Cell survival and death are intricately governed by apoptosis, a meticulously controlled programmed cell death. Apoptosis is vital in facilitating embryonic development and maintaining tissue homeostasis and immunological functioning. It is a complex interplay of intrinsic and extrinsic signaling pathways that ultimately converges on executing the apoptotic program. The extrinsic pathway is initiated by the binding of death ligands such as TNF-α and Fas to their respective receptors on the cell surface. In contrast, the intrinsic pathway leads to increased permeability of the outer mitochondrial membrane and the release of apoptogenic factors like cytochrome c, which is regulated by the Bcl-2 family of proteins. Once activated, these pathways lead to a cascade of biochemical events, including caspase activation, DNA fragmentation, and the dismantling of cellular components. Dysregulation of apoptosis is implicated in various disorders, such as cancer, autoimmune diseases, neurodegenerative disorders, and cardiovascular diseases. This article focuses on elucidating the molecular mechanisms underlying apoptosis regulation, to develop targeted therapeutic strategies. Modulating apoptotic pathways holds immense potential in cancer treatment, where promoting apoptosis in malignant cells could lead to tumor regression. This article demonstrates the therapeutic potential of targeting apoptosis, providing options for treating cancer and neurological illnesses. The safety and effectiveness of apoptosis-targeting drugs are being assessed in ongoing preclinical and clinical trials (phase I–III), opening the door for more effective therapeutic approaches and better patient outcomes.

Cancer is a multifaceted disease influenced by genetic mutations and environmental factors, including exposure to carcinogens. This review presents an in-depth analysis of the mechanisms driving cancer initiation, focusing on the roles of carcinogenic chemicals, anticancer therapies, and chemo-preventive agents. The discussion encompasses a broad spectrum of carcinogens: chemical agents like polycyclic aromatic hydrocarbons, physical agents such as ionizing radiation, biological agents like viruses, and certain therapeutic drugs. The multistep nature of carcinogenesis—comprising initiation, promotion, and progression phases—is detailed, with an emphasis on genetic and epigenetic alterations. Methods for testing carcinogenicity, including in vitro and in vivo studies and epidemiological approaches, are highlighted for their significance in identifying potential carcinogens and understanding their mechanisms. To classify and regulate carcinogenic exposures, the review also looks at the risk management plans and regulatory frameworks used by agencies like the European Chemicals Agency (ECHA), the Environmental Protection Agency (EPA), and the International Agency for Research on Cancer (IARC). Additionally, emerging trends in cancer treatment, such as precision oncology, immunotherapy, and early detection technologies, are explored, alongside ongoing challenges like health disparities and ethical issues. The review emphasizes the necessity of a multidisciplinary approach, involving collaboration among researchers, clinicians, regulatory bodies, and public health organizations, to translate scientific findings into effective cancer prevention, detection, and treatment strategies.

Non-enzymatic glycation of DNA both in vivo and in vitro results in generation of free radicals, known as glycoxidation. Glycoxidation leads to structural perturbation of DNA resulting in generation of neo-antigenic epitopes having implication in autoimmune disorders like diabetes mellitus. In this study human placental DNA was glycated with methylglyoxal (MG) and lysine (Lys) in the presence of Cu²⁺ and its auto-antibody binding was probed in Type 1 diabetes patients. Glycation was carried out by incubating DNA with MG, Lys and Cu²⁺ for 24 h at 37 °C. Carboxyethyl deoxyguanosine (CEdG) formed in glycation reaction was studied by LC-MS and the pathway for Amadori formation was studied by ESI-MS techniques. Furthermore, binding characteristics of auto-antibodies in diabetes patients were assessed by direct binding, competitive ELISA and band shift assay. DNA glycation with MG, Lys and Cu²⁺ results in the formation of CEdG (marker of DNA glycation) which was confirmed by LC-MS. The intermediate stages of glycation were confirmed by ESI-MS technique. Serum from diabetes patients exhibited enhanced binding and specificity for glycated DNA as compared to native form. Glycation of DNA has resulted in structural perturbation causing generation of neo-antigenic epitopes thus recognizing auto-antibodies in diabetes.