global demand for food, it is imperative that we guarantee that resistance is not transmitted or propagated during the treatment and disposal of animal waste, particularly from intensive farming. It is also crucial to formulate a research agenda to investigate how antibiotic resistance in animal faeces from livestock farming is affected by intensified farming activities. The review analyses the environment’s role in the transmission resistance chain and reviews methodologies for disrupting the link. A particular focus is placed on the limitations of the applied methodologies to reduce antimicrobial resistance in global animal production.

Colorectal cancer (CRC) is a multistep process that arises in the colic tissue microenvironment. Oxidative stress plays a role in mediating CRC cell survival and progression, as well as promoting resistance to therapies. CRC progression is associated with Wnt/β-Catenin signaling dysregulation and loss of proper APC functions. Cancer recurrence/relapse has been attributed to altered ROS levels, produced in a cancerous microenvironment. The effect of oxidative distress on Wnt/β-Catenin signaling in the light of APC functions is unclear. This study evaluated the effect of H₂O₂-induced short-term oxidative stress in HCT116, SW480 and SW620 cells with different phenotypes of APC and β-Catenin. The modulation and relationship of APC with characteristic molecules of Wnt/β-Catenin were assessed in gene and protein expression. Results indicated that CRC cells, even when deprived of growth factors, under acute oxidative distress conditions by H₂O₂ promote β-Catenin expression and modulate cytoplasmic APC protein. Furthermore, H₂O₂ induces differential gene expression depending on the cellular phenotype and leading to favor both Wnt/Catenin-dependent and -independent signaling. The exact mechanism by which oxidative distress can affect Wnt signaling functions will require further investigation to reveal new scenarios for the development of therapeutic approaches for CRC, in the light of the conserved functions of APC.

Primary liver cancers (PLCs) are steadily increasing in incidence and mortality in the world. They have a poor prognosis due to their silent nature, late discovery and resistance to common chemotherapy. At present, there are limited treatment alternatives, and the understanding of PLC molecular aspects is essential to develop more efficient drugs and therapeutic surgical and loco-regional strategies. A clear causal link with liver damage, inflammation, and regeneration has been found in the occurrence of PLC over the last few decades. Physiologically, Wingless/It (Wnt)-β-catenin signaling plays a key role in liver development, metabolic zonation and regeneration. Loss of functional homeostasis of this pathway appears to be a major driver of carcinogenesis in the liver parenchyma. In the hepatic microenvironment, molecular deregulations that exceed the Wnt signaling biological capacity can induce tumor initiation and progression. Indeed, somatic mutations are identified in key components of canonical and non-canonical Wnt signaling and in PLCs and precancerous lesions. In this review, the altered functions of Wnt/β-catenin signaling are considered in human PLCs, with emphasis on hepatocellular carcinomas (HCC), cholangiocarcinomas (CCA) and hepatoblastomas (HB). Based on recent literature, we also focused on liver cancerogenesis through Wnt deregulation. An overview of preclinical and clinical studies on approved and experimental drugs, targeting the Wnt/β-catenin cascade in PLCs, is proposed. In addition, the clinical implication of molecule inhibitors that have been shown to possess activity against the Wnt pathway in association with conventional surgical and loco-regional therapies are reviewed.

The accelerated spread of bacterial resistance has been demonstrated to reduce the effectiveness of antibiotic treatments for infections, resulting in higher morbidity and mortality rates, as well as increased costs for livestock producers. It is expected that the majority of future antimicrobial use will be in animal production. The management of AMR in the livestock sector poses significant challenges due to the multifaceted nature of the problem. In order to identify appropriate solutions to the rise of antimicrobial resistance, it is imperative to have a comprehensive understanding of the disease dynamics underpinning the ways in which antimicrobial resistance is transmitted between humans and animals. Furthermore, in consideration of the anticipated requirement to satisfy the global demand for food, it is imperative to guarantee that resistance is not transmitted or propagated during the treatment and disposal of animal waste, particularly from intensive farming. It is also crucial to formulate a research agenda to investigate how antibiotic resistance in animal feces from livestock farming is affected by intensified farming activities. The review analyses the environment's role in the transmission resistance chain and reviews methodologies for disrupting the link. A particular focus is placed on the limitations of the applied methodologies to reduce antimicrobial resistance in global animal production.

Interaction between infectious agents and liver tissue, as well as repeated and extreme biological events beyond adaptive capacities, may result in pathological conditions predisposing people to development of primary liver cancers (PLCs). In adults, PLCs mainly comprise hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA). Various infectious agents in the hepatic microenvironment can destabilize normal liver cell functions by modulating the Wnt/β-catenin pathway components. Among them, hepatotropic viruses B, C, and D are involved in Wnt/β-catenin signaling dysregulation. Other microbial agents, including oncogenic viruses such as Epstein–Barr virus (EBV) and human papilloma virus (HPV), bacteria, e.g., Mycoplasma hyorhinis and Salmonella Typhi, the protozoan parasite Toxoplasma gondii, the fungus Aspergillus flavus, and liver flukes such as Clonorchissinensis or Opisthorchis viverrini, may induce malignant transformation in hepatocytes or in target cells of the biliary tract through aberrant Wnt signaling activation. This review focuses on new insights into infectious agents implicated in the deregulation of Wnt signaling and PLC development. Since the Wnt/β-catenin pathway is a driver of cancer following viral and bacterial infections, molecules inhibiting the complex axis of Wnt signaling could represent novel therapeutic approaches in PLC treatment.