8.12 Glossary

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anoikis: a form of programmed cell death in which anchorage-dependent cells are detached from their surrounding extracellular matrix (ECM).  In metastasis, tumor cells may avoid anoikis and invade other organs.


Apomab: a pro-apoptotic anticancer agonist monoclonal antibody against death receptor 5 (DR5)/TNF-related apoptosis inducing ligand-receptor 2 (TRAIL-R2).


apoptosis: is the collection morphological and biochemical events that leads to the process of programmed cell death in multicellular organisms.


apoptosome complex: a protein structure formed triggered by the release of cytochrome c from the mitochondria in response to an intrinsic or extrinsic cell death stimulus.  Death stimuli can range from DNA damage to normal developmental cues.


autophagy: cellular degradation of unnecessary or dysfunctional components through the actions of lysosomes.  This can ensure survival during starvation by maintaining cellular energy levels.  Targeted cytoplasmic constituents are isolated from the rest of the cell within the autophagosome, which are then fused with lysosomes and degraded or recycled.


caspases: are a family of cysteine proteases that play important roles in apoptosis, necrosis, and inflammation.


curcumin: a diarylheptanoid. Research has identified curcumin as the agent responsible for most of the biological activity of turmeric, which is involved in inflammation attenuation.   In vitro studies show curcumin modulates the inflammatory response by down-regulating the activity of cyclooxygenase-2, lipoxygenase, and inducible nitric oxide synthase enzymes.


cytochrome c: a small heme protein associated with the inner membrane of the mitochondrion, as a part of the electron transport chain.  It is capable of undergoing oxidation and reduction, but does not bind oxygen.  Cytochrome c is also an intermediate in apoptosis.


effector (executioner) caspase:  Effector caspases (e.g., CASP3, CASP6, CASP7), when activated by initiator caspases, cleave other protein substrates within the cell, to trigger the apoptotic process.  The initiation of this cascade reaction is regulated by caspase inhibitors.


Hayflick limit:  The maximum number of cell divisions possible in a non-immortal cell. This limit is determined by the length of telomeres, which are serially shortened by each cell division.


inhibitor of apoptosis proteins: a family of functionally and structurally related proteins which serve as endogenous inhibitors of programmed cell death.  Most of them bind to and inhibit caspases as a mechanism.


initiator caspase: Initiator caspases (e.g., CASP2, CASP8, CASP9, and CASP10) cleave inactive pro-forms of effector caspases, thereby activating them and starting the cascade.


intrinsic pathway: also known as contact activation pathway, this pathway is involved in the innate inflammation response, beginning with the formation of tissue factors on collagen.


necrosis: a form of cell injury that results in the premature death of cells in living tissue by autolysis.    Caused by external factors such as infection, toxins, or trauma that result in the unregulated digestion of cell components.  This is in contrast to apoptosis.  While apoptosis often provides beneficial effects to the organism, necrosis is almost always detrimental and can be fatal.


oncogene-induced senescence: a DNA damage response triggered by DNA hyper-replication from the activity rapidly dividing cells transformed by oncogenes.


programmed cell death (PCD): death of a cell in any form, mediated by an intracellular program.  PCD is carried out in a regulated, normal process, which usually a part of an organism's life-cycle.   Apoptosis and autophagy are both forms of programmed cell death, but necrosis is a non-physiological process that occurs as a result of infection or injury.


PTEN-induced senescence: Similar to oncogene-induced senescence, loss of a tumor suppressor can also trigger cell senescence.  This was first illustrated for PTEN and NF1 TSGs.


pyknosis: irreversible chromatin condensation occurring before apoptosis or necrosis of a cell.


reactive oxygen species: exogenous or endogenous oxygen-containing compounds that readily react with cellular components, including free radicals, peroxides, and oxygen ions. Some have a benefical role in the cell (necessary for electron transport chain) while others are produced in response to stress or as a byproduct of ionizing radiation and will damage the cell.


retinoids: Vitamin A-related chemical compounds, containing a hexagonal ring structure, an unsaturated carbon chain, and a polar end group such as –OH. Retinoids are currently used to treat several skin conditions, as they downregulate epithelial cell proliferation. They are currently being tested for use in cancer therapy.


senescence: A cellular phase in which cells remain alive but have permanently finished cycling for the course of their normal lifespan.


senescence-associated secretory phenotype: the array of proteins, hormones, and other signaling molecules secreted by senescent cells.


stress-induced premature senescence: the long-term appearance of cellular markers of senescence on cells that have been exposed to some type of stress, such as oxidative stress or extracellular chemical signals.


survivin: a protein (encoded by the BIRC5 gene in humans) that inhibits apoptosis by inhibiting caspase activation.


zymogen: an inactive, precursor form of an enzyme requiring chemical activation to function as a normal enzyme.