Help Resources/Cellucidate Content
Catalogue of public cBooks: Oncology
Cellucidate Support Dec 08, 2009
This list includes publicly available cBooks on Cellucidate with rich content that will be of interest to other Cellucidate users, either for the purposes of demonstrating how Cellucidate can be used or as sets of agents and rules that could serve as a foundation for new models or be incorporated into existing models. This list is by no means complete and will updated periodically.
Do you have a cBook that you are willing to make publicly available and that you think might be of interest to others?
Just respond to this discussion topic with a link to your cBook and a brief description of why you think it might be of interest to other users and we might incorporate it into a future edition of the catalog :-)
So without further ado, the nominations in the category Oncology are ...
This book simulates the sequential activation of the Raf/MEK/ERK cascade from the Map Kinase Cascades. The
Raf/MEK/ERK cascade is essential part of many RTK induced signaling
networks. ERK activation induces transcription which ultimately leads
to numerous cellular processes such as growth, division and death. Due
to its integral part in vital cell processes, aberrant regulation of
this cascade is implicated in many cancers. Numerous drugs are
currently under clinical investigation to attempt to inhibit this
pathway’s key players ( 2002 S. Karger GmbH, Freiburg).
mTOR
The mTOR cBook gives a general overview of the pathway that mTOR is involved in. It begins from IRS1/2 and goes all the way down to capture the eIF-4E and S6 transcription factors.The model shows how well Cellucidate simulations mimic actual published, literature results. This model can be extended to incorporate various other arms related to Akt’s phosphorylation and can be used to shed light on such hazy areas. It can also be expanded to incorporate the negative feedback loop that is initiated by mTOR’s indirect activation of S6K1.
The ErbB Signaling Network
This cBook demonstrates the basal activation and normal ligand-induced activation of the ErbB receptor network and the kinetics of the formation of the various species of ErbB homodimers and heterodimers.
From EGF to Akt
This book explores the effect of cMET levels on Akt activation with low levels of ligand. The Hepatocyte Growth Factor Receptor (or cMET) pathway interacts closely with the EGFR pathway which is implicated in numerous types of cancers.
The Intrinsic Apoptosis Pathway
This cBook describes the intrinsic apoptosis pathway including the mitochondrial apoptosis circuits.
The Role of ErbB2 in Cancer
This cBook demonstrates the basal activation and normal ligand-induced activation of the ErbB receptor network and contrast these situations to the activation of the network that results from the overexpression of ErbB2. It also demonstrates the kinetics of the formation of the various species of ErbB homodimers and heterodimers.
mTOR
The mTOR cBook gives a general overview of the pathway that mTOR is involved in. It begins from IRS1/2 and goes all the way down to capture the eIF-4E and S6 transcription factors.The model shows how well Cellucidate simulations mimic actual published, literature results. This model can be extended to incorporate various other arms related to Akt’s phosphorylation and can be used to shed light on such hazy areas. It can also be expanded to incorporate the negative feedback loop that is initiated by mTOR’s indirect activation of S6K1.
The ErbB Signaling Network
This cBook demonstrates the basal activation and normal ligand-induced activation of the ErbB receptor network and the kinetics of the formation of the various species of ErbB homodimers and heterodimers.
From EGF to Akt
This book explores the effect of cMET levels on Akt activation with low levels of ligand. The Hepatocyte Growth Factor Receptor (or cMET) pathway interacts closely with the EGFR pathway which is implicated in numerous types of cancers.
The Intrinsic Apoptosis Pathway
This cBook describes the intrinsic apoptosis pathway including the mitochondrial apoptosis circuits.
The Role of ErbB2 in Cancer
This cBook demonstrates the basal activation and normal ligand-induced activation of the ErbB receptor network and contrast these situations to the activation of the network that results from the overexpression of ErbB2. It also demonstrates the kinetics of the formation of the various species of ErbB homodimers and heterodimers.
Met Levels and Akt Activation
This cBook explores the effect of cMET levels on Akt activation with low levels of ligand. The Hepatocyte Growth Factor Receptor (or cMET) pathway interacts closely with the EGFR pathway which is implicated in numerous types of cancers. On the receptor level, cMET can bind and dimerize HER3 to activated ErbB family effectors. Further downstream, cMET activates the Akt pathway - also activated by EGFR and heavily implicated in cell survival. Under normal levels of receptors and in the absence of ligand, only a basal level of activating signal reaches Akt. However, when cMET levels are overexpressed which is a common condition in gastric cancer, higher levels of Akt are activated even in the absence of ligand.
The Extrinsic Apoptosis Pathway
This book provides a general collation of the extrinsic apoptosis pathway starting with the death receptors. Extrinsic Apoptosis (programmed cell death) is an elegant example of the cell’s harmony between cellular signaling and spatial temporal mechanisms. Due to the important regulatory nature of apoptosis, it is a very heavily regulated mechanism. Intuitively, aberrant regulation in apoptosis can result in numerous types of disease including cancers, when a cell loses its ability to systematically destroy itself the breaks are cut.
This cBook explores the effect of cMET levels on Akt activation with low levels of ligand. The Hepatocyte Growth Factor Receptor (or cMET) pathway interacts closely with the EGFR pathway which is implicated in numerous types of cancers. On the receptor level, cMET can bind and dimerize HER3 to activated ErbB family effectors. Further downstream, cMET activates the Akt pathway - also activated by EGFR and heavily implicated in cell survival. Under normal levels of receptors and in the absence of ligand, only a basal level of activating signal reaches Akt. However, when cMET levels are overexpressed which is a common condition in gastric cancer, higher levels of Akt are activated even in the absence of ligand.
The Extrinsic Apoptosis Pathway
This book provides a general collation of the extrinsic apoptosis pathway starting with the death receptors. Extrinsic Apoptosis (programmed cell death) is an elegant example of the cell’s harmony between cellular signaling and spatial temporal mechanisms. Due to the important regulatory nature of apoptosis, it is a very heavily regulated mechanism. Intuitively, aberrant regulation in apoptosis can result in numerous types of disease including cancers, when a cell loses its ability to systematically destroy itself the breaks are cut.