Cell death plays a critical role in cancer development and treatment. There are two main forms of cell death relevant to cancer: apoptosis and necrosis. Apoptosis, (or programmed cell death, PCD), is a tightly regulated and essential biological process that occurs in multicellular organisms. It serves as a natural mechanism to eliminate damaged, aged, or unwanted cells, including potentially cancerous cells as well as playing key roles during development. Apoptosis can be triggered by various internal and external signals, such as DNA damage, cellular stress, or immune system activation. Key features of apoptosis include: 1) morphological changes. Apoptosis involves cell shrinkage, nuclear condensation, and the formation of apoptotic bodies. These changes allow an organized demise of the cell without causing inflammation or damage to neighbouring cells; 2) Caspase Activation. Caspases, a family of proteases, play central roles in apoptosis. Activation of caspases initiates a series of events leading to apoptosis. Two pathways for caspase activation have been identified, the intrinsic pathway (mitochondrial pathway) and the extrinsic pathway (death receptor pathway). The intrinsic pathway is triggered by various intracellular stress signals, such as DNA damage or loss of cell survival signals. It involves the release of cytochrome c from mitochondria, which leads to the formation of the apoptosome, a complex that activates caspase-9 and subsequently caspase-3, resulting in cell death. In the extrinsic pathway specific death receptors on the cell surface, such as Fas receptor or tumor necrosis factor receptor (TNFR) are activated, initiating a signalling cascade leading to the activation of caspase-8 and caspase-3. Death ligands, such as Fas ligand (FasL) or tumor necrosis factor (TNF), are involved in the extrinsic pathway. The regulation of apoptosis involves a delicate balance between pro-apoptotic and anti-apoptotic proteins. Bcl-2 family proteins are key regulators of this balance and control mitochondrial membrane permeability, promoting or inhibiting apoptosis. Apoptosis is thought to play multiple crucial roles in the development and progression of cancer. It acts as a tumour suppressor mechanism, eliminating cells with DNA damage or mutations that could potentially lead to cancer. Cancer cells often acquire alterations that allow them to evade apoptosis, resulting in their prolonged survival. For example, they can downregulate pro-apoptotic factors or upregulate anti-apoptotic proteins, such as members of the Bcl-2 family, which block the apoptotic pathway. Apoptosis is also involved in immune surveillance, where immune cells recognize and eliminate cancer cells. Cancer cells frequently develop mechanisms to evade immune detection and destruction by manipulating the apoptotic pathway. For example, they may alter the expression of cell surface molecules or secrete anti-apoptotic factors to suppress immune responses. Many cancer treatments, such as chemotherapy and radiation therapy, induce apoptosis in cancer cells. The success of these therapies relies on their ability to trigger apoptosis in cancer cells selectively. However, cancer cells often develop resistance to apoptosis, making them less responsive to these treatments and leading to treatment failure. Understanding the apoptotic pathways and dysregulation in cancer has led to the development of novel therapeutic approaches aiming to restore or enhance apoptosis. These include the use of targeted therapies, small molecules, and immunotherapies that specifically target anti-apoptotic proteins or activate pro-apoptotic pathways. We provide a comprehensive product catalogue of research reagents for investigating apoptosis, including Bcl-2 antibodies, AKT1 antibodies, NF-kB p65 antibodies, NF-kB p65 ELISA Kits, and IGFBP3 ELISA Kits. Explore our full apoptosis product range below and discover more, for less. Alternatively, you can explore our Metabolism, Apoptotic Markers, and Receptors product ranges.