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Annotation Apoptosis is a form of programmed cell death that enables the removal of damaged, infected, or otherwise unwanted cells in a controlled manner. Apoptosis can be initiated by multiple independent pathways that ultimately converge at a point where proteolytic enzymes belonging to the caspase family are activated, which dismantle the apoptotic cell. Multicellular organism have employed apoptotic mechanisms during host defence in response to viral infection to limit or prevent viral spread and replication. Consequently, viruses have evolved sophisticated molecular countermeasures to disarm host apoptotic defences, and this series of reviews and primary research articles in this Special Issue explores the intricate molecular interplay between viruses and their hosts when they battle for control of host apoptotic check-points.

Apoptosis. --- Cell death

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During our lifetime, the genome is constantly being exposed to different types of damage caused either by exogenous sources (radiations and/or genotoxic compound) but also as byproducts of endogenous processes (reactive oxigen species during respiration, stalled forks during replication, eroded telomeres, etc). From a structural point of view, there are many types of DNA damage including single or double strand breaks, base modifications and losses or base-pair mismatches. The amount of lesions that we face is enormous with estimates suggesting that each of our 1013 cells has to deal with around 10.000 lesions per day [1]. While the majority of these events are properly resolved by specialized mechanisms, a deficient response to DNA damage, and particularly to DSB, harbors a serious threat to human health [2]. DSB can be formed [1] following an exposure to ionizing radiation (X- or γ-rays) or clastogenic drugs; [2] endogenously, during DNA replication, or [3], as a consequence of reactive oxygen species (ROS) generated during oxidative metabolism. In addition, programmed DSB are used as repair intermediates during V(D)J and Class-Switch recombination (CSR) in lymphocytes [3], or during meiotic recombination [4]. Because of this, immunodeficiency and/or sterility problems are frequently associated with DDR-related pathologies.

Apoptosis. --- DNA repair. --- Phosphorylation.

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This book looks at the latest research studies on apoptosis in medicine. It is divided into three sections for convenient and easy reading. The first section which comprises two chapters is an introduction of the subject of apoptosis to the uninitiated. The second section which comprises a single solitary chapter looks at apoptosis in normal physiology during bone resorption under mechanical stress. The third and the final section reviews apoptosis in a number of pathological conditions with an emphasis on cancer.

Apoptosis. --- Cell death --- Medical genetics

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Apoptosis --- Cell death --- Apoptose --- Cellules --- Mort --- Cell Death --- physiology --- Apoptosis. --- Cell death. --- Cell Death - physiology --- Apoptosis - physiology

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Cancer cells --- Growth. --- Cells --- Pathology, Cellular --- Cancer cell growth --- Tumor Suppressor Proteins. --- Apoptosis. --- Apoptosis, Extrinsic Pathway --- Apoptosis, Intrinsic Pathway --- Caspase-Dependent Apoptosis --- Classic Apoptosis --- Classical Apoptosis --- Programmed Cell Death --- Programmed Cell Death, Type I --- Apoptoses, Extrinsic Pathway --- Apoptoses, Intrinsic Pathway --- Apoptosis, Caspase-Dependent --- Apoptosis, Classic --- Apoptosis, Classical --- Caspase Dependent Apoptosis --- Cell Death, Programmed --- Classic Apoptoses --- Extrinsic Pathway Apoptoses --- Extrinsic Pathway Apoptosis --- Intrinsic Pathway Apoptoses --- Intrinsic Pathway Apoptosis --- Necrosis --- Cell Death --- Clonal Deletion --- Superantigens --- Caspases --- Caspase 1 --- In Situ Nick-End Labeling --- Cellular Apoptosis Susceptibility Protein --- Genes, Transgenic, Suicide --- Growth Suppressor Proteins --- Metastasis Suppressor Proteins --- Proteins, Growth Suppressor --- Proteins, Metastasis Suppressor --- Proteins, Tumor Suppressor --- Genes, Tumor Suppressor --- Apoptosi