Apoptosis and Cancer Therapy: From Cutting-edge Science to by Klaus-Michael Debatin, Simone Fulda, Editors

By Klaus-Michael Debatin, Simone Fulda, Editors

Right here, a world and hugely distinctive group of authors leads readers from the rules of programmed phone dying to the position of apoptosis in melanoma improvement and rising remedy ideas. Divided into designated components, the 1st makes a speciality of apoptosis signaling, protecting extensive such issues as mitochondria, effector platforms, the Bcl-2 kinfolk, IAPs, survival pathways, tumor suppressor genes, modulators, lysosomes and phagocytosis. the second one part is going directly to examine apoptosis in melanoma and melanoma treatment, with an in depth examine version platforms, molecular prognosis, mobile rigidity, DNA harm and service, molecular goals and healing features. With its powerful specialize in contemporary advancements in melanoma treatment, this e-book is aimed toward oncologists, molecular and telephone biologists, biochemists, and people operating within the pharmaceutical and biotechnological industries.

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In T cells, expression of CD95L is strictly regulated. CD95L is not present on resting T cells, but is highly expressed upon activation of T cells by crosslinking of the T cell receptor (TCR) with an antigen or by reagents that mimic the antigen signal like agonistic anti-CD3 antibodies. The CD95/CD95L system plays a major role in regulation of the fate of T cells. During an immune response, activated T cells undergo rapid proliferation and differentiation. In turn, termination of an immune response requires elimination of activated T lymphocytes in a CD95L-dependent manner, called activation-induced cell death (AICD).

Caspase-9 activates caspase-3, resulting in induction of apoptosis. Bcl-2 family member Bid [49, 50]. This cleavage results in a proapoptotic fragment termed truncated Bid (tBid). This fragment induces proapoptotic functions of mitochondria by causing aggregation of Bax and Bak [51], and subsequent loss of cytochrome c from the mitochondrial intermembrane space. Apaf-1, cytochrome c and ATP form a large protein complex, the apoptosome, a sort of cytosolic DISC at which caspase-9 as the initiator caspase is activated [52].

Therefore, disruption of CD95-mediated apoptosis may lead to prolonged survival of B lymphocytes and subsequent accumulation of additional mutations in oncogene or tumor suppressor genes. Furthermore, in families characterized by germline CD95 mutations leading to autoimmunoproliferative syndrome (ALPS), the incidence of lymphomas is generally increased. Additional data suggesting the importance of the CD95/CD95L system for tumor progression emerged from studies on lpr and gld mouse strains, carrying mutations in CD95 and CD95L, respectively.

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