2009
DOI: 10.1136/jmg.2009.066944
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Apoptosis and cancer: mutations within caspase genes

Abstract: The inactivation of programmed cell death has profound effects not only on the development but also on the overall integrity of multicellular organisms.

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Cited by 597 publications
(451 citation statements)
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References 194 publications
(195 reference statements)
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“…Pro-caspase-8 is recruited to DISC by FADD, and dimerization or trimerization triggers pro-caspase-8 activation via reciprocal cleavage. Caspase-8, in turn, cleaves and activates caspase-3, -7, Bid, and also NF-kB [52,53]. Caspase-8 activation is regulated by cFLIP that is structurally homologous to caspase-8 but does not have caspase activity [54].…”
Section: Caspase Family Membersmentioning
confidence: 99%
“…Pro-caspase-8 is recruited to DISC by FADD, and dimerization or trimerization triggers pro-caspase-8 activation via reciprocal cleavage. Caspase-8, in turn, cleaves and activates caspase-3, -7, Bid, and also NF-kB [52,53]. Caspase-8 activation is regulated by cFLIP that is structurally homologous to caspase-8 but does not have caspase activity [54].…”
Section: Caspase Family Membersmentioning
confidence: 99%
“…Blebs are the progenitors of apoptotic bodies with small, nearly spherical cytoplasmic fragments encapsulated in cell membranes. Apoptotic bodies may contain functional organelles surrounded by intact plasma membranes (Elmore 2007;Ghavami et al 2009). Phosphatidylserine, a phospholipid embedded in the plasma membrane, is exposed on the outer side of apoptotic bodies.…”
Section: Introductionmentioning
confidence: 99%
“…Phosphatidylserine, a phospholipid embedded in the plasma membrane, is exposed on the outer side of apoptotic bodies. They act as ''eat me'' signals, thus attracting macrophages, and are efficiently phagocytosed (Elmore 2007;Ghavami et al 2009). …”
Section: Introductionmentioning
confidence: 99%
“…Conversely, the reduced expression or mutation of pro-apoptotic Bax/Bak or caspases has been reported in different cancers and correlated with poor clinical prognosis (Rampino et al, 1997;Shivapurkar et al, 2002;Fecker et al, 2006;Ghavami et al, 2009). Nevertheless, it is important to note that the abrogation of apoptotic pathways alone is unlikely to be sufficient to promote tumourigenesis since cancer often arises from a complex interplay of genetic aberrations and deregulated pathways.…”
Section: Apoptosis and Cancermentioning
confidence: 99%