Modeling Inherited Disorders of Post-Lanosterol Cholesterol Biosynthesis: From Animal Models to Patient-Derived Stem Cells.

Dietary and lifestyle factors are recognized as major determinants of cancer risk. Indeed, the development of several malignancies, including colorectal cancer (CRC), breast cancer, ovarian cancer, and lung cancer, has been strongly associated with nutritional habits []. In particular, imbalanced diets can disrupt cellular redox homeostasis, leading to excessive production of reactive oxygen species (ROS) and impaired antioxidant defenses. This condition promotes oxidative damage to DNA, lipids, and proteins, thereby contributing to genomic instability, aberrant cell signaling, and tumor initiation and progression [,]. A high intake of red and processed meats has been linked to increased oxidative stress, partly due to the presence of heme iron, which can catalyze the formation of ROS through Fenton-like reactions. Additionally, high-temperature cooking methods such as grilling or frying can also lead to the formation of pro-oxidant compounds, including heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs), further contributing to oxidative damage and carcinogenesis [,]. Moreover, variations in the levels of certain nutrients, including vitamins, trace elements and dietary fat, may also contribute to the establishment of a cancer-promoting environment []. Considerable research has investigated the role of nutrients as adjunctive strategies in the treatment of cancer. Conventional anticancer therapies particularly chemotherapy, remain the cornerstone of cancer treatment. However, chemotherapy is frequently associated with severe adverse effects including anemia, nausea, organ damage and neutropenic enterocolitis. Moreover, although it is highly effective for certain tumors, its therapeutic efficacy remains limited in other cancer types []. Recent evidence suggests that combining dietary strategies with chemotherapy may enhance treatment efficacy []. Preclinical and clinical studies have also demonstrated that nutritional approaches such as fasting or fasting-mimicking diets may promote differential stress resistance, protecting normal cells from oxidative damage while sensitizing cancer cells to treatment-induced cytotoxicity []. This narrative review was written by examining peer-reviewed literature relevant to bioactive compounds, nutritional approaches in cancer prevention and therapy. A broad non-systematic search of scientific literature was conducted using PubMed and Scopus, combined with Google Search to identify additional evidence. This search focused on publications from 2002 to 2025. This time frame was chosen to capture contemporary evidence generated in the era of modern nutritional approaches and medicine research. The search was conducted using the following key words: “cancer”, “diet”, “nutrition”, “chemotherapy”, “cancer treatment”, “fasting”, “short-term fasting”, “intermittent fasting”, “ketogenic diet”, “caloric restriction”, “oxidative stress”, “Mediterranean diet”, “antioxidant supplements”, “nutrients”, “polyphenols”, “bioactive compounds”, “reactive oxygen species”, “clinical trials”. Inclusion criteria were as follows: (1) studies involving adult male and female participants; (2) studies investigating fasting, caloric restriction, or ketogenic diets during cancer treatment; (3) studies evaluating bioactive compounds in cancer prevention; and (4) studies reporting treatment-related outcomes, patient-reported outcomes, or changes in circulating biomarkers associated with insulin sensitivity, cancer-promoting growth factors, or oxidative stress. The following exclusion criteria were applied: (1) fasting performed as a religious practice; (2) studies conducted exclusively in pediatric or veterinary populations; (3) studies not related to cancer prevention or treatment; and (4) conference abstracts, editorials, non-peer-reviewed publications, and unpublished data. Original studies, systematic reviews, and meta-analyses published in English were eligible for inclusion when they provided relevant evidence on dietary interventions and cancer. Randomized controlled trials in humans were regarded as the primary source of evidence for clinical conclusions, whereas animal and in vitro studies were used mainly to explain biological mechanisms and generate hypotheses. Approximately 240 original studies, systematic reviews, and meta-analyses were reviewed.