Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA129037 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE17768: An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: gene expression GSE17769: An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: DNA methylation GSE21347: An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: allelic status GSE21540: An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: CGH Refer to individual Series
2010-12-31 | E-GEOD-21541 | biostudies-arrayexpress
Project description:An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: CGH
| PRJNA129511 | ENA
Project description:An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: DNA methylation
| PRJNA129039 | ENA
Project description:An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: allelic status
| PRJNA129507 | ENA
Project description:One of the most fertile applications of next generation sequencing will be in the field of cancer genomics. Here, we report a high-throughput multi-dimensional sequencing study of primary non-small cell lung adenocarcinoma tumors and adjacent normal tissues of 6 never-smoker Korean female patients. Our data encompass results from exome-seq, RNA-seq, small RNA-seq, and MeDIP-seq. We identified and validated novel genetic aberrations including 47 somatic mutations and 20 fusion transcripts. We also characterized gene expression profiles which we sought to integrate with genomic aberrations and epigenetic regulations into functional networks. Importantly, among others the gene network module governing G2/M cell check point emerged as the primary source of disturbance in these patients. In addition, our study strongly suggests that microRNAs make key regulatory inputs into this gene network module. Our study offers a paradigm for integrative genomics analysis and proposes potential target pathways for the control of non-small cell lung adenocarcinoma. Study of primary non-small cell lung adenocarcinoma tumors and normal tissues of 6 patients.
2013-05-10 | E-GEOD-37764 | biostudies-arrayexpress
Project description:One of the most fertile applications of next generation sequencing will be in the field of cancer genomics. Here, we report a high-throughput multi-dimensional sequencing study of primary non-small cell lung adenocarcinoma tumors and adjacent normal tissues of 6 never-smoker Korean female patients. Our data encompass results from exome-seq, RNA-seq, small RNA-seq, and MeDIP-seq. We identified and validated novel genetic aberrations including 47 somatic mutations and 20 fusion transcripts. We also characterized gene expression profiles which we sought to integrate with genomic aberrations and epigenetic regulations into functional networks. Importantly, among others the gene network module governing G2/M cell check point emerged as the primary source of disturbance in these patients. In addition, our study strongly suggests that microRNAs make key regulatory inputs into this gene network module. Our study offers a paradigm for integrative genomics analysis and proposes potential target pathways for the control of non-small cell lung adenocarcinoma. Study of primary non-small cell lung adenocarcinoma tumors and normal tissues of 6 patients.
2013-05-10 | E-GEOD-37759 | biostudies-arrayexpress
Project description:Padala2017- ERK, PI3K/Akt and Wnt signalling
network (EGFR overexpression)
Crosstalk model of the ERK, Wnt and Akt
signalling pathways with EGFR overexpression.
This model is described in the article:
Cancerous perturbations
within the ERK, PI3K/Akt, and Wnt/?-catenin signaling network
constitutively activate inter-pathway positive feedback
loops.
Padala RR, Karnawat R, Viswanathan
SB, Thakkar AV, Das AB.
Mol Biosyst 2017 May; 13(5):
830-840
Abstract:
Perturbations in molecular signaling pathways are a result
of genetic or epigenetic alterations, which may lead to
malignant transformation of cells. Despite cellular robustness,
specific genetic or epigenetic changes of any gene can trigger
a cascade of failures, which result in the malfunctioning of
cell signaling pathways and lead to cancer phenotypes. The
extent of cellular robustness has a link with the architecture
of the network such as feedback and feedforward loops.
Perturbation in components within feedback loops causes a
transition from a regulated to a persistently activated state
and results in uncontrolled cell growth. This work represents
the mathematical and quantitative modeling of ERK, PI3K/Akt,
and Wnt/?-catenin signaling crosstalk to show the dynamics of
signaling responses during genetic and epigenetic changes in
cancer. ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk
networks include both intra and inter-pathway feedback loops
which function in a controlled fashion in a healthy cell. Our
results show that cancerous perturbations of components such as
EGFR, Ras, B-Raf, PTEN, and components of the destruction
complex cause extreme fragility in the network and
constitutively activate inter-pathway positive feedback loops.
