scispace - formally typeset
Open AccessJournal Article

Cell death via apoptosis and its relationship to growth, development and differentiation of both tumour and normal cells.

TLDR
Apoptosis is an energy requiring process requiring intact energy generating systems, unlike that of necrosis, and is the mechanism by which cytotoxic T cells kill tumour target cells; it may also be the mechanism which accounts for the high loss of cells in growing tumour masses.
Abstract
Cell death can occur by two possible mechanisms, necrosis or apoptosis. Necrosis is the classically recognised form of cell death and is characterised by high amplitude swelling of the mitochondria, nuclear flocculation and uncontrolled cell lysis. Tissue necrosis is normally seen following severe trauma to cells. The alternative form of cell death is via a programmed sequence of events and is termed apoptosis. Apoptosis occurs under a variety of physiological conditions and cells dying by this process undergo cytoplasmic and nuclear condensation, coupled with cleavage of the cell's DNA into nucleosome size fragments. DNA cleavage is due to the activation of a specific endogenous endonuclease. The cell finally fragments into apoptotic bodies which are engulfed by neighbouring cells and degraded. Apoptosis is an energy requiring process requiring intact energy generating systems, unlike that of necrosis. In relation to malignant disease, apoptosis is the mechanism by which cytotoxic T cells kill tumour target cells; it may also be the mechanism which accounts for the high loss of cells in growing tumour masses. Extensive apoptosis is seen in regressing tumours and also in those treated with chemotherapeutic agents. This form of death may require the activation of specific death genes, although in view of work carried out in this and other laboratories, demonstrating that inhibitors of both protein and RNA synthesis will readily induce apoptosis, this may not be universal. Finally, apoptosis has far reaching implications for the treatment of malignant disease, since only by understanding how cells die will be able to develop more effective means of killing them.

read more

Citations
More filters
Journal ArticleDOI

Induction of apoptosis in fibroblasts by c-myc protein

TL;DR: It is demonstrated that deregulated c-myc expression induces apoptosis in cells growth arrested by a variety of means and at various points in the cell cycle.
Journal ArticleDOI

Reperfusion injury induces apoptosis in rabbit cardiomyocytes.

TL;DR: Parts of apoptosis (programmed cell death) in myocytes are identified as a response to reperfusion but not ischemia, which indicates that apoptosis may be a specific feature of reperfusions injury in cardiac myocytes, leading to late cell death.
Journal Article

The "bystander effect": tumor regression when a fraction of the tumor mass is genetically modified.

TL;DR: It is demonstrated that genetic modification of tumor cells may be useful for developing cancer therapies and the mechanism of this "bystander effect" was related to the process of apoptotic cell death when HSV-TK-positive cells were exposed to GCV.
Journal ArticleDOI

Apoptosis induced by anticancer drugs.

TL;DR: It is suggested that identification of the gene products which couple the stimulus to the response, and so determine intrinsic cellular sensitivity (and resistance), will be important targets for new types of drugs which might allow responses to occur in the major cancers of man, which are chemoresistant.
Journal ArticleDOI

Intracellular K+ Suppresses the Activation of Apoptosis in Lymphocytes

TL;DR: Disruption of the natural K+electrochemical gradient suppressed the activity of both caspase and nuclease independent of the mode of activation of the apoptotic inducing agent, demonstrating that a decrease in intracellular K+ concentration is a necessary, early event in programmed cell death.
Related Papers (5)