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The role of apoptosis in the pathology of pancreatic cancer.

Samm N, Werner K, Rückert F, Saeger HD, Grützmann R, Pilarsky C - Cancers (Basel) (2010)

Bottom Line: Signal transduction of such stimuli includes a death receptor-mediated extrinsic pathway as well as an intrinsic pathway linked to the mitochondria.Defects in apoptotic pathways and the deregulation of apoptotic proteins, such as Survivin, Bcl-2, Bcl-xL and Mcl-1, play decisive roles in the development of pancreatic cancer.Investigation of the molecular mechanism allowing tumors to resist apoptotic cell death would lead to an improved understanding of the physiology and the development of new molecular strategies in pancreatic cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of Visceral-, Thoracic- and Vascular-Surgery, University Hospital Dresden, Dresden, Germany. christian.pilarsky@uniklinikum-dresden.de.

ABSTRACT
Pancreatic cancer is a disease with high resistance to most common therapies and therefore has a poor prognosis, which is partly due to a lack of reaction to apoptotic stimuli. Signal transduction of such stimuli includes a death receptor-mediated extrinsic pathway as well as an intrinsic pathway linked to the mitochondria. Defects in apoptotic pathways and the deregulation of apoptotic proteins, such as Survivin, Bcl-2, Bcl-xL and Mcl-1, play decisive roles in the development of pancreatic cancer. Investigation of the molecular mechanism allowing tumors to resist apoptotic cell death would lead to an improved understanding of the physiology and the development of new molecular strategies in pancreatic cancer.

No MeSH data available.


Related in: MedlinePlus

Apoptosis mediated by death receptors in type I and type II cells. In type I cells, the quantity of initiator caspases is adequate to induce apoptosis directly, whereas in type II cells, the enhancing effect of mitochondria is necessary.
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f3-cancers-03-00001: Apoptosis mediated by death receptors in type I and type II cells. In type I cells, the quantity of initiator caspases is adequate to induce apoptosis directly, whereas in type II cells, the enhancing effect of mitochondria is necessary.

Mentions: Two different cell types have been identified for the death receptor signaling pathway (Figure 3). In type I cells, the death receptor complex, together with the adaptor molecule FADD, recruits procaspase 8, which is then cleaved to the active caspase 8, thereby activating the effector caspases [37]. This action implies that, in type I cells, the activated initiator caspases are sufficient to induce executioner caspases directly.


The role of apoptosis in the pathology of pancreatic cancer.

Samm N, Werner K, Rückert F, Saeger HD, Grützmann R, Pilarsky C - Cancers (Basel) (2010)

Apoptosis mediated by death receptors in type I and type II cells. In type I cells, the quantity of initiator caspases is adequate to induce apoptosis directly, whereas in type II cells, the enhancing effect of mitochondria is necessary.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3756346&req=5

f3-cancers-03-00001: Apoptosis mediated by death receptors in type I and type II cells. In type I cells, the quantity of initiator caspases is adequate to induce apoptosis directly, whereas in type II cells, the enhancing effect of mitochondria is necessary.
Mentions: Two different cell types have been identified for the death receptor signaling pathway (Figure 3). In type I cells, the death receptor complex, together with the adaptor molecule FADD, recruits procaspase 8, which is then cleaved to the active caspase 8, thereby activating the effector caspases [37]. This action implies that, in type I cells, the activated initiator caspases are sufficient to induce executioner caspases directly.

Bottom Line: Signal transduction of such stimuli includes a death receptor-mediated extrinsic pathway as well as an intrinsic pathway linked to the mitochondria.Defects in apoptotic pathways and the deregulation of apoptotic proteins, such as Survivin, Bcl-2, Bcl-xL and Mcl-1, play decisive roles in the development of pancreatic cancer.Investigation of the molecular mechanism allowing tumors to resist apoptotic cell death would lead to an improved understanding of the physiology and the development of new molecular strategies in pancreatic cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of Visceral-, Thoracic- and Vascular-Surgery, University Hospital Dresden, Dresden, Germany. christian.pilarsky@uniklinikum-dresden.de.

ABSTRACT
Pancreatic cancer is a disease with high resistance to most common therapies and therefore has a poor prognosis, which is partly due to a lack of reaction to apoptotic stimuli. Signal transduction of such stimuli includes a death receptor-mediated extrinsic pathway as well as an intrinsic pathway linked to the mitochondria. Defects in apoptotic pathways and the deregulation of apoptotic proteins, such as Survivin, Bcl-2, Bcl-xL and Mcl-1, play decisive roles in the development of pancreatic cancer. Investigation of the molecular mechanism allowing tumors to resist apoptotic cell death would lead to an improved understanding of the physiology and the development of new molecular strategies in pancreatic cancer.

No MeSH data available.


Related in: MedlinePlus