We observed that the aberrant signaling response due to the
failure of specific network components is transmitted
throughout the network via crosstalk, generating an additive
effect on cancer growth and proliferation.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000656.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000656 | BioModels
Project description:Padala2017- ERK, PI3K/Akt and Wnt signalling
network (PTEN mutation)
Crosstalk model of the ERK, Wnt and Akt
Signalling pathways with PTEN mutation.
This model is described in the article:
Cancerous perturbations
within the ERK, PI3K/Akt, and Wnt/?-catenin signaling network
constitutively activate inter-pathway positive feedback
loops.
Padala RR, Karnawat R, Viswanathan
SB, Thakkar AV, Das AB.
Mol Biosyst 2017 May; 13(5):
830-840
Abstract:
Perturbations in molecular signaling pathways are a result
of genetic or epigenetic alterations, which may lead to
malignant transformation of cells. Despite cellular robustness,
specific genetic or epigenetic changes of any gene can trigger
a cascade of failures, which result in the malfunctioning of
cell signaling pathways and lead to cancer phenotypes. The
extent of cellular robustness has a link with the architecture
of the network such as feedback and feedforward loops.
Perturbation in components within feedback loops causes a
transition from a regulated to a persistently activated state
and results in uncontrolled cell growth. This work represents
the mathematical and quantitative modeling of ERK, PI3K/Akt,
and Wnt/?-catenin signaling crosstalk to show the dynamics of
signaling responses during genetic and epigenetic changes in
cancer. ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk
networks include both intra and inter-pathway feedback loops
which function in a controlled fashion in a healthy cell. Our
results show that cancerous perturbations of components such as
EGFR, Ras, B-Raf, PTEN, and components of the destruction
complex cause extreme fragility in the network and
constitutively activate inter-pathway positive feedback loops.
We observed that the aberrant signaling response due to the
failure of specific network components is transmitted
throughout the network via crosstalk, generating an additive
effect on cancer growth and proliferation.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000655.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000655 | BioModels
Project description:Padala2017- ERK, PI3K/Akt and Wnt signalling
network (normal)
Crosstalk model of the ERK, Wnt and Akt
signalling pathways under normal condition.
This model is described in the article:
Cancerous perturbations
within the ERK, PI3K/Akt, and Wnt/?-catenin signaling network
constitutively activate inter-pathway positive feedback
loops.
Padala RR, Karnawat R, Viswanathan
SB, Thakkar AV, Das AB.
Mol Biosyst 2017 May; 13(5):
830-840
Abstract:
Perturbations in molecular signaling pathways are a result
of genetic or epigenetic alterations, which may lead to
malignant transformation of cells. Despite cellular robustness,
specific genetic or epigenetic changes of any gene can trigger
a cascade of failures, which result in the malfunctioning of
cell signaling pathways and lead to cancer phenotypes. The
extent of cellular robustness has a link with the architecture
of the network such as feedback and feedforward loops.
Perturbation in components within feedback loops causes a
transition from a regulated to a persistently activated state
and results in uncontrolled cell growth. This work represents
the mathematical and quantitative modeling of ERK, PI3K/Akt,
and Wnt/?-catenin signaling crosstalk to show the dynamics of
signaling responses during genetic and epigenetic changes in
cancer. ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk
networks include both intra and inter-pathway feedback loops
which function in a controlled fashion in a healthy cell. Our
results show that cancerous perturbations of components such as
EGFR, Ras, B-Raf, PTEN, and components of the destruction
complex cause extreme fragility in the network and
constitutively activate inter-pathway positive feedback loops.
We observed that the aberrant signaling response due to the
failure of specific network components is transmitted
throughout the network via crosstalk, generating an additive
effect on cancer growth and proliferation.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000648.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000648 | BioModels